What is diabetes ?
Hormone increasing blood glucose level.Hormone decreasing blood glucose level.
Insulin
a.Insulin increases the activity of enzyme glucokinase which enhanced the uptake
of glucose from blood and initiate phospho-rilation of glucose in liver.
b.Insulin inhibits the enzme phosphorilase thus prevents break dowen of liver glycogen.
c.Insulin stimulate the enzyme glycogen synthetase thus promotes glycogensis .
d.Insulin promotes conversion of excess liver glucose into fatty acid.
e.Insulin inhibits gluconeogenesis.
when there is a vasopressin ( ADH ) deficiency or when the kidney fail to respond to the
hormone.
Types
1.Central diabetes insipidus.
2.Nephrogenic diabetes insipidus
Central diabetes insipidus ( Failure to produce ADH ) : An inability to produce or release ADH from the posterior pituitary can be caused by head injuries or infections, or it can be congenital.Because the distal tubular segments cannot reabsord water in the absence of ADH, this condition,called central diabetes insipidus.
response : The thirst mechanisms, are activated when excessive water is lost from the body; therefore,
as long as the person drinks enough water, large decreases in body fluid water do not occur. the primary
abnormality observed clinically in people with this condition is the large volume of dilute urine.However,
if water intake is restricted or the patient is unconscious for example, because of a head injury, severe
dehydration can rapidly occur.
Diabetes Mellitus
Definition: Diabetes mellitus is a syndrome of impaired carbohydrate, fat, and protein metabolism caused
by either lack of insulin secretim or decreased sensitivity of the tissues to insulin.
Types of diabetes mellitus: There are two general types of diabetes mellitus:
1.Type 1 diabetes, also called insulin-dependent diabetes mellitus (IDDM) :It is caused by lack of insulin
secretion.
2.Type 2 diabetes:Type 2 diabetes,also called non-insulin dependent diabetes mellitus (NIDDM) :It is caused by decreased sensitivity of target tissues to the metabolic effect of insulin.This reduced sensitivity to insulin is
often referred to as insulin resistance.
Effects of diabetes mellitus : In both types of diabetes mellitus, metabolism of all the main food stuffs is altered. The basic effect of insulin lack or insulin - resistance on glucose metabolism is to prevent the efficient uptake and utilization of glucose by most cells of body, except those of the brain. As a result, blood glucose concentration increases, cell utilization of glucose falls increasingly lower, and utilization of fats and proteins increases.
Chronic effects diabetes: The long stand elevation of blood glucose is widely believed ti cause the cornic complications of diabetes
1.Premature atherosclerosis
2.Retinopathy.
3.Nephropathy.
4.Neuropathy.
Intensive treatment with insulin delays the onset and slows the progression of these long-term complications. The benefits of tight control of blood glucose outweight the increased risk of severe hypoglycemia.How hyperglycemia causes the chonic complications of diabetes is unclear.In cells where entry of glucose is not dependent on insulin,elevated blood glucos leads to increased intracellular glucose and its metabolites.For example,increased intracellular sorbitol may contribute to the formation of cataracts.Further hyperglycemia may promote the condensation of glucos (or its metabolites,particularly glyceraldehyde 3 phosate) with cellular proteins, in a reaction analogous to the formation Hba1c. These glycated proteins may mediate some of the early microvascular changes of diabetes.
Insulin
Chemistry of insulin : Insulin is protein is nature with a molecular wt . of about 5,808 . It is composed of two amino acid chains connected to each other by disulfide linkages. A chain conteins 21 amino acid and B chain contain 30 amino acids. When the two amino acid chains are split apart the functional activity of insulin is lost.
Function of insulin
1.On carbohydrate metabolism : Insulin increases uptake, uses, storage of glucose by the liver, muscle and all the cells of the body and decreases blood glucose level as follows : Insulin increases the activity of enzyme glucokinase which enhanced the uptake of glucose from blood and initiate phosphorilation of glucose in liver. Insulin inhibits the enzyme phosphorilase thus prevents break down of liver glycogen. Insulin stimulate the enzyme glycogen synthetase thus promotes glycogenesis. Insulin promotes conversion of excess liver glucose into fetty acid.Insulin inhibits gluconeogenesis.
2. On fat metabolism : Insulin promotes fatty acid synthesis. Insulin increases fat storage in the adipose tissue. Insulin act as fat
sparer by increasing utilization of carbohydrate in presence of fat.
3.On protein metabolism : It increases the transport of amino acid to cells. It increases translation of m RNA on ribosome thus forming new protein. Insulin promotes the rate of transcription of DNA to from RNA, which increases protein synthesis. Insulin inhibits gluconeogenesis. Insulin depressed protein catabolism.
