Pharmacy No. 84. Delivery of medicines to your home and office.

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Trajenta, 30 pcs., 5 mg, film-coated tablets

The pharmacokinetics of linagliptin have been extensively studied when used in healthy volunteers and patients with type 2 diabetes mellitus. In healthy volunteers, after taking linagliptin at a dose of 5 mg, it was rapidly absorbed, the Cmax of linagliptin in plasma was reached after 1.5 hours.

The effective T1/2 after repeated doses of linagliptin at a dose of 5 mg is approximately 12 hours. When taking linagliptin at a dose of 5 mg 1 time per day, steady-state plasma concentrations of linagliptin are achieved after the third dose.

The pharmacokinetics of linagliptin in healthy volunteers and patients with type 2 diabetes mellitus were generally similar.

Suction.

The absolute bioavailability of linagliptin is approximately 30%.
Taking linagliptin with a high-fat meal does not have a clinically significant effect on pharmacokinetics. In vitro
studies have shown that linagliptin is a substrate for P-gp and the CYP3A4 isoenzyme. Ritonavir, as a potential inhibitor of P-gp and the CYP3A4 isoenzyme, may double the AUC value. Rifampin, as a potential inducer of P-gp and the CYP3A4 isoenzyme, may reduce the AUC value during steady-state pharmacokinetics.

Distribution.

Vd after a single intravenous administration of linagliptin at a dose of 5 mg to healthy volunteers is approximately 1.11 L, indicating extensive tissue distribution. The binding of linagliptin to plasma proteins depends on its concentration and is about 99% at a concentration of 1 nmol/l, and 75–89% at a concentration of more than 30 nmol/l, which reflects the saturation of the binding of linagliptin to DPP-4 as its concentration increases. At high concentrations, when complete saturation of DPP-4 occurs, 70–80% of linagliptin is bound to other plasma proteins (not DPP-4), and 30–20% of linagliptin is in the plasma in an unbound state.

Metabolism.

Approximately 5% of linagliptin is excreted by the kidneys. A small portion of linagliptin is metabolized. Metabolism plays a minor role in the elimination of linagliptin. There is one known major metabolite of linagliptin, which has no pharmacological activity.

Excretion.

The predominant route of elimination is through the intestines. 4 days after oral administration of [14C] labeled linagliptin in healthy volunteers, approximately 85% of the dose was excreted (80% intestinal and 5% renal) with a creatinine Cl of approximately 70 ml/min.

Pharmacokinetics in special groups of patients

Kidney failure.

In patients with mild renal impairment (Cl creatinine 50 to <80 mL/min), steady-state exposure to linagliptin was comparable to exposure in healthy subjects. In moderate renal impairment (creatinine Cl 30 to <50 ml/min), a slight increase in exposure was observed (approximately 1.7 times compared with healthy subjects). Exposure to linagliptin in patients with type 2 diabetes mellitus and severe renal impairment (Cl creatinine <30 mL/min) was increased approximately 1.4-fold compared with patients with diabetes mellitus and normal renal function. Modeling of linagliptin AUC values in patients with end-stage renal disease showed that exposure in these cases was comparable to exposure in patients with moderate or severe renal impairment. The use of hemodialysis or peritoneal dialysis is not expected to eliminate linagliptin to a therapeutically significant extent. Therefore, no changes in linagliptin dosage are required in patients with any degree of renal impairment.

Liver failure.

In patients with mild, moderate, and severe hepatic impairment (Child-Pugh classification), the mean AUC and Cmax values of linagliptin after multiple doses of 5 mg were similar to those in matched healthy subjects. No dosage changes are required for linagliptin in patients with mild, moderate or severe hepatic impairment.

BMI.

No changes in linagliptin dosage are required based on BMI.

Floor.

No changes in linagliptin dosing are required depending on gender.

Elderly patients.

No age-related dosing changes for linagliptin are required as age did not have a clinically significant effect on the pharmacokinetics of linagliptin in a population pharmacokinetic analysis performed in clinical studies. Plasma concentrations of linagliptin were comparable in both older patients (age 65–80 years) and younger patients.

Children.

The pharmacokinetics of linagliptin in children has not been studied.

Race.

