Top 5 best pills for diabetes - Endocrinology

Synthetic hypoglycemic oral antidiabetic agents are medications whose main function is to normalize blood glucose levels and alleviate the condition of patients with diabetes.

They achieve this in two ways: either they promote increased production of insulin by the pancreas, or they increase the sensitivity of tissues to this hormone. In addition, with such a diagnosis, additional medications are often prescribed to reduce the symptoms and consequences of the disease (to normalize blood pressure and weight, cleanse blood vessels, etc.).

Which tablets the attending physician prescribes depends on two factors: the type of diabetes and its clinical picture.

Tablets to lower blood sugar levels.

September 28, 2022
16058

4.5

Content

Types of diabetes
Causes of type 2 diabetes mellitus
How to choose diabetes pills
Top 5 diabetes pills
Diabetes
Siofor
Januvia
NovoNorm
Glucobay

To treat diabetes, it is not necessary to regularly inject insulin. In many cases, it is enough to simply lead a healthy lifestyle and take special medications. Let's figure out what types of diabetes there are and what pills doctors prescribe.

Diabetes mellitus is not one specific disease, but a group of diseases in which the metabolism in the body is disrupted (in particular, carbohydrate metabolism suffers).

Main

Twymeeg (imeglimin) is a new drug intended for the treatment of type 2 diabetes mellitus.
Imeglimin is the first representative of a completely new class of hypoglycemic drugs, characterized by the advantages of existing antidiabetic drugs. At the same time, imeglimin is devoid of serious negative side effects that come with all current medications without exception for the treatment of type 2 diabetes.

Twaymig, developed by the French company Poxel, was approved in Japan at the end of June 2022. Its commercial distribution in this country, as well as in China, South Korea and a number of countries in Southeast Asia, is carried out by the Japanese Sumitomo Dainippon Pharma.

The corresponding agreement between Poxel and Sumitomo Dainippon, concluded at the end of October 2022, stipulated that the latter would pay the former $42 million in advance, plus a potential $257 million as the project develops and sales of the finished drug, as well as a double-digit royalty from its implementation .

In February 2022, Roivant Sciences licensed imeglimin to market it in the United States, Europe and other countries outside of the Sumitomo Dainippon deal. For this, Poxel received an advance payment of $50 million and promises of future payments of up to $600 million plus royalties on sales. In November 2022, Metavant, which Royvant specially created for the development of imeglimin, returned the rights to the drug to Poxel due to a changed development strategy. Thus, the appearance of imeglimin in the West is still in question: Poxel clearly needs partners to conduct proper registration clinical trials.

According to industry forecasts, imeglimin is capable of achieving sales of over $3 billion a year, $600 million of which it will earn in Japan.

Types of diabetes

There are several types of diabetes.

Diabetes mellitus type 1.
Usually this disease develops at a young age (up to 30-35 years). A feature of this type of diabetes is insulin dependence. Symptoms of type 1 diabetes: increased appetite, but weight loss against this background, frequent urination, constant thirst. With this type of diabetes, carbohydrate metabolism is impaired, and the pancreas produces too little insulin.
Diabetes mellitus type 2.
This diabetes is non-insulin dependent. Most often, the disease develops in old age. Type 2 diabetes is often inherited. This kind of diabetes requires a special diet, physical activity (moderate) and strict adherence to the advice of your doctor.
Gestational diabetes.
This type of diabetes occurs in pregnant women and usually goes away after childbirth. Sometimes gestational diabetes can negatively affect the fetus or recur after a few years.
MODY-diabetes.
This kind of diabetes is rare; the disease occurs in 5% of diabetics. Develops at an early age. In MODY diabetes, a person has a very low need for insulin. The disease is considered an intermediate stage because it has features of the first two types of diabetes.

Treatment of diabetes depends on what caused it, how severe the disease is, what chronic diseases the person has, and what his age is. Tablets for diabetes, taking into account all the above factors, can only be prescribed by a doctor.

Causes of type 2 diabetes mellitus

There are certain factors that influence the occurrence of diabetes.

Some metabolic disorders in the body can increase the risk of disease. Among them:

presence of type 2 diabetes in close relatives;
obesity or overweight;
poor nutrition, an abundance of fatty or too carbohydrate foods in the diet;
lack of physical activity, sedentary lifestyle;
age factor;
high blood pressure;
impaired glucose tolerance (slight increase in blood sugar);
gestational diabetes in the past;
malnutrition during pregnancy.

In recent decades, due to changes in diet and physical activity, urbanization and the fast pace of life, the number of people with type 2 diabetes has increased sharply.

