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Diabetes Mellitus
Type I Diabetes Mellitus / IDDM
Autoimmune disorder that destroys the pancreatic beta cells
Insulin deficit hyperglycemia
Favored by genetic predisposition
1st degree children of diabetic parents: 5-10% risk
Risk is 5x higher for children of a diabetic father than of a
diabetic mother
Insulin deficit decreased glucose uptake by pancreatic cells
increased glucagon level:
hepatic glycogenolysis & gluconeogenesis
hepatic glucose output hyperglycemia
lypolisis FFA A-CoA TCA
ketone bodies
Hyperglycemia osmotic diuresis
glucosuria
Treated by insulin replacement
Diabetes Mellitus
Type II DM (90-95% of all diabetics western)
Insulin-independent DM / Non-insulin dependent DM (NIDDM) / adult
onset DM.
Resistance to insulin, rather than lack of insulin, or both (late stage)
Insulin levels may be normal, lowered or elevated
Strongly favored by genetic predisposition
Environment
Excessive caloric intake, obesity
Metabolic alterations are less pronounced than type I
Resistance to insulin
decreased glucose uptake by pancreatic cells increased
glucagon level
hepatic glucose output hyperglycemia
lipolysis increased FFA
decreased glucose uptake by insulin-sensitive cells hyperglycemia
Corrected by diet, weight loss
Exercise
Decreases insulin secretion (sympathetic effect on
Polyuria
Catabolism of macromulecules
Protein degradation
(muscle wasting)
Amino acids
Carbon skeletons
Polydipsia
Triglyceride degradation
(reduction of fat stores)
Fatty acid oxidation
ATP
Hepatic
glucose synthesis
Ketone synthesis
Ketonuria
Ketonemia
Decreased
glucose uptake
Hyperglycemia,
glycosuria,
osmotic diuresis,
electrolyte depletion
Increased
protein catabolism
Increased plasma
amino acids,
nitrogen loss in urine
Dehydration,
acidosis,
Coma,
death
Increased
lipolysis
Glycosylation of protein:
Glucose + Protein Schiffs base Glycosylated protein
Lens of the eyes, peripheral nerves, basement membrane of kidneys
Polyol formation:
Glucose sorbitol
Peripheral nerves, lens, renal glomeruli, seminal vesicles