There are no changes in linagliptin dosing based on race. Race did not significantly influence linagliptin plasma concentrations in a combined analysis of pharmacokinetic data obtained from Caucasian, Hispanic, African American, and Asian patients. In addition, the pharmacokinetic characteristics of linagliptin were similar in special studies conducted in healthy Caucasian volunteers and residents of Japan and China, as well as in African-American patients with type 2 diabetes mellitus.

Trajenta®

In vitro assessment of drug interactions

Linagliptin is a weak competitive inhibitor of the CYP3A4 isoenzyme.

Linagliptin does not inhibit other CYP isoenzymes and is not an inducer.

Linagliptin is a substrate for P-glycoprotein and inhibits to a small extent P-glycoprotein-mediated transport of digoxin.

In vivo assessment of drug interactions

Linagliptin does not have a clinically significant effect on the pharmacokinetics of metformin, glibenclamide, simvastatin, pioglitazone, warfarin, digoxin and oral contraceptives, which has been proven in vivo, and is based on the low ability of linagliptin to lead to drug interactions with substrates for CYP3A4, CYP2C9, CYP2C8, P-glycoprotein and transport molecules of organic cations.

Metformin.

The combined use of metformin (multiple daily doses of 850 mg 3 times/day) and linagliptin at a dose of 10 mg 1 time/day (above the therapeutic dose) in healthy volunteers did not lead to clinically significant changes in the pharmacokinetics of linagliptin or metformin. Thus, linagliptin is not an inhibitor of organic cation transport.

Sulfonylurea derivatives.

The pharmacokinetics of linagliptin (5 mg) did not change when combined with glibenclamide (single dose of glyburide 1.75 mg) and repeated oral administration of linagliptin (5 mg each). However, there was a clinically insignificant decrease in the AUC and Cmax values of glibenclamide by 14%. Because glibenclamide is metabolized primarily by CYP2C9, these data also support the conclusion that linagliptin is not a CYP2C9 inhibitor. Clinically significant interactions are not expected with other sulfonylureas (for example, glipizide and glimepiride), which, like glibenclamide, are mainly metabolized by CYP2C9.

Thiazolidinediones.

Co-administration of multiple doses of linagliptin 10 mg/day (above the therapeutic dose) and pioglitazone 45 mg/day (multiple doses), which is a substrate for CYP2C8 and CYP3A4, did not have a clinically significant effect on the pharmacokinetics of linagliptin or pioglitazone, or the active metabolites of pioglitazone. . This indicates that linagliptin in vivo is not an inhibitor of CYP2C8-mediated metabolism and supports the conclusion that linagliptin does not have a significant inhibitory effect on CYP3A4 in vivo.

Ritonavir.

Co-administration of linagliptin (single dose 5 mg orally) and ritonavir (multiple doses of 200 mg orally), an active inhibitor of P-glycoprotein and the CYP3A4 isoenzyme, increased the AUC and Cmax values of linagliptin by approximately 2-fold and 3-fold, respectively. However, these changes in linagliptin pharmacokinetics were not considered significant. Therefore, clinically significant interactions with other P-gp and CYP3A4 inhibitors are not expected and no dose adjustment is required.

Rifampicin.

Repeated co-administration of linagliptin and rifampicin, an active inducer of P-glycoprotein and the CYP3A4 isoenzyme, led to a decrease in the AUC and Cmax values of linagliptin by 39.6% and 43.8%, respectively, and to a decrease in the inhibition of basal dipeptidyl peptidase-4 activity by approximately 30%. Thus, the clinical efficacy of linagliptin when used in combination with active P-glycoprotein inducers is expected to be maintained, although it may not be fully realized.

Digoxin.

Combined repeated use of linagliptin (5 mg/day) and digoxin (0.25 mg/day) in healthy volunteers did not affect the pharmacokinetics of digoxin. Thus, linagliptin is not an inhibitor of P-glycoprotein-mediated transport in vivo.

Warfarin.

Linagliptin, administered repeatedly at a dose of 5 mg/day, did not change the pharmacokinetics of warfarin, which is a substrate for CYP2C9, indicating that linagliptin does not have the ability to inhibit CYP2C9.

Simvastatin.