Types 1 and 2 diabetes: differences

Photos from open sources

Introduction

According to the decision of a working meeting of the Austrian Society of Urology (1994), the changes in the body of men that occur as a result of testosterone deficiency were proposed to be called “ partial androgen deficiency in older men
,” or
PADAM syndrome (partial androgen deficiency in aging males).
But in domestic medicine, they are increasingly inclined to the term “
age-related androgen deficiency
” or “
age-related hypogonadism
”.
Age-related androgen deficiency
is a condition caused by an age-related decrease in the secretion of testosterone in Leydig cells. Recently, there has been extraordinary interest in this problem, associated primarily with the widespread prevalence of age-related hypogonadism. It is generally accepted that as men age, there is a gradual decrease in the level of sex hormones, the onset of which occurs between 30 and 40 years. It is known that from 40 to 50 years old, approximately 7% of men suffer from hypogonadism, from 60 to 80 years old - 20%, over 80 years old - already 35%. According to the results of numerous studies conducted in the USA, androgen deficiency is observed in almost 5 million men, and only 5% of them receive hormone replacement therapy. In addition, it has been shown that a decrease or absence of sexual function affects not only the quality of life, but also affects its duration. It is known that the main male sex hormone, which is responsible for the health and activity of a man throughout his life, is testosterone. Together with dihydrotestosterone, androstenedione and their metabolites, it creates the appropriate tone of the central nervous system, subcortical formations, centers of the autonomic nervous system, supporting the functional activity of the gonads and providing copulatory function. Testosterone, along with androgenic effects, can also have a powerful anabolic effect on various human tissues. It is not in vain that at the National Congress “Man and Medicine” (2006, Moscow), corresponding member of the Russian Academy of Medical Sciences O.B. Laurent said: “Changes in testosterone levels affect adenopituitary regulation in general, causing not only a decrease in creative potential, changes in emotionality, sexual activity, but also negatively affects mineral and carbohydrate metabolism, so androgen deficiency is a problem that unites doctors of many specialties.” One of the pressing problems, often combined with age-related androgen deficiency in men, is the presence of various concomitant diseases and, above all, type 2 diabetes mellitus. Diabetes mellitus is one of the most common chronic diseases and has a strong upward trend. Every year the number of patients increases by 6-7%, and by now it affects 2-4% of the population. According to official statistics from the Ministry of Health of the Russian Federation, more than 2 million people suffer from diabetes in our country, and up to 200 thousand new cases of this disease are registered annually. Approximately 88% of cases are type 2 diabetes. And the prevalence of androgen deficiency in these patients reaches 65%. Thus, almost every second patient with sexual dysfunction also suffers from type 2 diabetes. The most accurate data regarding the prevalence of sexual dysfunction in the general population and among patients with diabetes were obtained from the results of the long-term Massachusetts Study of Aging Men (1994) and the work of Vinik and Richardson. The results of the first study showed a relationship between levels of free testosterone, sex steroid binding globulin (SHBG), and the risk of developing insulin resistance and type 2 diabetes. With a decrease in free testosterone levels by 1 standard deviation (3.9 ng/dL), the risk of developing type 2 diabetes is 1.58, and with a decrease in SHBG by 1 standard deviation (15.8 nmol/L) – 1.89. According to a second study, testosterone levels in patients with type 2 diabetes are 10-15% lower than in people of the same age groups without diabetes. In addition, androgen deficiency in men closely correlates with the presence of insulin resistance and hyperinsulinemia, and the administration of testosterone drugs leads to their reduction. It is interesting to note that, according to the Scientific Research Center of the Russian Academy of Medical Sciences, testosterone levels in patients with type 2 diabetes mellitus on insulin therapy remain within normal values, in contrast to patients receiving oral hypoglycemic drugs (Kalinchenko S.Yu., Kozlov G.I. ,2003). Therefore, the influence of insulin on testosterone production in Leydig cells cannot be excluded. It has also been convincingly proven that the low level of free and total testosterone observed in type 2 diabetes mellitus, especially in obese patients, is not associated with the degree of diabetes decompensation. It is believed that the first reason for the development of age-related hypogonadism is probably a decrease in the number of Leydig cells due to a deterioration in the blood supply to the testicular tissue and a decrease in the number of receptors for luteinizing hormone on their surface. The second possible cause of androgen deficiency in obese patients with type 2 diabetes mellitus is the abdominal type of obesity, usually combined with this disease. There is now extensive evidence supporting the relationship between visceral obesity and decreased testosterone levels in men. Adipose tissue has an “affinity” for steroid hormones. Aromatase in adipose tissue in increased quantities converts androgens (testosterone and androstenedione) into estrogens, which suppress the secretion of both gonadotropin-releasing hormone and luteinizing hormone, which leads to a decrease in blood testosterone levels. In addition, the cause of androgen deficiency in obesity is leptin produced by white adipose tissue, which stimulates the secretion of gonadotropin-releasing hormone. It is believed that some resistance of central structures to leptin in obese patients leads to disruption of the rhythm of gonadotropin-releasing hormone secretion, which may be another reason for the development of hypogonadotropic hypogonadism.

How to choose diabetes pills

The most important thing in treating diabetes is proper nutrition and moderate physical activity, giving up bad habits and controlling weight. In the initial stages of the disease, these measures are enough to keep blood sugar levels normal, but over time, as diabetes progresses, only such measures become insufficient. Some people with type 2 diabetes need to take medications to lower their sugar levels. If one remedy is not enough, the doctor may prescribe both tablets and insulin in parallel.

Most often, type 2 diabetes is treated with the following groups of drugs:

Metformin from the biguanide group reduces insulin resistance and helps the body properly consume its own insulin. All over the world, drugs from this group are used as the main drugs in the treatment of type 2 diabetes.
Sulfonylureas are stimulants for the pancreas to produce insulin. This group includes active ingredients such as gliclazide, glipizide, glimepiride, tolbutamide and glibenclamide. Read also: Popular drugs for lowering cholesterol Top 5 drugs for lowering cholesterol levels in the blood.

Top 5 diabetes pills

Let us remind you once again that only a doctor can choose the right drug to lower blood sugar levels. Often a combination of several drugs or even parallel insulin injections may be needed. Self-medication for diabetes is unacceptable, because only an experienced endocrinologist, having studied the results of your tests, can prescribe a certain drug and then adjust its dosage. Without the participation of a doctor, such treatment can cause serious complications, including hypoglycemia and coma. We have compiled a list of the most effective and commonly prescribed diabetes pills.

Clinical manifestations and diagnosis

Most clinical manifestations of testosterone deficiency are nonspecific. Very often, the only symptom of age-related androgen deficiency may be a decrease or loss of sexual desire (libido). Other sexual symptoms are also noted (deterioration in the quality and frequency of erections, especially at night, difficulty achieving orgasm, decreased intensity of achieved orgasm, decreased sensitivity of the penis), changes in the neuro-emotional status occur (decreased intellectual activity, creative productivity, increased fatigue, decreased mood , depression, insomnia), changes in bones, muscles, skin and adipose tissue (decreased strength and volume of muscle mass, decreased body hair, the appearance of wrinkles, decreased bone density, increased visceral fat). In addition, the man is worried about the feeling of heat - “hot flashes”, fluctuations in blood pressure during the day, dizziness, increased sweating, cardialgia. Among laboratory research methods, the leading place in clinical practice is occupied by the determination of the level of total testosterone in blood serum. The concentration of this hormone below 12 nmol/l (normal values are 13-33 nmol/l) indicates the presence of androgen deficiency. Although it should be noted that the most informative is to determine the level of free or biologically active testosterone. But, unfortunately, currently conducting this laboratory research is technically difficult. In this regard, if necessary (with severe clinical symptoms and normal concentrations of total testosterone), it is determined by a calculation method based on the ratio of the levels of total testosterone/sex hormone binding globulin. In addition to a specific examination, it is also advisable to perform a general blood test (when testosterone levels decrease, anemia may occur) and densitometry (androgen deficiency is one of the main causes of osteoporosis in men).

Diabetes

Diabeton tablets from the group of sulfonylurea derivatives can only be purchased with a prescription. The active ingredient of the drug - gliclazide - is released slowly after taking the tablet, therefore it gently reduces blood sugar levels. “Diabeton” is prescribed to those patients who monitor their diet, eat regularly and get enough carbohydrate foods. These tablets are prescribed for type 2 diabetes, when diet, physical activity and weight correction do not help reduce sugar. The drug has also proven itself well as a prevention of diabetic complications (strokes, heart attacks, kidney diseases, eye diseases, etc.).

Contraindications:

allergies to the components of the drug, type 1 diabetes, severe kidney and liver diseases, ketoacidosis, taking antifungal drugs, age under 18 years, pregnancy and breastfeeding. When a doctor prescribes these pills for diabetes, he must evaluate the patient’s age, his diet, the state of the cardiovascular system, the presence of problems with the thyroid gland and the functioning of the adrenal glands.

