Glucose Homeostasis seminar by dr anita teli

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Glucose Homeostasis:

Glucose Homeostasis Speaker: Dr Anita . Teli

Introduction :

Introduction Glucose is the carbohydrate currency of the body. An adult human body contains about 18g free glucose. This amount is just sufficient to meet the basal energy requirements of the body for one hour. The liver has about 100g stored glycogen. Besides this it is capable of producing 125-150 mg of glucose/min or 180-220g/24hrs.

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Normal blood sugar level varies from 80-120 mg per 100 ml (fasting) & 100-120 mg per 100 ml (after meal). Plasma concentration of glucose is slightly higher (about 15%) than blood glucose. The glucose concentration of 180 mg/dl (plasma or blood) corresponds to 10mmol/l.

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Large quantities of sugar are constantly entering the blood stream ( absorption, gluconeogenesis , glycogenolysis ) & are constantly being removed from it ( glycogenesis , oxidation of sugar, lipid synthesis) . In spite of those opposing forces, blood sugar level remains fairly constant within this limited range. This indicates that there must be a strong machinery for blood sugar regulation in the body.

Regulation of blood glucose level:

Regulation of blood glucose level The mechanism involves the following factors: i ) ALIMENTARY MECHANISM a. Assimilation limits of glucose . 1). 200g glucose given by mouth- no sugar found in the urine. 2). 300-500g given- large amount of water is osmotically drawn in & stomach becomes distended. 3). >500g given at a time, subject develops nausea & the glucose is vomited out.

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b. Digestion of starch : slow & long process. Necessarily absorption becomes slow. So that sharp rise of blood sugar is prevented. c. Rate of absorption : maximum limit of absorption of glucose is about 1.84 g per kg per hour . What ever be the amount of sugar given, the rate of absorption does not go beyond it, hence blood sugar cannot have a sharp rise.

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ii). ROLE OF LIVER : a). Liver stores sugar as glycogen, when blood sugar rises & thus rise of blood sugar is checked. b). Liver mobilizes glycogen stores, when blood sugar level falls & speeds the rate of gluconeogenesis & thus restores the level to normal. iii). ROLE OF MUSCLES: a). Muscles stores glucose from blood stream & stores it as glycogen, thus tending to reduce blood sugar. b). In hypoglycemia or after severe muscular exercise, lactic acid is mobilized from the muscles, converted first to glycogen then to glucose in the liver & discharged into blood stream, raising the blood sugar level.

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iv). ROLE OF ENDOCRINES : endocrines are chief regulators of blood sugar level. 1 . Insulin : It is the strongest blood sugar reducing factor. It lowers blood sugar in three ways, a). Increasing glycogenesis b). Promoting glucose uptake in muscles & adipose tissues. c). Preventing gluconeogenesis

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2. Anterior pituitiary : These hormones increases blood sugar levels a). Growth hormone : Decreases peripheral utilizations of glucose & increases blood sugar levels. b). ACTH : Through adrenal cortex increases blood sugar. c). TSH : Through thyroid increases blood sugar.

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3). Posterior pituitary: large dose of vasopressin & oxytocin increases the blood sugar levels temporarily. 4). Adrenal cortex : Glucocorticoid work in following ways; a). Decreases peripheral utilization of glucose due to retardation of phosphorylation . b). Increases gluconeogenesis in the liver due to retarted amino acids incorporation into protein, thus making more glucogenic material available. Administration of glucocorticoids produces temporarily diabetes in a number of animal species. Partially pancreatectomised animals may be made permanently diabetic by administration of cortisol or cortisone.

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5). Epinephrine & Norepineprine : Raises blood sugar levels a). By stimulating glycogenolysis from liver. b). Converting muscle glycogen into lactic acid, increases blood sugar level. c). Also increases BMR by 20%, & increases the oxidation of glucose in the tissues. 6). Thyroid : effects are exhibited by thyroxine a). Increase in the peripheral utilization & combustion of glucose in the tissues. b). Stimulation of glycogenolysis & gluconeogenesis 7). Glucagon : Increases blood sugar due to glycogenolysis in liver & gluconeogenesis .

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v). ROLE OF NERVOUS SYSTEM: Hypothalamic lesions causes disturbances of carbohydrate metabolism , namely hypoglycemia, increased sensitivity to insulin. Autonomic nervous system takes a great part in blood glucose regulation by following ways a). Stimulation of the right vagus reduces blood sugar level by increasing insulin secretion. b). Stimulation of the sympathetic nerves increases blood sugar level by mobilizing liver glycogen & by stimulating epinephrine secretion.

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vi). ROLE OF BLOOD SUGAR : Blood sugar regulates its own level. Hyperglycemia stimulates insulin secretion a. directly acting on the beta cells, & b. stimulating the right vagus c. It also increases the rate of oxidation of sugar in the tissue independent of hormones d. Depresses the secretion of the growth hormone. In this way, the raised blood sugar is brought down to normal. On the other hand, hypoglycemia depresses insulin secretion by opposite effects.