Linagliptin, administered repeatedly to healthy volunteers at a dose of 10 mg/day (above the therapeutic dose), had minimal effect on the pharmacokinetic parameters of simvastatin, which is a sensitive substrate for CYP3A4. After taking linagliptin at a dose of 10 mg together with simvastatin, used at a daily dose of 40 mg for 6 days, the AUC value of simvastatin increased by 34%, and the Cmax value increased by 10%. Thus, linagliptin is a weak inhibitor of CYP3A4-mediated metabolism. Dose changes when taken concomitantly with drugs that are metabolized by CYP3A4 are considered inappropriate.

Oral contraceptives.

Co-administration of linagliptin at a dose of 5 mg with levonorgestrel or ethinyl estradiol did not change the pharmacokinetics of these drugs.

Description of the drug TRAZHENTA® (TRAZHENTA)

The pharmacokinetics of linagliptin have been extensively studied in healthy volunteers and in patients with type 2 diabetes mellitus. In healthy volunteers, after taking linagliptin at a dose of 5 mg, it was rapidly absorbed, the Cmax of linagliptin in plasma was reached after 1.5 hours.

The concentration of linagliptin in plasma decreases in three phases. Terminal T1/2 is long, more than 100 hours, which is mainly due to the stable binding of linagliptin to the DPP-4 enzyme, however, because the relationship is reversible, accumulation of linagliptin does not occur. The effective T1/2 after repeated doses of linagliptin at a dose of 5 mg is approximately 12 hours. When taking linagliptin at a dose of 5 mg 1 time / day, Css of linagliptin in plasma are achieved after the third dose.

The pharmacokinetics of linagliptin in healthy volunteers and in patients with type 2 diabetes mellitus was generally similar.

The absolute bioavailability of linagliptin is approximately 30%. Taking linagliptin with a high-fat meal does not have a clinically significant effect on pharmacokinetics. In vitro studies have shown that linagliptin is a substrate for P-glycoprotein and the CYP3A4 isoenzyme. Ritonavir, as a potential inhibitor of P-glycoprotein and the CYP3A4 isoenzyme, may double the AUC value. Rifampicin, as a potential inducer of P-glycoprotein and the CYP3A4 isoenzyme, may reduce the AUC value during the period of equilibrium pharmacokinetics.

Vd after a single intravenous administration of linagliptin at a dose of 5 mg to healthy volunteers is approximately 1110 L, indicating intensive tissue distribution. The binding of linagliptin to plasma proteins depends on its concentration and is about 99% at a concentration of 1 nmol/l, and 75-89% at a concentration of more than 30 nmol/l, which reflects the saturation of the binding of linagliptin to DPP-4 as its concentration increases. At high concentrations, when complete saturation of DPP-4 occurs, 70-80% of linagliptin is bound to other plasma proteins (not DPP-4), and 30-20% of linagliptin is in the plasma in an unbound state.

The predominant route of elimination is through the intestines. 4 days after oral administration of [14C] labeled linagliptin in healthy volunteers, approximately 85% of the dose was excreted (80% intestinal and 5% urinary) with a clearance clearance of approximately 70 ml/min.

Linagliptin (Linagliptinum)

Metformin. The combined use of metformin (multiple daily doses of 850 mg 3 times a day) and linagliptin at a dose of 10 mg 1 time per day (above the therapeutic dose) in healthy volunteers did not lead to clinically significant changes in the pharmacokinetics of linagliptin or metformin. Thus, linagliptin is not an inhibitor of organic cation transport.

Sulfonylurea derivatives. The pharmacokinetics of linagliptin (5 mg) did not change when combined with glibenclamide (single dose 1.75 mg) and repeated oral administration of linagliptin (5 mg each). However, there was a clinically insignificant decrease in the AUC and Cmax values of glibenclamide by 14%. Because glibenclamide is metabolized primarily by CYP2C9, these data also support the conclusion that linagliptin is not a CYP2C9 inhibitor. Clinically significant interactions are not expected with other sulfonylureas (for example, glipizide and glimepiride), which, like glibenclamide, are mainly metabolized by CYP2C9.