Diabeton MV

SERVIER (Servier), France

A drug to lower blood glucose levels.
Used for: Type 2 diabetes mellitus with insufficient effectiveness of diet therapy, physical activity and weight loss; - prevention of complications of diabetes mellitus: reducing the risk of microvascular (nephropathy, retinopathy) and macrovascular complications (myocardial infarction, stroke) in patients with type 2 diabetes mellitus through intensive glycemic control. from 140

5.0 1 review

1016

Like
Write a review

Drugs that can provoke hyperglycemia

Corticosteroids

Glucocorticosteroids can antagonize the action of insulin and stimulate gluconeogenesis, especially in the liver, leading to an overall increase in glucose production [1]. With normal carbohydrate metabolism, this property of steroids is not accompanied by changes in glycemia: the beta cells of the pancreas are able to produce sufficient amounts of insulin to compensate for excess glucose. However, in diabetes mellitus, when insulin levels are reduced and tissue sensitivity to it is impaired, the body is not able to neutralize the effect of steroids on glucose metabolism. Therefore, while taking corticosteroids with concomitant hyperglycemia in patients with diabetes or prediabetes (impaired glucose tolerance), blood glucose levels may increase and the need for insulin or oral antidiabetic drugs may increase [1, 2].

The severity of the hyperglycemic effect varies among corticosteroids, with prednisolone and dexamethasone having the most potent effects. However, there are limitations to systemic administration of most steroids [3].

Restrictions:

Prednisolone, methylprednisolone, dexamethasone and betamethasone are contraindicated for use in diabetes mellitus
Hydrocortisone is prohibited for decompensated severe diabetes
Triamcinolone is approved for disorders of carbohydrate metabolism, however, the instructions for use emphasize the likelihood of developing diabetes mellitus while taking the drug [3].

Atypical antipsychotic drugs

Drugs in this group are quite widely used to treat schizophrenia and more common mental disorders, such as recurrent depression. They can exhibit a number of serious side effects, including impaired glucose metabolism. Its severity can be so great that while taking antipsychotics, there is a possibility of developing diabetes mellitus or even diabetic ketoacidosis [1].

It is believed that hyperglycemia while taking antipsychotics develops due to changes in the regulation of glucose and insulin levels, as well as disorders of lipid metabolism. The ability of drugs in this group to stimulate appetite and promote weight gain plays a certain role. With increasing weight, the volume of adipose tissue sharply increases, which leads to a decrease in insulin sensitivity and, as a consequence, to the development of diabetes mellitus [4]. It is known that with every kilogram of excess weight, the risk of type 2 diabetes increases by 4.5% [4].

It should be noted that the severity of the negative effect of atypical antipsychotics on carbohydrate metabolism varies. Olanzapine is associated with the highest risk of impaired glycemia. Risperidone and quetiapine are considered “intermediate” risk drugs, and aripiprazole and ziprasidone have the least effect on carbohydrate metabolism [2, 4].

Restrictions

Olanzapine is prescribed with caution in diabetes mellitus. Other atypical antipsychotics, including clozapine, are used without restrictions according to the instructions [3].

Thiazide diuretics

Thiazide (hydrochlorothiazide) and thiazide-like diuretics are widely used to treat arterial hypertension, including in patients with diabetes mellitus. They are prescribed despite the fact that these drugs contribute to the development of hyperglycemia, and in some cases even induce the development of new cases of diabetes mellitus [1].

Hyperglycemia while taking diuretics of this group develops due to the implementation of several mechanisms. First, the drugs cause hypokalemia, which increases transport across beta cell membranes, leading to impaired insulin secretion. Secondly, against the background of their intake, the renin-angiotensin-aldosterone system is activated and, as a result, blood flow in the striated muscles worsens and glucose utilization decreases. This contributes to hyperglycemia and increased insulin resistance [1].

However, there is some good news. Firstly, the effect of drugs of this series on the level of glycemia is dose-dependent, and for the treatment of arterial hypertension they are used in low dosages. And secondly, the thiazide-like diuretic indapamide has virtually no negative effect on glucose metabolism, and its use in diabetes mellitus reduces the likelihood of hyperglycemia to zero [1].

Restrictions

Hydrochlorothiazide - contraindicated in diabetes mellitus
Chlorthalidone - contraindicated in severe forms of diabetes mellitus
Indapamide - used with restrictions for diabetes mellitus in the stage of decompensation. The importance of monitoring blood glucose concentrations in all patients with diabetes, especially in the presence of hypokalemia, is emphasized [3].

Statins

Statins are key drugs used to prevent cardiovascular diseases. Undoubtedly, they are prescribed for diabetes, despite their so-called diabetogenic effect. Research results indicate that statins can cause the development of diabetes. However, the hyperglycemic effect of statins is quite “modest”: for the development of one case of diabetes mellitus, it is necessary to treat 167 patients with rosuvastatin at a dose of 20 mg for 5 years [1].

The negative effect on glucose levels and the possibility of increased glycemia during use are already included in the instructions for the use of statins [1]. Unfortunately, this side effect is characteristic of the entire class of drugs, and there is no difference in the severity of the hyperglycemic effect among its different representatives.

The mechanism of development of the diabetogenic effect of statins is combined. The drugs suppress insulin secretion by reducing the sensitivity of beta cells to glucose and reduce insulin sensitivity in muscles. The diabetogenic effect of statins is dose dependent: the risk of developing diabetes increases with increasing dosages.

It is noteworthy that the likelihood of diabetes when taking lipid-lowering drugs of the statin group is not increased in all consumers. The risk of a hyperglycemic effect is much higher with increased blood glucose levels, increased triglycerides, obesity (BMI ≥30 kg/m2), hypertension and old age. The increased risk of statin-induced diabetes is also associated with a number of other factors, including the female gender of the patient [1].

Despite the proven diabetogenic effect, statins continue to be used in patients with diabetes, since it is obvious that the risk of developing diabetes while taking them is completely offset by the benefit - a significant reduction in the likelihood of developing cardiovascular diseases and complications.

Restrictions

There is no guidance on the use of statins for diabetes, but the instructions emphasize the possibility of developing type 2 diabetes mellitus while taking the drugs [3].

A nicotinic acid

Vitamin PP, or niacin, is involved in many redox reactions, the formation of enzymes, and the metabolism of lipids and carbohydrates in cells. The drug is converted in the body into nicotinamide, which is involved in the metabolism of fats, proteins, amino acids, purines, tissue respiration and biosynthesis processes.

