Normal blood glucose levels are maintained by the hormone. Other ways to determine the level of glucose and insulin. Functions of thyroid hormones
Diabetes is an extremely common disease these days. According to statistics, more than 80% of older people are affected by it. Moreover, middle-aged and even young people, as well as children, are increasingly at risk. This is due to malnutrition and excess weight, hereditary predisposition and metabolic disorders, autoimmune and various somatic diseases. Have you ever wondered why diabetes is called "diabetes"? And generally speaking,sugar in the hormonal system - what is its role? What is glucose and what hormones control its level in the blood?
Promote the storage structure of glycogen in the liver. . Glucagon is also a peptide hormone and acts on a membrane-bound receptor. This is what leads to the breakdown of glycogen and thus the release of glucose into the blood. If the blood sugar level is not correct: diabetes mellitus.
Blood sugar levels need to be regulated throughout the day. But sometimes there are persistent problems. The main disease here is diabetes mellitus. Diabetes is a metabolic disorder that manifests itself in a violation of the concentration and use of glucose. There are usually two types.
What is glucose?
Grape sugar or glucose is a carbohydrate of the monosaccharide group, one of the main components involved in the metabolic processes of the human body. It is glucose that provides living cells with energy and is the initial product of the biosynthesis of almost all substances.
Type 1 diabetes mellitus: hereditary, autoimmune disease, destruction of beta cells. A new compound that combines the effects of three gastrointestinal hormones lowers blood sugar and reduces body fat to unprecedented levels.
Triple Hormone Reduces Body Efficiency and Increases Insulin Sensitivity
Her main focus is on the development of new molecules that combine the effects of various metabolic hormones. The triagonist reduced body weight by about 30 percent, twice as much as the dual co-agonist at the same dosage. In addition, the triple hormone showed significantly improved insulin sensitivity.
Normally, the level of glucose in human blood is constant (100 mg), which is ensured in the process of synthesis and breakdown of glycogen. Sugar in the hormonal system plays almost the main role, as it is one of the main sources of energy that supports the stable functioning of muscle tissues, taking an active part in absolutely all chemical reactions occurring in the body of living beings, including humans.
The third hormone, glucagon, increases calorie burning in the long run. This triple hormonal action in one molecule demonstrates unparalleled effectiveness. This affects several centers of metabolic control in the pancreas, liver, adipose tissue and brain, explains lead author Brian Finan of the Helmholtz Diabetes Center.
“This latest breakthrough shows us that we are on the right track to develop better methods to fight obesity and diabetes,” Chop says. The most important next step is clinical trials. We also want to continue working on personalized therapy concepts and more efficient metabolism programming with combination molecules of four, five or more hormone components.
Responsible for the distribution of sugar throughout the cells of the body, as well as maintaining it normal level in the blood entrusted to the endocrine system. The endocrine glands produce hormones that regulate metabolic processes.
Glucose penetrates into the cells of all organs and tissues of the body from the blood, and the hormone insulin is responsible for this, produced by the endocrine part of the pancreas - a secretory organ digestive system. In addition to insulin, this organ produces the hormone glucagon and C-septide, which, along with insulin, are involved in humoral regulation, and pancreatic juice with special enzymes necessary for the digestion of food - carbohydrates, fats and proteins.
Carbohydrates are virtually indistinguishable from many string sugar molecules. And they tend to be so scary when it comes to weight loss. Simply put, starch becomes sugar. After a meal rich in carbohydrates, our blood is flooded with "sugar". At the same time, the pancreas releases insulin. Insulin now opens up the cells of the body so they can take in the sugar in the blood. At the same time, they close the fat cells so that the "starvation" stores are not attacked. The body has just received a signal that there is enough sugar.
Thus, people who eat mainly sugar and starch from grains have too high blood sugar levels. All civilizational diseases, such as overweight, iron deficiency, osteoporosis, from diabetes to cancer, favor a diet rich in grains and sugar.
The role of sugar in the hormonal system, as well as in all other systems and organs of the human body is invaluable. Violation of the functions of the pancreas, i.e., destabilization of hormone production, causes the development of many diseases, including diabetes mellitus.
Importance of insulin in humoral regulation
As already mentioned, the main task of insulin is to stimulate the penetration of glucose into the cells of the body from the blood. Under the influence of this hormone, all synthesizing processes are activated, the absorption of sugar by muscle and fat tissues increases, and the process of converting glucose into glycogen is stimulated.
What happens after carbohydrate meal? Most carbohydrates are quickly broken down into simple sugars, which are then absorbed. small intestine mostly in the form of glucose and absorbed into the blood. The glucose in the blood is then transported to the liver. When the glycogen stores in the liver are full, most of the blood sugar is released into the bloodstream.