Thiazolidinediones. Co-administration of multiple doses of linagliptin 10 mg per day (above the therapeutic dose) and pioglitazone 45 mg per day (multiple doses), which is a substrate for CYP2C8 and CYP3A4, did not have a clinically significant effect on the pharmacokinetics of linagliptin or pioglitazone, or the active metabolites of pioglitazone. . This indicates that linagliptin in vivo

is not an inhibitor of CYP2C8-mediated metabolism and supports the conclusion that linagliptin has no significant
in vivo
on CYP3A4.

Ritonavir. Co-administration of linagliptin (single dose 5 mg orally) and ritonavir (multiple doses of 200 mg orally), an active inhibitor of P-glycoprotein and the CYP3A4 isoenzyme, increased the AUC and Cmax values of linagliptin by approximately 2-fold and 3-fold, respectively. However, these changes in linagliptin pharmacokinetics were not considered significant. Therefore, clinically significant interactions with other P-gp and CYP3A4 inhibitors are not expected and no dose adjustment is required.

Rifampicin. Repeated co-administration of linagliptin and rifampicin, an active inducer of P-glycoprotein and the CYP3A4 isoenzyme, resulted in a decrease in the AUC and Cmax of linagliptin by 39.6% and 43.8%, respectively, and a decrease in the inhibition of basal dipeptidyl peptidase-4 activity by approximately 30%. Thus, the clinical efficacy of linagliptin when used in combination with active P-glycoprotein inducers is expected to be maintained, although it may not be fully realized.

Digoxin. Combined repeated use of linagliptin (5 mg per day) and digoxin (0.25 mg per day) in healthy volunteers did not affect the pharmacokinetics of digoxin. Thus, linagliptin in vivo

is not an inhibitor of P-glycoprotein-mediated transport.

Warfarin. Linagliptin, administered repeatedly at a dose of 5 mg per day, did not change the pharmacokinetics of warfarin, which is a substrate for CYP2C9, indicating that linagliptin does not have the ability to inhibit CYP2C9.

Simvastatin. Linagliptin, administered repeatedly to healthy volunteers at a dose of 10 mg per day (above the therapeutic dose), had minimal effect on the pharmacokinetic parameters of simvastatin, which is a sensitive substrate for CYP3A4. After taking linagliptin at a dose of 10 mg together with simvastatin, used at a daily dose of 40 mg for 6 days, the AUC value of simvastatin increased by 34% and the Cmax value by 10%. Thus, linagliptin is a weak inhibitor of CYP3A4-mediated metabolism. Changing the dose when taken concomitantly with drugs that are metabolized by CYP3A4 is considered inappropriate.

Oral contraceptives. Co-administration of linagliptin at a dose of 5 mg with levonorgestrel or ethinyl estradiol did not change the pharmacokinetics of these drugs.

Treatment of diabetes

Diabetes mellitus is a group of metabolic diseases characterized by high levels of glucose (“sugar”) in the blood.

Why do we need glucose

The norm of blood glucose (sugar) in whole capillary blood is 3.3-5.5 mmol/l in the morning on an empty stomach (i.e. after 7-14 hours of overnight fasting) and up to 7.8 mmol/l after meals (i.e. 1.5-2 hours after the last meal).

Normally, in the human body, glucose is used by the cell as an energy source (in other words, the body’s cells “feed” on glucose from the blood). The more a cell works, the correspondingly more energy (glucose) it requires.

Glucose (the expression “blood sugar” is more often used, but this is not entirely true) constantly circulates in the human blood. There are 2 ways for glucose to enter the human body: - the first is through food containing carbohydrates, - the second is through the production of glucose by the liver (this is the reason that in diabetes mellitus, even if the patient has not eaten anything, the blood glucose level can be increased).

However, in order to be used as energy, glucose from the blood must go to muscles (to do work), fat tissue, or the liver (the body's glucose storage facility). This occurs under the influence of the hormone insulin, which is produced by beta cells of the pancreas. As soon as the blood glucose level rises after a meal, the pancreas instantly releases insulin into the blood, which, in turn, connects with insulin receptors on muscle, fat or liver cells. Insulin, like a key, “opens” cells to allow glucose to enter them, resulting in the level of glucose (sugar) in the blood returning to normal. Between meals and at night, if necessary, glucose enters the blood from the liver's depot, so at night insulin controls the liver so that it does not release too much glucose into the blood.