The negative effect on glycemia is expressed in the ability to increase the level of plasma glucose and glycated hemoglobin due to the development of insulin resistance and a decrease in insulin secretion by pancreatic beta cells [1]. For a person suffering from diabetes, this effect can be critical.

Restrictions

If you have diabetes, it is prohibited to take nicotinic acid in high doses. It is also considered inappropriate to prescribe a drug for the correction of dyslipidemia in cases of impaired carbohydrate metabolism. The instructions also note that nicotinic acid can reduce the hypoglycemic effect of glucose-lowering drugs [3].

Siofor

You can buy Siofor tablets in different dosages, strictly according to your prescription. The active ingredient of Siofora is metformin. The drug belongs to the biguanide group and affects the uptake of glucose by cells. The drug is prescribed to people with type 2 diabetes (including those who are overweight). The drug is suitable for those who do not benefit from lifestyle changes. "Siofor" is used both as monotherapy and as part of a complex treatment of severe diabetes (together with other tablets or against the background of insulin injections). The drug is indicated for children over 10 years of age (as a single drug or in combination with insulin).

Contraindications:

ketoacidosis, intolerance to the drug components, serious kidney and liver diseases, pregnancy and breastfeeding, low-calorie diet. Also, Siofor should not be used simultaneously with contrast agents containing iodine.

Siofor

Berlin-Chemie/Menarini, Germany

- type 2 diabetes mellitus, especially in overweight patients with ineffective diet therapy and physical activity.
It can be used as monotherapy or in combination with other oral hypoglycemic drugs and insulin. from 208

1062

Like
Write a review

Insulin resistance and ways of its correction in type 2 diabetes mellitus

Insulin resistance is an insufficient biological response of cells to the action of insulin when its concentration in the blood is sufficient. The biological effects of insulin can be grouped into four groups:

very fast (seconds): hyperpolarization of cell membranes, changes in membrane transport of glucose and ions;
fast (minutes): activation or inhibition of enzymes, which leads to the predominance of anabolic processes (glycogenesis, lipogenesis and protein synthesis) and inhibition of catabolic processes;
slow (from minutes to hours): increased absorption of amino acids by cells, selective induction or repression of enzyme synthesis;
the slowest (from hours to days): mitogenesis and cell reproduction (DNA synthesis, gene transcription).

Thus, the concept of insulin resistance is not limited to parameters characterizing the metabolism of carbohydrates, but also includes changes in the metabolism of fats, proteins, endothelial function, gene expression, etc.

A number of diseases and physiological conditions can be identified that are accompanied by insulin resistance. The main ones are the following (M. I. Balabolkin, 2001):

physiological insulin resistance (puberty, pregnancy, diet rich in fat, night sleep);
metabolic (type 2 diabetes mellitus (DM), obesity, decompensation of type 1 DM, severe malnutrition, excessive alcohol intake);
endocrine (thyrotoxicosis, hypothyroidism, Cushing's syndrome, acromegaly, pheochromocytoma);
non-endocrine (essential hypertension, liver cirrhosis, rheumatoid arthritis, trauma, burns, sepsis, surgery).

The term “insulin resistance” should not be equated with the “insulin resistance syndrome” or “metabolic syndrome” described by G. Reaven (1988) and including: impaired glucose tolerance (or type 2 diabetes), arterial hypertension, hyperuricemia, hypercoagulability, microalbuminuria and some other systemic disorders.

Insulin carries out its biological action at the cellular level through the corresponding receptor. The insulin receptor is a protein consisting of two α and two β subunits. The α-subunit is located on the outer surface of the cell membrane, and insulin binds to it. The β subunit is a transmembrane protein and has tyrosine kinase activity, which is not observed in the absence of insulin. The attachment of insulin to the binding center on the α-subunits activates the enzyme, and this enzyme itself serves as a substrate, i.e., autophosphorylation of the β-subunit of the insulin receptor occurs at several tyrosine residues. Phosphorylation of the β-subunit, in turn, leads to a change in the substrate specificity of the enzyme: it is now able to phosphorylate other intracellular proteins—insulin receptor substrates (IRS). SIR-1, SIR-2, as well as some proteins of the STAT family (signal transducer and activator of transcription) are known. Phosphorylation of SIR leads to a pleiotropic response of the cell to the insulin signal. Laboratory mice lacking the CIR-1 gene exhibit insulin resistance and reduced tolerance during glucose loading. Insulin, mediated by SIR-1, activates phosphatidylinositol 3-kinase (PI-3-kinase). Activation of PI-3-kinase is the central link in the signaling pathway that stimulates the translocation of the glucose transporter GLUT-4 from the cytosol to the plasma membrane, and, consequently, the transmembrane transport of glucose into muscle and fat cells. PI-3-kinase inhibitors inhibit both basal and insulin-stimulated glucose uptake; in the latter case, the translocation of GLUT-4 to the membrane is inhibited (M. Reaven Gerald, 1999).

According to modern concepts, resistance of peripheral tissues (muscle, adipose and liver tissue) to the action of insulin underlies the pathogenesis of type 2 diabetes. Metabolic disorders observed due to insulin resistance in type 2 diabetes are presented in Table 1.

Insulin resistance of muscle tissue is the earliest and possibly genetically determined defect, which far precedes the clinical manifestation of type 2 diabetes. The results of studies using nuclear magnetic resonance spectroscopy (NMR) showed (GI Shulman, DL Rothman, 1990) that the synthesis of glycogen in muscles plays a fundamental role in insulin-mediated glucose uptake both in normal conditions and in type 2 diabetes, however, the impairment glycogen synthesis is secondary to defects in glucose transport and phosphorylation.

A decrease in insulin concentration in the liver is characterized by the absence of its inhibitory effect on the processes of gluconeogenesis, a decrease in glycogen synthesis, and activation of glycogenolysis processes, which ultimately leads to an increase in glucose production by the liver (RA DeFronzo, 1990).

Another link that plays a significant role in the development of hyperglycemia is the resistance of adipose tissue to the action of insulin, namely resistance to the antilipolytic action of insulin. As a result of uncontrolled lipid oxidation, large amounts of free fatty acids (FFA) are released. An increase in their level leads to inhibition of the processes of transport and phosphorylation of glucose and, as a consequence, to a decrease in glucose oxidation and glycogen synthesis in muscles (MM Hennes, E. Shrago, 1990). Thus, changes in fat metabolism, namely FFA metabolism, contribute to impaired tissue glucose utilization.

Excess FFA activates the processes of gluconeogenesis and affects the synthesis of lipoproteins in the liver, leading to increased formation of very low density lipoproteins (VLDL) and triglycerides, which is accompanied by a decrease in the level of high density lipoproteins (HDL) (RHUnger, 1995).

