Dysfunction of membrane-receptor system of blood cells and kidney tissue in experimental diabetes mellitus

Bull Exp Biol Med. 2013 Mar;154(5):610-3. doi: 10.1007/s10517-013-2011-x.

Abstract

The effect of streptozotocin-induced diabetes mellitus on some parameters of energy metabolism and functional status of cell membranes was studied in experiments on rats. It was found that the development of diabetes mellitus is associated with dramatic changes in the metabolism of blood cells and kidney tissue: inhibition of aerobic ATP synthesis, accumulation of lactate, uncoupling of oxidative phosphorylation, and development of lactic acidosis. Diabetes mellitus leads to restructuring of membrane lipids, changes in microviscosity, and suppression of insulin receptors and membrane-bound Na(+), K(+)-ATPase, and Ca(2+)-ATPase. Sharply increased levels of LPO products and lactic acidosis during DM indicate an imbalance in the LPO-antioxidant system and development of oxidative stress.

MeSH terms

  • Acidosis, Lactic / metabolism
  • Adenosine Triphosphate / biosynthesis
  • Animals
  • Blood Glucose / metabolism
  • Cell Membrane / physiology
  • Diabetes Mellitus, Experimental / blood*
  • Diabetes Mellitus, Experimental / metabolism*
  • Energy Metabolism
  • Erythrocytes / metabolism*
  • Glycolysis
  • Kidney / metabolism*
  • Lactic Acid / metabolism
  • Lipid Peroxidation
  • Male
  • Membrane Lipids / metabolism
  • Oxidative Phosphorylation
  • Oxidative Stress
  • Rats
  • Rats, Wistar
  • Receptor, Insulin / metabolism
  • Sodium-Potassium-Exchanging ATPase / metabolism
  • Streptozocin

Substances

  • Blood Glucose
  • Membrane Lipids
  • Lactic Acid
  • Streptozocin
  • Adenosine Triphosphate
  • Receptor, Insulin
  • Sodium-Potassium-Exchanging ATPase