Gimner Reddy Drugs Of Carbohydrate Metabolism

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polyphagia

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too much hunger

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polyuria

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too much urine; too much glucose in urine;

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polydipsia

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too much thirst

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type I diabetes

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10 of cases, lack of insulin

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Type II diabetes

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insuline resistance

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complications of diabetes:

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microvascular complications
neuropathy (nerve damage)
nephropathy (kidney disease)
vision disorders
macrovascular complications (heart disease, stroke)
peripheral vascular disease

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progression of diabetes

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insulin resistance, hyperinsulinemia, impaired glucose tolerance, decline of B-cell function, type II diabetes

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Hemoglobin A1c

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glucose-containing goblin.
Hemoglobin A1C levels has positive, linear coorelation with blood glucose level. A1C can be used to monitor progress of therapy.

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glucose --> ____ --> fructose

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sorbitol.
lens, retina, nerves, and kidneys don't have sorbitol dehydrogenase. therefore, sorbitol gets stuck in those cells and results in cel swelling and pathology.

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increased sorbitol =

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decrease glutathione.
glutathione is main reducing agent in the body, which increases oxidative stress.

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high plasma glucose = __ glucose and __ inositol inside cells

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low and low

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inositol

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many second messengers.
enters cell through glucose transporters. high glucose competes with inositol and results in low intracellular inositol levels. causes some problems, esp those associated with the nervous system.

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insulin _____ cell division, nutrient uptake into cells, syntehsis of lipids, glycogen and proteins

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increases.
insulin is a growth factor.

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AGE

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advanced glycation end products.alters gene transcription.

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addition of n-acetylglucoseamine

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alters protein activity. it alters gene transcription.

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excess glucose

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electron transport system is unable to handle increased proton gradients and more reactive oxygen species is made. leads to pathology in cells.

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6 explanations for complications of diabetes mellitus

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1. nonenzymatic addition of glucose to proteins (ex. hemoglobin A1c)
2. addition of glucose derviatibes (N-acetylglucoseamine) to proteins
3. altered gene expression and chronic immune response against altered proteins now seen as foreign poteins
4. cell swelling because of sorbitol formation
5. decreased levels of inositol in cells
6. formation of reactive oxygen species.

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starch blockers

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less dietary glucose enters blood stream.

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alpha glucosidase (amylase) inhibitors

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acarbose and miglitol.
disaccharides with a nonhydrolyzable bond (like sulfur) and have high affinity for enzymes

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sulfonylureas

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bind K- chanels, inhibitthem and depolarize cells, leading to release of more insulin from Beta cells of panceas.

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normal regulation of insulin release from beta cells

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high glucose = high ATP, low ADP

low glucose = high ADP, low ATP

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ADP and K+ channels

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open K+ channels, hyperpolarizes

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ATP and K+ channels

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closes K+ channels and depolarizes

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insulin sensitizers

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biguanides/metformin, and TZDs

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biguanides - metformin

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works in the liver. decreases gluconeognesis, and fatty acid degradation.

increaes glucose transporters and increases glucose consumption.

bottom line: less glucose released into blood stream.

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TZDs

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rosiglitazone and pioglitazone

works in adipose tissue; activates PPAR-gamma receptors. adipose uses more glucose and maes triglycerides. hormone-sensitive lipase is inhibied and less fatty acids are released.

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Glucagon-like peptide

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GLP-1.

made by eneteroendocrine cells in ileum and released into plasma. decreases appetite, decreases intestinal motility, increaes insulin release by beta cells, decreases glucagon release by alpha cells.

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exenatide

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GLP-1 analog

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sitagliptin

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increases half-life of GLP-1

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adverse effects of insulin

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hypoglycemia

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adverse effects of sulfonylureas

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hypoglycemia

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adverse effects of starch blockers

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flatulence, bloating, GI disturbances

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adverse effecs of metformin

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lactic acid acidosis

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adverse effects of TZDs

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weight gain