Long-term increases in FFA levels have a direct damaging effect on pancreatic β-cells, which is described as a lipotoxic effect, resulting in a decrease in the secretory capacity of pancreatic islet β-cells.

The state of insulin resistance and a high risk of developing type 2 diabetes is typical for individuals with a visceral rather than a peripheral distribution of fatty tissue. This may be due to the biochemical characteristics of visceral adipose tissue: it responds poorly to the antilipolytic effect of insulin. In visceral adipose tissue, an increase in the synthesis of tumor necrosis factor was noted, which reduces the activity of insulin receptor tyrosine kinase and phosphorylation of SIR proteins. Hypertrophy of adipocytes in the abdominal type of obesity leads to a change in the conformation of the insulin receptor molecule and disruption of its binding to insulin.

As long as the β-cells of the pancreas are able to produce sufficient amounts of insulin to compensate for these defects and maintain a state of hyperinsulinemia, hyperglycemia will be absent. However, when β-cell reserves are depleted, a state of relative insulin deficiency occurs, which is manifested by an increase in blood sugar levels and the manifestation of diabetes. As research results have shown (Levy et al., 1998), in patients with type 2 diabetes who are only on a diet, after 5–7 years from the onset of the disease, there is a significant decrease in β-cell function, while tissue sensitivity to insulin remains virtually unchanged . There is a lot of clinical evidence that hyperinsulinemia is an independent risk factor for the development of coronary heart disease both in individuals without type 2 diabetes and in patients with type 2 diabetes (S. Lebto et al., 2000).

Treatment tactics for type 2 diabetes should be aimed at normalizing the pathogenetic processes underlying the disease, i.e., reducing insulin resistance and improving β-cell function.

Currently, there are non-pharmacological and pharmacological methods for correcting insulin resistance. Non-pharmacological methods include a low-calorie diet aimed at reducing body weight and physical activity - the foundation on which the treatment of all patients with type 2 diabetes with insulin resistance is based. Weight loss can be achieved by following a low-calorie diet containing less than 30% fat, less than 10% saturated fat and more than 15 g/kcal fiber, as well as a regular exercise regimen.

Patients may be recommended regular moderate-intensity aerobic physical activity (hiking, swimming, cross-country skiing, cycling) lasting 30–45 minutes 3 to 5 times a week, as well as any feasible set of physical exercises (J. Eriksson, S. Taimela, 1997). Exercise stimulates insulin-independent glucose uptake, and the exercise-induced increase in glucose uptake is independent of insulin action. Moreover, during physical activity there is a paradoxical decrease in blood insulin levels. Muscle glucose uptake increases despite a drop in insulin levels, and exercise is accompanied by a shift of GLUT-4 from a different pool than under the action of insulin (NS Peirce, 1999).

During the onset of the disease, before the formation of a persistent decrease in the secretory function of pancreatic β-cells, especially with overweight or obesity, the drugs of choice are drugs that reduce insulin resistance of peripheral tissues. This group of drugs includes biguanides and thiazolidinediones (glitazones).

In Russia, as in all countries of the world, only metformin (Siofor, Glucophage, Gliformin) is used from the biguanide group.

The main mechanism of action of metformin is aimed at eliminating the production of glucose by the liver, as well as reducing insulin resistance in muscle and fat tissue. The drug has the ability to suppress gluconeogenesis by blocking the enzymes of this process in the liver. In the presence of insulin, biguanides increase peripheral glucose utilization by muscles by activating insulin receptor tyrosine kinase and the translocation of GLUT-4 and GLUT-1 in muscle cells. Biguanides increase the utilization of glucose by the intestines (increasing anaerobic glycolysis), which is manifested by a decrease in the level of glucose in the blood flowing from the intestines. Long-term use of metformin has a positive effect on lipid metabolism: it leads to a decrease in the level of cholesterol and triglycerides in the blood. The mechanism of action of metformin is antihyperglycemic, not hypoglycemic. The drug does not reduce blood glucose levels below its normal level - which is why there are no hypoglycemic conditions with metformin monotherapy. According to a number of authors, metformin has an anorectic effect. Patients receiving metformin experience a decrease in body weight, mainly due to a decrease in adipose tissue. The drug has also been proven to have a positive effect on the fibrinolytic properties of the blood due to the suppression of plasminogen activator inhibitor-1.

Results from a UK prospective study (UKPDS) showed that metformin use from the time of diagnosis reduced diabetes-related mortality by 42%, all-cause mortality by 36%, and diabetic complications by 32% (Lancet , 1998). The data obtained indicate that taking metformin significantly improves survival and reduces the risk of developing complications of type 2 diabetes. However, in the UKPDS study, the average daily dose of metformin (Glucophage) was 2000 mg or higher for most patients. It is the dose of 2000 mg/day that is the optimal daily dose at which the best control of blood sugar is observed.

The indication for the use of metformin is type 2 diabetes against the background of overweight or obesity, with unsatisfactory compensation of carbohydrate metabolism due to diet and physical activity.

The initial daily dose of metformin is 500 mg. After 1 week from the start of therapy, if there are no side effects, the dose of the drug is increased. The maximum daily dose of the drug is 3000 mg. Take the drug 2-3 times a day with meals, which is extremely important for maximum effectiveness. The duration of action of the drug is 8–12 hours.

Side effects of metformin include diarrhea, dyspeptic disorders, and a metallic taste in the mouth. Side effects usually disappear when the dose of the drug is reduced. Persistent diarrhea is a contraindication for discontinuation of the drug.

By inhibiting gluconeogenesis, biguanides contribute to an increase in the content of lactate, pyruvate, alanine (substances that are precursors of glucose in the process of gluconeogenesis), which in extremely rare cases can lead to the development of lactic acidosis. The risk of developing lactic acidosis increases when taking excessively large doses of the drug, in patients with renal and liver failure, as well as in the presence of conditions accompanied by tissue hypoxia.

Contraindications to the use of metformin are impaired renal function (a decrease in creatinine clearance below 50 ml/min or an increase in creatinine in the blood above 1.5 mmol/l), alcohol abuse, pregnancy, lactation, as well as hypoxic conditions of any nature: circulatory failure, respiratory failure , anemia, acute infections, acute myocardial infarction, shock, intravenous administration of iodinated contrast agents.

Studies in recent years have shown that the frequency of fatal increases in blood levels of lactic acid during long-term treatment with metformin is only 0.084 cases per 1000 patients per year. Compliance with contraindications to the prescription of metformin eliminates the risk of developing this complication.