If a violation occurs at any stage of this process, diabetes mellitus occurs.

Types of diabetes

Diabetes mellitus type 1

(previously used the name: insulin-dependent diabetes mellitus) develops mainly at a young age (usually before 30 years of age, although type 1 diabetes mellitus can also develop at a later age).

Type 1 diabetes mellitus is caused by the cessation of insulin production by the pancreas due to the death of β-cells (responsible for the production of insulin in the pancreas). The development of type 1 diabetes mellitus occurs against the background of a special genetic predisposition (i.e. a person was born with it), which, when exposed to some external factors (for example, viruses), leads to a change in the state of the body’s immune system. The body of a patient with type 1 diabetes begins to perceive its pancreatic β-cells as foreign and protects itself from them by producing antibodies (similar to what happens when protecting against infection), leading to the death of pancreatic β-cells, which means severe insufficiency insulin.

Diabetes mellitus 1

type develops when at least 90% of the β cells of the pancreas die. Let us recall the mechanism of action of insulin, its function as a “key” that opens cells to sugar. In type 1 diabetes mellitus, this key disappeared from the blood (see figure).

Lack of insulin in type 1 diabetes mellitus The onset of type 1 diabetes mellitus is acute, always accompanied by severe symptoms of hyperglycemia (high blood sugar): - weight loss (the patient involuntarily loses weight), - a constant feeling of hunger, - thirst, dry mouth (the patient drinks a lot fluids, including at night), - frequent urination (in regular or large portions, including at night), - weakness.

If you do not consult a doctor in time and do not start treating type 1 diabetes with insulin, the condition worsens, and diabetic coma very often develops.

Diabetes mellitus type 2

(previously called insulin-dependent diabetes mellitus) is much more common than type 1 diabetes mellitus. The incidence of type 2 diabetes mellitus is typical for older people: it is detected, as a rule, after 40 years of age, although recently, according to WHO experts, the average age of patients with type 2 diabetes mellitus is getting younger.

About 80% of people with type 2 diabetes are overweight. Also, type 2 diabetes is characterized by heredity - a high prevalence among close relatives.

In type 2 diabetes, the pancreas continues to produce insulin, often in larger quantities than usual. Although there are also cases of type 2 diabetes mellitus with reduced insulin secretion.

The main defect in type 2 diabetes is that the cells do not “sense” insulin well, that is, they do not open well in response to interaction with it, so sugar from the blood cannot fully penetrate inside (see figure). Blood sugar level remains elevated. This state of decreased sensitivity to insulin is called insulin resistance.

Low sensitivity to insulin in type 2 diabetes mellitus You can figuratively imagine that the “keyholes” (scientifically speaking - insulin receptors) on the cell doors are deformed, and there is no perfect match with the keys - insulin molecules. It takes more effort (more keys, i.e. more insulin) to overcome the insulin receptor defect. The pancreas cannot supply a sufficient amount of insulin into the blood to overcome insulin resistance and completely normalize blood sugar levels, because In type 2 diabetes mellitus, the capabilities of β cells are still limited.

As a result, with type 2 diabetes, a paradoxical situation arises when there is a lot of both insulin and sugar in the blood at the same time.

Type 2 diabetes mellitus, unlike type 1 diabetes mellitus, begins gradually, often completely unnoticed by the patient. Therefore, a person can be sick for quite a long time, but not know about it. Elevated blood sugar (glucose) levels may be detected by chance during an examination for some other reason.

At the same time, there are cases with clear manifestations of hyperglycemia:

- weakness, fatigue, - thirst, dry mouth (the patient drinks a lot of fluids, including at night),
- frequent urination (regular or large portions, including at night),
- itching of the skin (especially in the perineal area),
- slow wound healing, - frequent infections, - blurred vision.
Diabetic coma develops much less frequently, usually
- if type 2 diabetes mellitus is accompanied by some other very serious disease: pneumonia, serious injury, suppurative processes, heart attack, etc.

Treatment of diabetes

Treatment for diabetes differs depending on the type of diabetes.