Control of insulin secretion
1.Blood glucose level : Increased blood glucose level increases insulin secretion. As concentration of blood glucose rise above 100 mg / dl of blood, the rate os insulin secretion rises rapidly, reaching a peak some 10 to 30 times the basal level at blood glucose concentration between 400 and 600 mg/ dl.
2. Amino acids : Addition of excess amino acids stimulste insulin secretion.
3. GI tract hormones : Some GI tract hormones gastrin, secretin GIP, CCK - PZ etc, moderately stimulate insulin secretion.
4. Some other hormones of autonomic nervous system : Glucagon, growth hormone, cortisol, and to a lesser extent, progesterone
and estrogen either directly stimulate insulin secretion or potentiate the glucose stimulus for insulin secretion.Under some conditions stimulation of the parasympathetic nerves to the pancrease can increase insulin secretion. Howover it is doubtful that this effect is of physiological significance for regulating insulin secretion.
Metabolic changes in type I diabetes : Hyperglycemia and ketoacidasis are the hall marks of untreated diabetes mellitus. Hyperglycemia ia caused by increased hepatic production of glucose combined with diminished peripheral utilization. Ketosis results from increased mobilization of fatty acids from adipose tissue combined with accelerated hepatic synthesis of 3-hydroxybutyrate and acetoacetate. However,not all the fatty acids flooding the liver can be disposed of through oxidation or ketone body synthesis Fatty
Hormone increasing blood glucose level.Hormone decreasing blood glucose level.
Insulin
a.Insulin increases the activity of enzyme glucokinase which enhanced the uptake
of glucose from blood and initiate phospho-rilation of glucose in liver.
b.Insulin inhibits the enzme phosphorilase thus prevents break dowen of liver glycogen.
c.Insulin stimulate the enzyme glycogen synthetase thus promotes glycogensis .
d.Insulin promotes conversion of excess liver glucose into fatty acid.
e.Insulin inhibits gluconeogenesis.
Adrenal diabetes
Both the increased rate of gluconeogenesis and the moderate reduction in the rate of glucose utilisation by the cell cause the blood glucose concentration to rise.The rise in blood glucose in turn stilumates secretion of insulin.The increased plasma levels of insulin, however, are not as effective in maintaining plasma glucose as they are under normal conditions.For reasons that are not entirely clear high levels of glucocorticoid reduce the sensitivity of many tissues especially skeletal muscle and adipose tissue,to the stimulatory effects of insulin on glucose uptake and utilision.One possible explanation is that high levels of fatty acids caused by the effect of glucocorticoids to mobilise lipids from fat depots may impair insulins actions on the tissue. In this way excess secretion of glucocorticoids may produce disturbances of carbohydrate metabolism very similar to those found in patients with excess levels of growth hormone.The increase in blood glucose concentration is occasionally great enough ( 50 per sent or more above normal ) that the condition is called adrenal diabetes.Administration of insulin lowers the blood glucose concentration is only a moderate amount in adrenal diabetes-not nearly as much as it does in pancreatic diabetes-because the tissues are resistant to the effects of insulin.Diabetes inspidus
Diabetes insipidus is the syndrome charactreised by polyuria and polydipsia that resultswhen there is a vasopressin ( ADH ) deficiency or when the kidney fail to respond to the
hormone.
Types
1.Central diabetes insipidus.
2.Nephrogenic diabetes insipidus
Central diabetes insipidus ( Failure to produce ADH ) : An inability to produce or release ADH from the posterior pituitary can be caused by head injuries or infections, or it can be congenital.Because the distal tubular segments cannot reabsord water in the absence of ADH, this condition,called central diabetes insipidus.
response : The thirst mechanisms, are activated when excessive water is lost from the body; therefore,
as long as the person drinks enough water, large decreases in body fluid water do not occur. the primary
abnormality observed clinically in people with this condition is the large volume of dilute urine.However,
if water intake is restricted or the patient is unconscious for example, because of a head injury, severe
dehydration can rapidly occur.
Diabetes Mellitus
Definition: Diabetes mellitus is a syndrome of impaired carbohydrate, fat, and protein metabolism caused
by either lack of insulin secretim or decreased sensitivity of the tissues to insulin.
Types of diabetes mellitus: There are two general types of diabetes mellitus:
1.Type 1 diabetes, also called insulin-dependent diabetes mellitus (IDDM) :It is caused by lack of insulin
secretion.