Metformin can be used as monotherapy or in combination with sulfonylureas in patients with type 2 diabetes. The combination of biguanides and sulfonylurea derivatives is rational because it affects both parts of the pathogenesis of type 2 diabetes: it stimulates insulin secretion and improves tissue sensitivity to insulin. Currently, combination drugs with a fixed dose of metformin and sulfonylurea derivatives have been developed and are actively used:

glibomet (glibenclamide 2.5 mg + metformin 400 mg);
glucovance (glibenclamide 2.5 mg + metformin 500 mg; glibenclamide 5 mg + metformin 500 mg);
Metaglip (glipizide + metformin).

Combination drugs have a number of advantages. Due to lower therapeutic doses of combined drugs, their tolerability is better, and fewer side effects are observed than with monotherapy or with separate administration of combined drugs. When taking combined drugs, higher compliance is observed, since the quantity and frequency of taking tablet drugs is reduced. The use of combination drugs makes it possible to prescribe three-component therapy. The presence of different dosages of drugs included in the combined drug (as for the drug glucovance) makes it possible to more flexiblely select the optimal, desired ratio of the combined drugs. However, a strictly fixed dose of drugs also causes a number of difficulties when it is necessary to change the dose of only one of the combined drugs.

Also, in patients with type 2 diabetes, metformin can be used in combination with insulin in cases of severe insulin resistance, which can improve compensation of carbohydrate metabolism.

Glitazones (sensitizers, i.e., agents that increase insulin sensitivity) represent a new class of drugs that have proven effective in the treatment of type 2 diabetes (J. Clifford, Bailey et al., 2001). Medicines in this group (pioglitazone, rosiglitazone) are synthetic ligands of nuclear peroxisome proliferator-activated receptor γ-receptors - PPARγ (peroxisome proliferator-activated receptor). The nuclear receptor PPARγ belongs to the family of nuclear hormonal receptors that play the role of transcription factors. The PPARγ receptor is predominantly expressed in fat cells and monocytes, less so in skeletal muscles, liver, and kidneys. Several isoforms of PPAR are known: PPARα, PPARγ (subtypes 1, 2) and PPARβ/PPARδ.

Activation of PPARγ changes the expression of genes involved in metabolic processes such as adipogenesis, insulin signal transmission, and glucose transport (Y. Miyazaki et al., 2001), which leads to a decrease in tissue resistance to the action of insulin in target cells. In adipose tissue, the action of glitazones leads to inhibition of lipolysis processes and the accumulation of triglycerides, which results in a decrease in the level of FFAs in the blood. In turn, a decrease in the level of FFA in plasma enhances the processes of glucose uptake by muscles and reduces gluconeogenesis. Since FFAs have a lipotoxic effect on β-cells, their reduction improves the function of the latter.

Glitazones are able to increase the expression and translocation of the glucose transporter GLUT4 on the surface of the adipocyte in response to the action of insulin, which enhances the utilization of glucose by adipose tissue. Glitazones influence the differentiation of preadipocytes, which leads to an increase in the proportion of smaller, but more insulin-sensitive cells. In vivo and in vitro, glitazones reduce leptin expression, thereby indirectly affecting adipose tissue mass (BM Spiegelman, 1998), and also promote the differentiation of brown adipose tissue.

Glitazones improve glucose utilization in muscles. As is known, in patients with type 2 diabetes there is a disturbance in the insulin-stimulated activity of the insulin receptor PI-3-kinase in muscles. In a comparative study, it was shown that during therapy with troglitazone, insulin-stimulated PI-3-kinase activity increased almost 3-fold. No changes in the activity of this enzyme were observed during metformin therapy (Yoshinori Miyazaki et al., 2003).

The results of laboratory studies suggested that glitazones (rosiglitazone) have a protective effect on β-cells, preventing the death of β-cells by enhancing their proliferation (P. Beales et al., 2000).

The action of glitazones, aimed at overcoming insulin resistance and improving β-cell function, leads not only to the maintenance of satisfactory glycemic control, but also prevents disease progression, further decline in β-cell function and progression of macrovascular complications. By affecting virtually all components of the metabolic syndrome, glitazones potentially reduce the risk of developing cardiovascular diseases.

PPARγ receptors are present in all cells of the vascular wall and involved in the development of atherosclerosis: endothelial cells, vascular smooth muscle cells (VSM), monocytes and macrophages. PPARγ ligands inhibit differentiation, proliferation and migration of all types of cells. PPARγ ligands inhibit the growth and migration of VSM cells by arresting the cell cycle in the G1 phase. They also inhibit two processes required for VSM cell movement: chemoattractant-induced migration and matrix metalloproteinase production. In addition to inhibiting monocyte chemotaxis protein (MCP)-1-induced monocyte migration, PPARγ ligands inhibit the expression of adhesion molecules in endothelial cells, resulting in decreased monocyte adhesion to endothelial cells and decreased inflammatory effects of macrophages (A. Greenberg et al., 2001).

Currently, two drugs from the group of thiazolidinediones are registered and approved for use: pioglitazone (Actos) and rosiglitazone (Avandia).

The indication for the use of glitazones as monotherapy is newly diagnosed type 2 diabetes with signs of insulin resistance with ineffective diet and exercise regimen. Glitazones are indicated as combination therapy in the absence of adequate glycemic control when taking metformin or sulfonylurea derivatives. A triple combination (glitazones, metformin and sulfonylureas) can also be used to improve glycemic control.

Januvia

These tablets from the gliptin group are sold exclusively by prescription. The active substance of the drug is sitagliptin. Januvia is used in combination therapy: together with metformin or with insulin injections. The dosage of the drug is selected very carefully, only after collecting all the data on the patient’s health. Januvia tablets are prescribed to lower sugar levels while following a diet and physical activity. In combination with other means, if lifestyle changes have not shown positive results.

Contraindications:

age under 18 years, type 1 diabetes, ketoacidosis, pregnancy and breastfeeding. The drug is prescribed with caution to people with kidney disease, pancreatitis and while taking other medications.

Januvia

Merck Sharp and Dome, Netherlands

Monotherapy: as an adjunct to diet and exercise to improve glycemic control in type 2 diabetes mellitus. Combination therapy: in type 2 diabetes mellitus to improve glycemic control in combination with metformin or a PPAR-γ agonist (eg, thiazolidinedione) when diet and physical activity in combination with monotherapy with the listed drugs does not lead to adequate glycemic control.
from 1429

673

Like
Write a review

"Tvaymig": effectiveness and safety of imeglimin

To evaluate the effectiveness and safety of imeglimin in the treatment of type 2 diabetes mellitus, the TIMES clinical program consisted of three phase III pivotal studies involving over a thousand Japanese patients:

TIMES 1 (JapicCTI-173769): 24-week clinical trial (randomized, double-blind, placebo-controlled, multicenter) testing imeglimine alone;

TIMES 2 (JapicCTI-173782): A 52-week clinical trial (randomized, open-label, placebo-controlled, multicenter) examining imeglimin alone or in combination with other antidiabetic agents: sulfonylureas, glinides, metformin, alpha-glucosidase inhibitors, glitazones , DPP4 inhibitors, GLP-1R agonists, SGLT2 inhibitors;

TIMES 3 (JapicCTI-183846): A 16-week clinical trial (randomized, double-blind, placebo-controlled, multicenter) followed by a 36-week open-label period testing the addition of imeglimine to insulin therapy.