With 500 calories of protein and the same amount of sugar, insulin levels explode. But our cells cannot absorb these amounts of sugar, i.e. glucose. They are not genetically engineered for this. Therefore, the body now tries to help itself and notifies the "emergency center": the pancreas is now producing the hormone insulin. This hormone is released to lower blood sugar levels. Excess glucose is thus removed from the bloodstream, converted to fat, and deposited in the body's fat cells.
The same insulin promotes the synthesis of fatty acids, thanks to which fat is deposited in adipose tissues, plus, the breakdown of fat is inhibited and, accordingly, the formation of toxic ketone bodies. Among other things, this hormone prevents the formation of glucose and other biological substances in the liver, that is, it controls the processes of glycogenesis and gluconeogenesis.
If they are already filled, new body fat cells are created and filled. Glucose levels that went up in the first 45 minutes just as quickly hit the "basement" over the next 45 minutes. The next "hypoglycemia" causes cravings, and it is preferable to use again quickly used simple sugars. This starts the "cycle" from the beginning.
The dietary advice of 5 to 7 small meals a day has a devastating effect: insulin levels are constantly at the limit, and access to body fat is always closed. This is why carbohydrate diets can't work. Thus, we can say that insulin is a growth hormone hormone: it lowers blood sugar levels, increases hunger and increases body fat. Just as it can become the purest "fat hormone", it provides invaluable care services for every single cell.
If for some reason the pancreas does not cope with its direct duties and insulin is produced in insufficient or excessive quantities, its content in the blood is disturbed. As a result, all chemical processes in which glucose is involved are disrupted, resulting in the occurrence of a disease state. In other words, diabetes mellitus and a number of other serious diseases develop. Treatment of such pathologies requires the use of serious drug therapy, and in some cases, surgical intervention.
If the pancreas is constantly used, it often leads to diabetes in old age, with the pancreas eventually unable to produce enough insulin. It's like she's stopped production. In addition to insulin, the pancreas also produces the hormone glucagon. This has the opposite effect.
Glucagon causes an increase in blood sugar levels, the breakdown of adipose tissue and inhibition of appetite. Thus, it can be called a hormone for weight loss. In the case of defatted flour, glucagon levels rise, remain at a maximum for several hours, and fall very slowly over several hours. Glucagon ensures that fat burning is on. The fat reserves of the body are now being used - they are finally there.
A. Carbohydrates contained in the diet.
Most dietary carbohydrates are hydrolyzed to form glucose, galactose, or fructose, which enter the liver through the portal vein. Galactose and fructose are rapidly converted in the liver to glucose (see figures 21.2 and 21.3).
B. Various glucose-forming compounds entering the path of gluconeogenesis (Fig. 22.2). These compounds can be divided into two groups: (1) compounds that convert to glucose and are not products of its metabolism, such as amino acids and propionate; (2) compounds that are products of partial glucose metabolism in a number of tissues; they are transported to the liver and kidneys, where glucose is resynthesized from them. So, lactate, which is formed in skeletal muscles and red blood cells from glucose, is transported to the liver and kidneys, where glucose is again formed from it, which then enters the blood and tissues. This process is called the Korn cycle or the lactic acid cycle (Fig. 22.6). The source of glycerol necessary for the synthesis of triacylglycerols in adipose tissue is blood glucose, since the use of free glycerol in this tissue is difficult. Acylglycerols in adipose tissue undergo constant
This also explains why defatted flour fills up before 11 o'clock. Insulin is produced after carbohydrate meal. Blood sugar levels are subject to high fluctuations. Insulin must be produced continuously. Glucagon is produced after defatted flour. Equality of hunger remains, blood sugar levels are constant. We only need a small amount of insulin, but now the glucagon is released. Your own fat burning in the body occurs.
Note. The hormone insulin is absolutely essential and naturally performs important functions. Insulin must be injected. The peptide hormone insulin is hypoglycemic and is produced by the body. The pancreas produces little or no insulin. However, since insulin cannot be effectively taken in the diet, insulin-deficient patients must be administered.
Rice. 22.6. The lactic acid cycle (Cori cycle) and the glucose-alanine cycle.
hydrolysis, which results in the formation of free glycerol, which diffuses from the tissue into the blood. In the liver and kidneys, it enters the path of gluconeogenesis and turns back into glucose. Thus, a cycle is constantly functioning in which glucose from the liver and kidneys is transported to adipose tissue, and glycerol from this tissue enters the liver and kidneys, where it is converted into glucose.
