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Diabetes Mellitus - Biochemistry
DIAGNOSIS
- Diabetes: fasting blood glucose > 126 mg/dl
- Normal: fasting blood glucose < 100 mg/dl
- Prediabetes: 125 > fasting blood glucose > 100
Type I
- Autoimmune destruction of pancreatic beta cells
- Rarer than Type II
- Sudden onset
Type II
- Most common type
- Symptoms tend to be milder than Type I
- Gradual onset of symptoms
- Normally insulin-sensitive tissues become insulin resistant
Hyperglycemia: elevated blood glucose
1. Tissues cannot use glucose (no insulin or insulin resistance)
2. Liver increases gluconeogenesis
- Adipose breaks down TAG to FFA & glycerol (gluconeogenic)
- Skeletal muscle breaks down proteins: releases glucogenic amino acids
- Pancreatic alpha cells secrete abnormally high levels of glucagon
Dyslipidemia: elevated blood lipid levels
- Adipose breaks down TAG and releases FFA & glycerol
- Liver releases TAG in VLDL
- VLDL & chylomicrons accumulate because of low lipoprotein lipase (LPL) concentrations
- Insulin normally stimulates LPL synthesis
Ketoacidosis: Type I only
- Increased glucagon secretion promotes ketogenesis
- Adipose FFA shunt into ketogenesis
- Type II diabetics: hyperglycemia & hypertriglyceridemia w/o ketoacidosis
Polyphagia: extreme hunger
- Mass mobilization of adipose TAG & muscle proteins
- Overproduction of glucagon
Polyuria: frequent urination
- Ketoacidosis and hyperglycemia inhibit kidney urine filtration
- Glycosuria (glucose in the urine)
- Ketonuria (ketone bodies in the urine): Type I ONLY
- Leads to extreme thirst
Polydipsia: extreme thirst
- Extreme conditions: polyuria can lead to volume depletion
- Volume depletion and ketoacidosis can produce diabetic coma