TIMES 1

The TIMES 1 clinical trial recruited patients (n=212) aged 20 years or older with type 2 diabetes mellitus following diet and exercise. The initial level of glycated hemoglobin (HbA1c) was in the range of 7.0–10%.

Participants were assigned to receive 1000 mg of imeglimine twice daily or a placebo.

After 24 weeks of treatment, HbA1c levels in the imeglimin group decreased by an average of 0.72% (95% CI: −0.86 - −0.58) versus an increase of 0.15% (95% CI: 0.01 - 0.29) in the placebo group: the difference was −0.87% (95% CI: −1.04 - −0.69; p<0.0001).

35.8% of patients receiving imeglimin reached the target HbA1c level below 7%, versus 7.5% in the control group (p<0.0001).

Among patients with previously untreated diabetes, HbA1c levels fell by an average of 0.81% (95% CI: −0.96 to −0.67) versus an increase of 0.06% (95% CI: −0.08 - 0.20): the difference was equal to -0.87% (95% CI: -1.07 - -0.67; p<0.0001). Among patients who were previously treated for diabetes, HbA1c levels decreased by an average of 0.51% (95% CI: −0.73 - −0.29) versus 0.33% (95% CI: 0.09 - 0.56): the difference was −0.84% (95% CI: −1.16 - −0.52; p<0.0001).

The absolute reduction in HbA1c levels was greater among patients who had not previously adhered to diabetes pharmacotherapy. Perhaps imeglimin is better suited to this category of patients due to its ability to improve glucose-stimulated insulin secretion without too much death of beta cells.

Other clinical outcomes are as follows:

Fasting plasma glucose (FPG): change of −0.31 mmol/L in the imeglimine group versus +0.71 mmol/L in the placebo group (p<0.0001).

Proinsulin to fasting insulin ratio: change -0.0138 versus +0.0036 (p=0.0579). An increase in this ratio reflects beta cell dysfunction associated with the onset and progression of type 2 diabetes.

Fasting proinsulin to C-peptide ratio: change -0.0003 versus +0.0002 (p=0.0012). An increase in this ratio is considered the best indicator of impaired beta cell status, since C-peptide does not undergo hepatic clearance, that is, its concentration is less dependent on insulin resistance.

Quantitative Insulin Sensitivity Control Index (QUICKI): change +0.0017 versus −0.0076 (p=0.0050). The lower this indicator, determined by the inverse sum of the logarithms of insulin and fasting glucose, the greater the insulin resistance.

Insulin resistance index according to homeostasis model assessment (HOMA-IR): change by +0.1961 versus +0.1321 (p=0.7325).

Beta cell function index according to homeostasis model assessment (HOMA-β): change by +3.5276 versus −2.7121 (p=0.0002).

Total cholesterol levels increased by 3.3% in the imeglimin group compared to the placebo group (p=0.0439), and low-density lipoprotein (LDL) cholesterol levels increased by 7.2% (p=0.0051). The differences were not clinically significant.

The safety profile of imeglimin was favorable. The proportions of subjects experiencing adverse events were similar in the drug and placebo groups. There were no serious adverse reactions that were related to treatment. Positive tolerability of imeglimin has been documented: very rare ailments from the gastrointestinal tract were of mild severity. The administration of imeglimin did not lead to an increase in the incidence of hypoglycemia: although imeglimin potentiates beta cell function and insulin secretion, this compound causes insulin secretion only in response to glucose.

TIMES 2

The TIMES 2 clinical trial recruited patients (n=714) aged 20 years or older with type 2 diabetes mellitus. The initial HbA1c level was in the range of 7.0–10% or 7.5–10.5%, respectively, in the case of monotherapy or combination treatment.

Participants were prescribed 1000 mg of imeglimine twice a day or it along with other antidiabetic drugs.

After 52 weeks of treatment, the results were as follows:

monoadministration of imeglimin reduced HbA1c levels by 0.46% (95% CI: −0.59 - −0.33);

combination of imeglimin with DPP4 inhibitors: −0.92% (95% CI: −1.14 - −0.71);

combination of imeglimin with glitazones: −0.88% (95% CI: −1.10 - −0.67);

combination of imeglimin with alpha-glucosidase inhibitors: −0.85% (95% CI: −1.03 - −0.67);

combination of imeglimin with glinides: −0.70% (95% CI: −0.95 - −0.45);

combination of imeglimin with metformin: −0.67% (95% CI: −0.86 - −0.48);

combination of imeglimine with SGLT2 inhibitors: −0.57% (95% CI: −0.71 - −0.43);

combination of imeglimine with sulfonylurea derivatives: −0.56% (95% CI: −0.71 - −0.40);

combination of imeglimin with GLP-1R agonists: −0.12% (95% CI: −0.39 - −0.15).

TIMES 3

The TIMES 3 clinical trial included patients (n=208) aged 20 years and older with type 2 diabetes mellitus who adhered to insulin therapy. Baseline HbA1c levels ranged from 7.5–11.0%.

During the double-blind 16-week treatment period, participants were prescribed 1000 mg of imeglimine twice daily or placebo on their usual insulin therapy. In the drug group, there was a decrease in HbA1c levels by an average of 0.60% (95% CI: −0.80 - −0.40) relative to the control group (p<0.0001).

In the subsequent open-label 36-week treatment period, all subjects received the above dose of imeglimine. Those patients who initially followed the course of imeglimin showed a decrease in HbA1c levels by an average of 0.64% relative to baseline. In patients who were prescribed imeglimin after placebo, the drop in HbA1c levels averaged 0.54% compared to baseline.

NovoNorm

This is a prescription drug for diabetes from the group of glinides, the main active ingredient of which is repaglinide. Effectively reduces blood sugar against the background of metabolic disorders in people with diabetes. NovoNorm is prescribed for type 2 diabetes, when diet and exercise are ineffective. Also, taking these tablets is indicated when treatment with metformin is low (in this case, combination treatment is indicated).

Contraindications:

type 1 diabetes, ketoacidosis, surgical interventions, conditions requiring insulin, pregnancy and breastfeeding, intolerance to drug components, age under 18 years. Diabetes tablets should be used with caution in those who have liver and kidney diseases, and also have an unhealthy diet.