Tasks and functions of insulin
Insulin is a vital hormone produced in the pancreatic beta cells of the islets of Langerhans and released into the bloodstream. Insulin lowers blood sugar levels and acts as an anabolic hormone. The function of insulin is especially dependent on the regulation of blood sugar. In addition to insulin, this requires the hormone glucagon. While insulin lowers blood sugar levels, glucagon is able to increase blood sugar levels by releasing carbohydrates in the muscles and liver.
In addition to glucagon, adrenaline, cortisone, and certain thyroid hormones, blood sugar levels are raised. Blood sugar levels rise, in particular, from grape sugar found in food. This is followed by the release of insulin into the blood. Insulin has a key function on the cells of the body. Here, so to speak, it closes the cells and allows blood sugar from the blood to enter the bloodstream. Insulin also affects the metabolism of fats and proteins, as well as the balance of potassium. In chronic metabolic diseases, insulin is completely or partially absent or may not work enough.
It should be noted that among the amino acids transported during fasting from the muscles to the liver, alanine predominates. This made it possible to postulate the existence of a glucose-alanine cycle (Fig. 22.6), through which glucose flows from the liver to the muscles, and alanine from the muscles to the liver, thereby ensuring the transfer of amino nitrogen from the muscles to the liver and "free energy" from the liver to the muscles. The energy needed to synthesize glucose from pyruvate in the liver comes from fatty acid oxidation.
Production of insulin in the pancreas
Insulin production occurs in the beta cells of the islets of Langerhans in the pancreas. It can be stored in the pancreas as a hexamer. A micronutrient is needed to store insulin and produce insulin. Many diabetics suffer from a zinc deficiency and benefit from zinc supplements.
Insulin as a drug for the treatment of diabetes
Insulin plays a vital role in medicinal product in the treatment of diabetes mellitus. It can be obtained from the pancreas of pigs and cattle. In addition, insulin can be produced biosynthetically as human insulin. There are also so-called insulin analogues. In principle, it is impossible to treat diabetes mellitus through insulin tablets, since the hormone will be digested into gastrointestinal tract and may not have any effect.
B. Liver glycogen. Blood glucose concentration
In humans, between meals, the concentration of glucose in the blood varies from 80 to. After eating a meal rich in carbohydrates, the concentration of glucose increases to. During fasting, the concentration of glucose drops to approximately. In ruminants, the concentration of glucose is much lower - about in sheep and in cattle. This is apparently due to the fact that in these animals almost all carbohydrates supplied with food are broken down into lower (volatile) fatty acids, which replace glucose as an energy source in tissues during normal nutrition.
Insulin is administered by insulin-dependent diabetics with or the so-called insulin pen into the subcutaneous fat. Insulin can also be given through a catheter connected to an insulin pump. Important in the history of insulin was the discovery of insulin-producing islet cells in the pancreas by Paul Langerhans over 20 years later, Oskar Minkowski and Joseph von Mehring were able to prove that the pancreas protects people from diabetes. The real discoverers of insulin are Frederick Banting and Charles Best.
Researchers have already built several monomolecular hormones that combine the effects of two metabolic hormones. For the first time, researchers have been able to produce a drug of unprecedented potency using a finely tuned combination of three metabolically active ingredients. Matthias Zop, Brian Finan: Source: Helmholtz Zentrum Munich.
Regulation of blood glucose concentration
Maintaining blood glucose at a certain level is an example of one of the most advanced mechanisms of homeostasis, which involves the liver, extrahepatic tissues and some hormones. Glucose easily penetrates into the cells of the liver and relatively slowly into the cells of extrahepatic tissues. Therefore, passage through the cell membrane is the rate-limiting step in the uptake of glucose by extrahepatic tissues. Glucose entering the cells is rapidly phosphorylated under the action of hexokinase. On the other hand, it is possible that some other enzyme activities and concentrations of key intermediates have a greater effect on glucose uptake or glucose output from the liver. However, blood glucose concentration is an important factor regulating the rate of glucose uptake by both the liver and extrahepatic tissues.
It also affects several centers of metabolic control in the pancreas, liver, adipose tissue and brain, explains lead author Brian Finan of the Helmholtz Diabetes Center. In addition, we want to continue working on personalized therapy concepts and try to use combined molecules of four, five or more hormone components to individually program metabolism even more efficiently. like german Research Center Health and Environment, Helmholtz Zentrum Munich is committed to developing personalized medicine for the diagnosis, treatment and prevention of common diseases such as diabetes and lung disease.
