The onset of Type II diabetes is gradual and typically occurs in adulthood.
Both Type I and Type II
Normal - in the first stage, the problem is not about secretion, it is about resistance.
Target organs respond less to the insulin message in the first stage of Type II diabetes.
Lipotoxicity and inflammation promote insulin resistance.
Intestinal cells primarily absorb carbohydrates in the form of Monosaccharides.
Insulin promotes fusion of intracellular GLUT-4 vesicles to the plasma membrane.
Glucagon causes muscle to decrease glucost uptake by altering GLUT-4 levels present on the plasma membrane.
Auto-phosphorylates and Activates IRS-1
Activate PI3K
Insulin receptor dephosphorylation
Proteolytic degradation of insulin receptor and IRS-1
IRS-1 phosphorylation on Threonine residue
Accumulation of misfolded insulin in the Golgi system.
In Type II diabetes both glucose and fatty acid levels increase in the blood.
Reduced glucose uptake due to insulin resistance.
Increased liver glucose production through glycogenolysis and gluconeogenesis.
Lifestyle modifications such as exercise, reduced caloric intake, and better diet.
Drugs that increase insulin production and sensitivity.
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