The effect of mitochondrial dysfunction on glucose metabolism during shock.
Hepatic glycogen content, blood glucose and lactate concentrations, and hepatic mitochondrial energy-linked functions were measured in rats in late hemorrhagic shock. As judged by correlation coefficients, the following significant relationships were noted: (formula: see text). Glycogen depletion, hypoglycemia, and lactic acidemia occurred frequently. However, alone or in combination, these variables did not relate significantly to need for or amount of shed blood uptake prior to sacrifice. Neither hepatic glycogen depletion nor uncoupled hepatic mitochondrial oxidative phosphorylation alone accounted for hypoglycemia. The genesis of hypoglycemia was determined by the occurrence of both these events in either sequence. When hepatic mitochondrial oxidative phosphorylation became uncoupled, the blood glucose concentration and hepatic glycogen content were linearly related (r = 0.94). This effect probably results from impaired gluconeogenesis due to mitochondrial dysfunction.
D000818:Animals; D005947:Glucose / Q000378:metabolism*; D006439:Hemodynamics; D007773:Lactates / Q000378:metabolism; D008112:Liver Glycogen / Q000378:metabolism; D008297:Male; D008930:Mitochondria, Liver / Q000378:metabolism*; D010085:Oxidative Phosphorylation; D051381:Rats; D012771:Shock, Hemorrhagic / Q000378:metabolism* / Q000503:physiopathology
D007773:Lactates; D008112:Liver Glycogen; D005947:Glucose