The role of glucoconnase. Of particular note is that glucose-6-phosphate inhibits hexokinase and thus extrahepatic glucose uptake, which is dependent on hexokinase, which catalyzes glucose phosphorylation and is feedback regulated. This does not happen in the liver because glucose-6-phosphate does not inhibit glucokinase. This enzyme has a higher value (lower affinity) for glucose than hexokinase; glucokinase activity increases within physiological glucose concentrations (Fig. 22.7); after eating a carbohydrate-rich meal, the enzyme "tunes" to high concentrations of glucose entering the liver through the portal vein. Note that this enzyme is absent in ruminants, in which only a small amount of glucose enters the portal venous system from the intestine.
To do this, he explores the interplay of genetics, environmental factors, and lifestyle. The headquarters of the center is located in Neuerberg in the north of Munich. Institute of Diabetes and Obesity investigates disorders metabolic syndrome using systems biology and translational approaches based on cell systems, genetically modified mouse models and clinical intervention research. The aim is to discover new signaling pathways for the development of multidisciplinary innovative therapeutic approaches for personalized prevention and treatment of obesity, diabetes and their comorbidities.
Under normal blood glucose levels, the liver appears to supply glucose to the blood. With an increase in the level of glucose in the blood, its exit from the liver stops, and at sufficiently high concentrations, the flow of glucose into the liver begins. As shown by experiments conducted on rats, at a concentration of glucose in the portal vein of the liver, the rate of glucose entry into the liver and the rate of its exit from the liver are equal.
The role of insulin. In a state of hyperglycemia, the supply of glucose to both the liver and peripheral tissues increases. The hormone plays a central role in the regulation of blood glucose levels.
Rice. 22.7. Dependence of the glucose phosphorylating activity of hexokinase and glucokinase on the concentration of glucose in the blood. The value for glucose in hexokinase is 0.05 (0.9 mg / 100 ml), and in glucokinase - 10
insulin. It is synthesized in the pancreas by the B cells of the islets of Langerhans, and its entry into the bloodstream increases with hyperglycemia. The concentration of this hormone in the blood changes in parallel with the concentration of glucose; its introduction quickly causes hypoglycemia. Substances that cause insulin secretion include amino acids, free fatty acids, ketone bodies, glucagon, secretin, and the drug tolbutamide; epinephrine and norepinephrine, on the contrary, block its secretion. Insulin rapidly causes an increase in glucose uptake by adipose tissue and muscle by accelerating the transport of glucose through cell membranes by moving glucose transporters from the cytoplasm to the plasma membrane. However, insulin has no direct effect on the entry of glucose into liver cells; this is consistent with the data that the rate of glucose metabolism by liver cells is not limited by the rate of its passage through cell membranes. Insulin, however, acts indirectly by affecting the activity of enzymes involved in glycolysis and glycogenolysis (see above).
The anterior pituitary gland secretes hormones whose action is opposite to that of insulin, that is, they increase blood glucose levels. These include growth hormone, ACTH (corticotropin) and probably other "diabetogenic" factors. Hypoglycemia stimulates the secretion of growth hormone. It causes a decrease in the supply of glucose to certain tissues, such as muscles. The action of growth hormone is to some extent indirect, since it stimulates the mobilization of free fatty acids from adipose tissue, which are inhibitors of glucose uptake. Long-term administration of growth hormone leads to diabetes. By causing hyperglycemia, it stimulates a constant secretion of insulin, which ultimately leads to the depletion of B cells.
Glucocorticoids (-hydroxysteroids) are secreted by the adrenal cortex and play an important role in carbohydrate metabolism. The introduction of these steroids enhances gluconeogenesis by intensifying protein catabolism in tissues, increasing the consumption of amino acids by the liver, as well as increasing the activity of transaminases and other enzymes involved in the process of gluconeogenesis in the liver. In addition, glucocorticoids inhibit the utilization of glucose in extrahepatic tissues. In these cases, glucocorticoids act like insulin antagonists.
Adrenaline is secreted by the adrenal medulla in response to stressful stimuli (fear, intense excitement, bleeding, oxygen deficiency, hypoglycemia, etc.). By stimulating phosphorylase, it causes glycogenolysis in the liver and muscles. In muscles, due to the absence of glucose-6-phosphatase, glycogenolysis reaches the stage of lactate, while in the liver, the main product of glycogen conversion is glucose, which enters the blood, where its level rises.
Glucagon is a hormone secreted by the A cells of the islets of Langerhans in the pancreas (its secretion is stimulated by hypoglycemia). When glucagon enters the liver through the portal vein, it, like adrenaline, activates phosphorylase and causes glycogenolysis. Most of the endogenous glucagon is retained in the liver. Unlike adrenaline, glucagon does not affect muscle phosphorylase. This hormone also enhances gluconeogenesis from amino acids and lactate. The hyperglycemic effect of glucagon is due to both glycogenolysis and gluconeogenesis in the liver.