In type 1 diabetes mellitus, which occurs as a result of an absolute insufficiency of insulin secretion by the own pancreas, constant self-monitoring and insulin treatment are required to preserve life. It should be emphasized that treatment with externally administered insulin is the only treatment option in this situation. The selection of doses and treatment regimens for diabetes mellitus with insulin is carried out individually, taking into account age, gender, physical activity, and individual sensitivity to insulin.

For type 1 diabetes mellitus

sometimes, at the very beginning of the disease, after normalization of blood glucose during treatment of diabetes mellitus with insulin, the need for it suddenly begins to decrease until it is completely canceled. But this is not recovery. This phenomenon is called the “honeymoon” of diabetes, or scientifically, remission. This is explained by the fact that after blood sugar is normalized with the help of insulin, the β cells that have not yet died can work for some time. Subsequently, they all die, and the person needs treatment for diabetes mellitus with insulin for life. Anyone who develops type 1 diabetes for the first time should be warned by their doctor about the possible occurrence of such a situation and what to do in this case.

Treatment of diabetes mellitus with insulin can be carried out using insulin syringes, pens or an insulin pump.

Insulin pump therapy is an alternative treatment for diabetes mellitus in people who heavily use a syringe or pen to inject insulin and regularly measure their blood sugar levels. Insulin pump therapy is used instead of treating diabetes with injections. The pump is worn on the body or on clothing, for example, on a belt. Currently, about 250 thousand people around the world use insulin pumps.

The main goal of treating type 2 diabetes is to improve the sensitivity of cells to insulin. The causes of poor insulin sensitivity are not yet fully understood. However, it has long been known that the most powerful factor in the formation of insulin resistance is excess weight, i.e. excessive accumulation of fat in the body. Numerous scientific studies and long-term observations of patients show that weight loss during the treatment of type 2 diabetes in most patients can achieve a significant improvement in blood sugar levels.

In type 2 diabetes, normalizing weight can lead to complete normalization of blood sugar for a long time, although this cannot be called a complete recovery.

If diet and exercise aimed at weight loss do not provide sufficient effect in the treatment of type 2 diabetes, you have to resort to medication. They are available in tablets. Some of them act on the pancreas, increasing insulin production, while others improve its effect (reduce insulin resistance). Thus, the drugs themselves used to treat type 2 diabetes mellitus do not lower blood sugar; insulin does this; therefore, to obtain the effect of tablets in the treatment of diabetes mellitus, a preserved reserve of pancreatic β-cells is necessary. This makes it clear why it is pointless to use tablet drugs in the treatment of type 1 diabetes, because most of the β cells have already died.

Insulin is often used to treat type 2 diabetes. Treatment with insulin for type 2 diabetes mellitus can be prescribed as a temporary measure, for example, during surgery, severe acute illnesses, or as permanent treatment. This is why it is currently not recommended to call type 2 diabetes mellitus non-insulin dependent. The type of diabetes treatment does not determine the type of diabetes.

Diet plays the most important role in the treatment of diabetes.

Diet for diabetes

Despite the common goals in the treatment of different types of diabetes (elimination of symptoms of high blood sugar, minimizing the risk of hypoglycemia, prevention of complications), diet patterns for type 1 and type 2 diabetes mellitus differ significantly. There is no single diet plan for diabetes mellitus.

In type 1 diabetes mellitus, the occurrence of which is associated with the death of beta cells of the pancreas and insulin deficiency, the main method of treatment is insulin replacement therapy, and dietary restrictions, according to modern views, are of an auxiliary nature and should be given only to the extent that insulin therapy differs from insulin production in a healthy person.

The fundamental principles of prescribing a diet for type 1 diabetes mellitus have been subject to critical revision in recent years.

One of the principles of the traditional diet for diabetes is the recommendation to consume a strictly defined, identical amount of calories every day. Each patient was prescribed a daily calorie requirement based on their “ideal weight.” This makes no sense and is impossible for the following reasons:

a) in healthy individuals with normal weight, the balance between energy intake and expenditure varies greatly from day to day. Energy expenditure in healthy individuals is variable because their physical activity is variable. Consequently, if a patient with type 1 diabetes is prescribed a given diet with a daily consumption of a fixed, identical amount of calories, then in order to maintain a normal weight, one would have to recommend an equally given, strict plan of physical activity for every day, which is absolutely unrealistic.

b) in patients with type 1 diabetes mellitus with normal weight and a properly selected insulin treatment regimen for diabetes mellitus, appetite regulation does not differ from that in healthy individuals. The fact that they sometimes have to be forced to eat to prevent hypoglycemia, even in the absence of appetite, is most often a consequence of not entirely adequate insulin therapy.