2.Type 2 diabetes:Type 2 diabetes,also called non-insulin dependent diabetes mellitus (NIDDM) :It is caused by decreased sensitivity of target tissues to the metabolic effect of insulin.This reduced sensitivity to insulin is
often referred to as insulin resistance.
Effects of diabetes mellitus : In both types of diabetes mellitus, metabolism of all the main food stuffs is altered. The basic effect of insulin lack or insulin - resistance on glucose metabolism is to prevent the efficient uptake and utilization of glucose by most cells of body, except those of the brain. As a result, blood glucose concentration increases, cell utilization of glucose falls increasingly lower, and utilization of fats and proteins increases.
Chronic effects diabetes: The long stand elevation of blood glucose is widely believed ti cause the cornic complications of diabetes
1.Premature atherosclerosis
2.Retinopathy.
3.Nephropathy.
4.Neuropathy.
Intensive treatment with insulin delays the onset and slows the progression of these long-term complications. The benefits of tight control of blood glucose outweight the increased risk of severe hypoglycemia.How hyperglycemia causes the chonic complications of diabetes is unclear.In cells where entry of glucose is not dependent on insulin,elevated blood glucos leads to increased intracellular glucose and its metabolites.For example,increased intracellular sorbitol may contribute to the formation of cataracts.Further hyperglycemia may promote the condensation of glucos (or its metabolites,particularly glyceraldehyde 3 phosate) with cellular proteins, in a reaction analogous to the formation Hba1c. These glycated proteins may mediate some of the early microvascular changes of diabetes.
Insulin
Chemistry of insulin : Insulin is protein is nature with a molecular wt . of about 5,808 . It is composed of two amino acid chains connected to each other by disulfide linkages. A chain conteins 21 amino acid and B chain contain 30 amino acids. When the two amino acid chains are split apart the functional activity of insulin is lost.
Function of insulin
1.On carbohydrate metabolism : Insulin increases uptake, uses, storage of glucose by the liver, muscle and all the cells of the body and decreases blood glucose level as follows : Insulin increases the activity of enzyme glucokinase which enhanced the uptake of glucose from blood and initiate phosphorilation of glucose in liver. Insulin inhibits the enzyme phosphorilase thus prevents break down of liver glycogen. Insulin stimulate the enzyme glycogen synthetase thus promotes glycogenesis. Insulin promotes conversion of excess liver glucose into fetty acid.Insulin inhibits gluconeogenesis.
2. On fat metabolism : Insulin promotes fatty acid synthesis. Insulin increases fat storage in the adipose tissue. Insulin act as fat
sparer by increasing utilization of carbohydrate in presence of fat.
3.On protein metabolism : It increases the transport of amino acid to cells. It increases translation of m RNA on ribosome thus forming new protein. Insulin promotes the rate of transcription of DNA to from RNA, which increases protein synthesis. Insulin inhibits gluconeogenesis. Insulin depressed protein catabolism.
Control of insulin secretion
1.Blood glucose level : Increased blood glucose level increases insulin secretion. As concentration of blood glucose rise above 100 mg / dl of blood, the rate os insulin secretion rises rapidly, reaching a peak some 10 to 30 times the basal level at blood glucose concentration between 400 and 600 mg/ dl.
2. Amino acids : Addition of excess amino acids stimulste insulin secretion.
3. GI tract hormones : Some GI tract hormones gastrin, secretin GIP, CCK - PZ etc, moderately stimulate insulin secretion.
4. Some other hormones of autonomic nervous system : Glucagon, growth hormone, cortisol, and to a lesser extent, progesterone
and estrogen either directly stimulate insulin secretion or potentiate the glucose stimulus for insulin secretion.Under some conditions stimulation of the parasympathetic nerves to the pancrease can increase insulin secretion. Howover it is doubtful that this effect is of physiological significance for regulating insulin secretion.
Metabolic changes in type I diabetes : Hyperglycemia and ketoacidasis are the hall marks of untreated diabetes mellitus. Hyperglycemia ia caused by increased hepatic production of glucose combined with diminished peripheral utilization. Ketosis results from increased mobilization of fatty acids from adipose tissue combined with accelerated hepatic synthesis of 3-hydroxybutyrate and acetoacetate. However,not all the fatty acids flooding the liver can be disposed of through oxidation or ketone body synthesis Fatty
acids are also converted to triacylglycerol, which is packaged and secreted in VLDL. Chylomicrons are synthesized from dietary lipids by the intestinal mucosal cells following a meal. Because lipoprotein degradation catalyzed by lipoprotein lipase in adipose tissue is low in diabetics, the plasma chylomicron and VLDL levels are elavated, resuting in hypertiglyceridemia.
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