Enhanced glucose cycling and suppressed de novo synthesis of glucose-6-phosphate result in a net unchanged hepatic glucose output in ob/ob miceBandsma, RHJ., Grefhorst, A., van Dijk, TH., van der Sluijs, FH., Hammer, A., Reijngoud, DJ. & Kuipers, F., Nov-2004, In : Diabetologia. 47, 11, p. 2022-2031 10 p.
Research output: Contribution to journal › Article › Academic › peer-review
Aims/hypothesis. Leptin-deficient ob/ob mice are hyperinsulinaemic and hyperglycaemic; however, the cause of hyperglycaemia remains largely unknown.
Methods. Glucose metabolism in vivo in 9-h fasted ob/ob mice and lean littermates was studied by infusing [U-C-13]-glucose, [2-C-13]-glycerol, [1-H-2]-galactose and paracetamol for 6 h, applying mass isotopomer distribution analysis on blood glucose and urinary paracetamol-glucuronide.
Results. When expressed on the basis of body weight, endogenous glucose production (109 23 vs 152 +/- 27 mumol.kg(-1).min(-1), obese versus lean mice, p
Conclusions/interpretation. Unaffected total hepatic glucose output in the presence of hyperinsulinaemia reflects hepatic insulin resistance in ob/ob mice, which is associated with markedly increased rates of glucose cycling. Hyperglycaemia in ob/ob mice primarily results from a decreased metabolic clearance rate of glucose.
|Number of pages||10|
|Publication status||Published - Nov-2004|
- glucose-6-phosphate, gluconeogenesis, glycogen, glycogenolysis, hepatic glucose production, mass isotopomer distribution analysis, ob/ob mice, stable isotopes, OB-OB MICE, DIABETES-MELLITUS, MASS ISOTOPOMER, CONSCIOUS MICE, GLUCONEOGENESIS, INSULIN, GLYCOGEN, METABOLISM, TURNOVER, HUMANS