Improved treatment regimens for diabetes mellitus using insulin and self-monitoring of metabolism based on blood sugar levels give the patient the opportunity to regulate food intake only depending on the feeling of hunger and satiety, like healthy people. Thus, the diet of a patient with type 1 diabetes mellitus corresponds to a complete healthy diet (balanced in calories and content of essential nutrients). The only difference is that the insulin injected does not “know” when or how much you eat. Therefore, you yourself must ensure that the action of insulin corresponds to your diet. Therefore, you need to know which foods increase your blood sugar.

The main treatment method for type 2 diabetes is normalization of body weight through a low-calorie diet and increased physical activity. Diet for type 2 diabetes is very important; it is one of the significant components that allows you to achieve success.

All food products consist of three components: proteins, fats and carbohydrates. They all contain calories, but not all increase blood sugar.

Only carbohydrates have a pronounced blood sugar-raising effect. What foods contain carbohydrates? It's easy to remember: most foods are plant-based, and animal foods are limited to liquid dairy products. It is important for you to know whether blood sugar rises after certain foods, and if so, by how much. There are types of carbohydrate foods after which blood sugar either does not rise at all or rises only slightly.

All carbohydrates can be roughly divided into two groups: those containing rapidly absorbed (“fast”) carbohydrates and slowly absorbed (“slow”) carbohydrates. Products with “fast” carbohydrates contain refined sugars and include preserves and jams, candies, sweets, fruits, and fruit juices. “Fast” carbohydrates cause a sharp increase in blood sugar (depending on the amount of food eaten) because they are quickly absorbed into the blood, so it is better to exclude them from the diet for diabetes. “Slow” carbohydrates are much more beneficial for patients with diabetes, because they take much longer to be absorbed. In addition, the absorption of sugars is slowed down by the fiber contained in food, so the diet when treating diabetes should be enriched with foods rich in fiber.

Here are a few simple rules to follow when treating diabetes: food should be taken in small portions and often (4-6 times a day); adhere to the established diet - try not to skip meals; do not overeat - eat as much as recommended by your doctor; use bread made from wholemeal flour or with bran; vegetables (except potatoes and legumes) should be eaten daily; Avoid eating “fast” carbohydrates.

Exercise for Diabetes Physical exercise in the treatment of diabetes is very important: it increases the sensitivity of body tissues to insulin and, thus, helps reduce blood sugar levels.

Housework, walking, and jogging can be considered physical activity. Preference should be given to regular and dosed physical exercise: sudden and intense exercise can cause problems with maintaining normal sugar levels.

If you are an athlete or sportswoman, you have no contraindications to playing sports, provided that your blood sugar levels are well controlled and all necessary measures are taken to prevent a significant decrease in it.

Prevention of complications of diabetes Patients with diabetes have an increased risk of developing complications from the heart and blood vessels (especially in the legs and kidneys). Regular physical activity, sometimes just walking, is enough to prevent circulatory problems in the feet.

If you have diabetes, an untreated wound or abrasion on the foot can develop into a serious problem. Even minor cuts or scrapes on the feet take longer to heal than in patients without diabetes and require increased attention. The key to preventing these problems is wearing well-fitting shoes and checking your feet frequently. Use a mirror if you find it difficult to examine all areas of your feet, and remember that foot injuries are often painless at first and may go unnoticed for a long time if you are not careful enough.

Patients with diabetes have an increased risk of kidney dysfunction and heart disease several years after diagnosis. There is good evidence that good blood sugar control reduces this risk. Also, to prevent complications of diabetes mellitus, it is necessary to undergo preventive treatment 2 times a year.

Blood pressure control is also important. Check your blood pressure regularly. If it is elevated, your doctor will prescribe treatment for you.