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vii). ROLE OF TISSUES, TISSUE FLUID & SKIN : a). The tissues fluid(30 lit), having nearly the same glucose content as plasma, can store a large amount of glucose. Any rise or fall of blood sugar is at once compensated by appropriate exchange with tissue fluid. b). The skin & subcutaneous tissue can store a large amount of glucose temporarily. c). The tissues in general use up sugar in a number of ways- such as, conversion into lipids, synthesis of other substances, oxidation of glucose.

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viii). ROLE OF KIDNEYS : Kidneys act as the last outposts. Glucose is continuously filtered by the glomeruli , reabsorbed & returned to the blood. When blood sugar goes above the renal threshold(180 mg per 100 ml), it leaks out through the kidneys. This value is referred to as renal threshold for glucose. The maximum ability of the renal tubules to reabsorb glucose per minute is known as tubular maximum for glucose. The value is 350 mg/min.

Hypoglycemia:

Hypoglycemia Is a condition in which blood sugar level is below the normal level i.e., below 80 mg per 100ml. In diabetic subjects whose tissues are accustomed to high blood sugar, hypoglycemia symptoms may start at a blood sugar level much above normal Hypoglycemic symptoms depends on three factors:

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1). The actual blood sugar level. 2). The rapidity of blood sugar reduction. 3). The previous blood sugar level. Since nerve cells have very little stored food & since they use sugar mostly as a sole source of energy, hypoglycemia will, therefore, affect the nerve cells first. Hence, the earliest manifestation will be nervous in origin & they are

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1). A feeling of fatigue, weakness & hunger. 2). Extreme anxiety & irritability 3). Abnormal behavior as in alcohol poisoning. 4). Tremors develop & fine movements are not possible. 5). Vasomotor disturbances, such as flushing or pallor, perspiration & chilliness. 6). Lastly there may be delirium, diabetic coma, convulsion & loss of deep reflexes. Hypoglycemia symptoms are relieved by administration of glucose.

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Compensatory reactions of hypoglycemia: 1). Stimulates hypothalamus which in its return promotes the secretion of ACTH & other hormone which oppose the actions of insulin & restore the blood sugar level to normal. 2). Hypoglycemia also stimulates the secretion of epinephrine which stimulates glycogenolysis & raises the blood sugar level.

Hyperglycemia :

Hyperglycemia Is a condition in which blood sugar increases above the normal level, i.e., above 120mg per 100 ml. When blood sugar level exceeds the renal threshold (180 mg per 100 ml), sugar appears in the urine. Persistent hyperglycemia occurs when there is diminished utilization of glucose, & discharge of excess sugar from the liver. Hyperfunction of some of the endocrine glands causes hyperglycemia. Lack or diminished secretion of insulin is the main factor which produces hyperglycemia & glycosuria as in diabetes milletus .

Glycosuria:

Glycosuria Is a condition when the blood glucose level exceeds 180 mg glucose per 100 ml blood above the normal blood glucose level. The renal tubular cells are not able to reabsorb all the glucose, some glucose reaches the urinary bladder & glycosuria results.

Diabetes milletus:

Diabetes milletus The term diabetes means that a large volume of urine is passed. The term mellitus means (sweet) dates from the time when the urine was tested by tasting. It is a disorder of metabolism characterized by high blood sugar level & excretion of sugar in urine. It is being broadly divided into 2 groups i ). IDDM ii). NIDDM

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Principal abnormalities of DM are, 1). An increased liberation of glucose in circulation from liver 2). Reduced entrance of glucose in peripheral tissues. Hyperglycemia, glycosuria , ketosis, acidosis, diabetic coma, polyuria , weight loss in spite of polyphagia & polydipsia are the abnormal characteristics of diabetes.

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Major metabolic changes in diabetes i ). Hyperglycemia ii). Ketoacidosis iii). Hypertriglyceridemia

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Insulin stimulates oxidation of glucose. Hence in diabetes mellitus, glucose combustion will be depressed. This is shown by the following facts: a). RQ falls to about 0.7 & arteriovenous glucose difference is low. This shows that tissues are utilizing very little glucose & fats are being burnt. b). Isolated organs or limbs, if perfused with glucose plus insulin, remove glucose much more quickly than when perfused with glucose alone. Studies after administration of glucose labeled with radio active 14 C have shown that insulin directly increases the rate of glucose oxidation.

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Long term effects of diabetes 1). Atherosclerosis 2). Retinopathy 3). Nephropathy 4). Neuropathy

Management of diabetes:

Management of diabetes Diet , exercise, drug & finally , insulin are the management options in diabetics. Dietary management : diabetic patient is advised to consume low calories, high protein & fiber rich diet. Carbohydrates should be taken in the form of starch & complex sugars. Refined sugars should be avoided. Fat intake should be drastically reduced so as to meet the nutritional requirements of unsaturated fatty acids. Diet control & exercise will help to a large extent obese NIDDM patients.

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Hypoglycemic drugs ; Sulfonylureas ( acetohexamide , tolbutamide & gibenclamide ) & Biguanides . These drugs promote the secretion of endogenous insulin & reduces blood glucose levels. Insulin : 2 types of insulin preparation are commercially available a. short acting b. long acting

References :

References Human physiology- Dr C C Chatterjee Text book of Biochemistry- Dr U. Satyanarayana Text book of medical physiology- Guyton

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