It should be noted that thyroid hormone also affects blood glucose levels. Experimental data indicate that thyroxin has a diabetogenic effect, and the removal of the thyroid gland prevents the development of diabetes. It was noted that glycogen is completely absent in the liver of animals with thyrotoxicosis. In people with an overactive thyroid, fasting blood sugar is high, while in people with an underactive thyroid, it is low. In hyperthyroidism, glucose appears to be used at a normal or increased rate, while in hypothyroidism, the ability to utilize glucose is reduced. It should be noted that patients with hypothyroidism are less sensitive to the action of insulin than healthy people and patients with hyperthyroidism.
Renal threshold for glucose, glycosuria
When the blood glucose reaches a relatively high level, the kidneys are also included in the regulation process. Glucose is filtered by the renal glomeruli and usually completely returned to the blood as a result of reabsorption (reabsorption) in the renal tubules. The process of glucose reabsorption is associated with the consumption of ATP in the cells of the renal tubules. The maximum rate of glucose reabsorption in the renal tubules is about 350. At elevated content blood glucose glomerular filtrate contains more glucose than can be reabsorbed in the tubules. Excess glucose is excreted in the urine, i.e., glycosuria occurs. At healthy people Glycosuria occurs when glucose levels in venous blood exceeds 170-180 mg/100 ml; this level is called the renal glucose threshold.
In experimental animals, glycosuria can be induced using phloridzin, which inhibits
Rice. 22.8. Test for glucose tolerance. Curves of blood glucose levels in a healthy and diabetic person after ingestion of 50 g of glucose. Please note that in a diabetic patient, the initial blood glucose level is increased. An indicator of normal tolerance is a return to the initial level of glucose in the blood within two hours.
reabsorption of glucose in the renal tubules. This glycosuria due to impaired glucose reabsorption is called renal glycosuria. Renal glycosuria can be caused by a hereditary defect in the kidneys, or it can develop as a result of a number of diseases. Glycosuria is often an indication of diabetes mellitus.
Glucose tolerance
The ability of the body to use glucose can be judged by its tolerance to it. After the introduction of a certain amount of glucose, blood glucose dynamics curves are built (Fig. 22.8), which characterize glucose tolerance. At diabetes it is lowered due to a decrease in the amount of secreted insulin; with this disease, the blood glucose level rises (hyperglycemia), glycosuria occurs, and changes in fat metabolism may occur. Glucose tolerance is reduced not only in diabetes, but also in some conditions accompanied by impaired liver function, in a number of infectious diseases, obesity, action series medicines and sometimes atherosclerosis. A decrease in glucose tolerance can also be observed with hyperfunction of the pituitary or adrenal cortex due to antagonism between the hormones secreted by these endocrine glands and insulin.
Insulin increases the body's tolerance to glucose. With its introduction, the content of glucose in the blood decreases, and its consumption and content in the form of glycogen in the liver and muscles increase. With the introduction of excess insulin, severe hypoglycemia may occur, accompanied by convulsions; if glucose is not administered quickly in this state, then a lethal outcome may occur. In humans, hypoglycemic seizures appear with a rapid decrease in blood glucose to 20 mg / 100 ml. Increased tolerance to glucose is observed with insufficient function of the pituitary gland or the adrenal cortex; this is a consequence of the decrease in the antagonistic effect of the hormones secreted by these glands in relation to insulin. As a result, the "relative content" of insulin in the body increases.
LITERATURE
Cohen P. Control of Enzyme Activity, 2nd ed. Chapman and Hall, 1983.
Hers H. G. The control of glycogen metabolism in the liver, Annu. Rev. Biochem., 1976, 45, 167.
Hers H. G., Hue L. Gluconeogenesis and related aspects of glycolysis. Annu. Rev. Biochem., 1983, 52, 617.
Hers H. G., Van Schaftingen E. Fructose 2-6-bisphosphate two years after its discovery, Biochem. J., 1982, 206, 1.
Hue L., Van de Werve G. (eds). Short-Term Regulation of Liver Metabolism, Elsevier/North Holland, 1981.
Newsholme E.A., Crabtree B. Flux-generating and regulatory steps in metabolic control, Trends Biochem. Sc., 1981, 6, 53.
Newsholme E.A., Start C. Regulation in Metabolism. Wiley, 1973.
Storey K. B. A re-evalution of the Pasteur effect, Mol. Physiol., 1985, 8, 439.
