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Diabetes Mellitus: Pathophysiology

 PATHOPHYSIOLOGY OF DM

IMPAIRED INSULIN SECRETION

  • A pancreas with normal Beta cell function is able to adjust insulin production to maintain normal blood glucose levels.
  • Hyperinsulinemia or high blood levels of insulin is an early finding of T2 DM.
  • More insulin is secreted to maintain normal blood glucose levels until eventually the pancreas can no longer produce sufficient insulin.
  • Impaired Beta cell function results in reduced ability to produce a first-phase insulin response sufficient to signal the liver to stop producing glucose after a meal.
  • As DM progresses, large numbers of patients with T2DM eventually loses all beta cell function and require exogenous insulin to maintain the blood glucose levels. 


INSULIN RESISTANCE

  • Insulin resistance is the primary factor that differentiates T2DM from other forms of diabetes.
  • Insulin resistance maybe present for several years prior to the diagnosis of DM.
  • Insulin resistance occurs more significantly in skeletal muscles and liver.
  • Insulin resistance in the liver poses a double threat because the liver becomes nonresponsive to insulin for glucose uptake and hepatic production of glucose after a meal does not cease which leads to elevated fasting and post-meal glucose levels.


IMAPIRED GLUCAGON SECRETION

  • Glucagon is the counter regulatory hormones produced by the beta cells that raises blood glucose levels.
  • The release of insulin and the inhibition of glucagon is glucose stimulated.
  • Most patients with a 10–20-year history of T1DM have lost their ability to release glucagon, which increases their risk of hypoglycemic unawareness.



GLUCAGON LIKE PEPTIDE AND GIP IMAPIRED 

People with T2DM have impaired phase 2 insulin release, and some have impaired glucagon-like peptide (GLP-Q) and glucose-dependent insulinotropic polypeptide (GIP) release, which further reduces the release of insulin.

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