New norm

Novo Nordisk (Novo Nordisk), Denmark

NovoNorm is a short-acting oral hypoglycemic drug. Rapidly reduces blood glucose levels, stimulating the release of insulin by the pancreas. Binds on the β-cell membrane to a receptor protein specific for this drug. This leads to blocking of ATP-dependent potassium channels and depolarization of the cell membrane, which in turn promotes the opening of calcium channels. The entry of calcium into the β-cell stimulates the secretion of insulin.
from 139

962

Like
Write a review

Drugs that may cause hypoglycemia

Beta blockers

Members of this group may attenuate β2-adrenergic receptor-mediated glucose release from the liver in response to hypoglycemia. Along with this, beta-blockers “lubricate” the clinical picture, reducing the severity of adrenergic-mediated symptoms of a critical drop in sugar levels, with the exception of sweating. Let us recall that adrenergic clinical manifestations of hypoglycemia include cardiac arrhythmias, agitation, anxiety, muscle tremors, pallor of the skin and increased blood pressure [5].

Thus, when taking beta-blockers, hypoglycemia may be longer lasting and also less noticeable, which is doubly dangerous. Therefore, ideally, for concomitant diabetes mellitus, only selective β1-blockers, for example, bisoprolol, should be used [5].

Restrictions

Non-selective beta blockers - propranolol and sotalol - can be used with caution while monitoring blood glucose levels.
Selective β1-blockers (bisoprolol, metoprolol, carvedilol) are also used with restrictions, that is, when controlling blood glucose levels [3].

GLUCOMETER CONTOUR PLUS ONE - LOOK AT DIABETES IN A NEW WORLD!

For people with diabetes who want to effectively manage their disease

The smart system of the Contour Plus One Glucose Meter and the free Contour Diabetes App helps you better manage your diabetes*
The Smart Backlight feature helps you quickly interpret results and receive prompts for action.
Data on blood glucose levels are automatically included in the Application with the ability to upload reports - no need to keep a paper diary anymore
The system helps take care of loved ones using remote control

THERE ARE CONTRAINDICATIONS. BEFORE USE, YOU MUST READ THE INSTRUCTIONS

No. FSZ 2008/02237 dated 12/18/2018, No. RZN 2015/2584 dated 12/17/2018.

* Freckmann G. et all. User Performance Evaluation of Four Blood Glucose Monitoring Systems Applying ISO 15197:2013 Accuracy Criteria and calculation of Insulin Dosing Errors. Diabetes Ther. 2018 Apr; 9(2):683–697

Antibacterial agents of the fluoroquinolone series

Fluoroquinolones are closely associated with dysregulation of glucose and insulin levels. Hypoglycemia is considered a class-specific undesirable effect of drugs in this group [1]. Most reports of the development of hypoglycemia were recorded during treatment with gatifloxacion, although it is believed that all representatives of fluoroquinolones are capable of inducing a drop in sugar levels [5].

The hypoglycemic effect of gatifloxacin is associated with an increase in insulin levels and a decrease in blood glucose. Other fluoroquinolones (ciprofloxacin, levofloxacin, moxifloxacin, norfloxacin, ofloxacin), according to some data, are also capable of lowering plasma sugar levels.

The exact mechanism of the hypoglycemic effect of drugs in this group is still unknown. But it is obvious that fluoroquinolones can potentiate the effect of various hypoglycemic agents, including sulfonylureas. This effect is independent of the dose and manifests itself within the first three days of antibiotic therapy, provoking asymptomatic episodes of hypoglycemia. If fluoroquinolone treatment is continued for more than 3 days, severe hypoglycemia may occur, requiring hospitalization [5].

Restrictions

Gatifloxacin is contraindicated in diabetes mellitus
Other fluoroquinolones can be used with caution, with regular monitoring of blood sugar levels [3].

Salicylates

NSAID salicylates, the most prominent representative of which is acetylsalicylic acid, exhibit a hypoglycemic effect, which is most pronounced when these drugs are used together with drugs to lower blood sugar levels. Hypoglycemia develops due to the ability of salicylates to increase insulin secretion (especially in patients with type 2 diabetes mellitus) and increase tissue sensitivity to insulin. In addition, drugs in this group displace sulfonylurea from binding to proteins and at the same time block its excretion by the kidneys [5]. This mechanism explains the ability of salicylates to increase the effect of hypoglycemic drugs.

Restrictions

The instructions for use of acetylsalicylic acid emphasize its ability to enhance the hypoglycemic effect of glucose-lowering drugs, which affects the dosage of the latter.

Glucobay

Prescription tablets "Glucobay" are an alpha-glucosidase inhibitor, the active substance of the drug is acarbose. Glucobay is prescribed for type 2 diabetes while following a diet. The drug perfectly lowers blood sugar levels.

Contraindications:

gastrointestinal diseases (ulcers, flatulence, intestinal obstruction, malabsorption of nutrients), severe kidney disease, pregnancy and breastfeeding, intolerance to the components of the drug. Glucobay should be taken with caution against the background of infectious diseases, at elevated temperatures, after operations and injuries. In the first six months of taking diabetes pills, it is important to monitor your liver function.

Glucobay

Bayer AG, Germany

Glucobay is a hypoglycemic agent for oral use.
Indicated for the treatment of type 2 diabetes mellitus in combination with diet. The medication is recommended for people with a predisposition to developing diabetes, in combination with exercise and diet. from 528

5.0 1 review

735

Like
Write a review

Auxiliary tablets

Diabetes mellitus of any type is characterized not only by a pathological increase in blood glucose. The disease is accompanied by a number of symptoms that worsen the patient's quality of life. In addition, over time, improper functioning of the pancreas and high sugar levels affect the functioning of many internal organs and provoke the development of complications.

Therefore, the goal of therapy is not only to normalize blood counts, but also to improve well-being and minimize undesirable consequences. In this regard, depending on the patient’s health condition, the doctor additionally prescribes tablets of various pharmacological effects.

Enzyme preparations

For diabetes of various types, take pills for the pancreas, the functioning of which is impaired. They improve its enzymatic function, replenish the deficiency of amylase (for the breakdown of carbohydrates), protease (proteins) and lipase (fats). Here is a list of enzyme preparations that a doctor can prescribe for diabetics in this group:

Abomin;
Actovegin;
Betaine;
Wobenzym;
Digestal;
Creon;
Mezim;
Pangrol;
Panzinorm;
Pancreatin;
Pezital;
Festal;
Phlogenzyme;
Enzistal;
herbal enzyme tablets: Solizim, Somilase, Unienzyme.

Tablets for the pancreas
As a result of correct and regular use of enzyme preparations, not only the functioning of the pancreas improves, but also digestion and metabolism.