Effect of Global ATGL Knockout on Murine Fasting Glucose Kinetics

J Diabetes Res. 2015:2015:542029. doi: 10.1155/2015/542029. Epub 2015 Jul 5.

Abstract

Mice deficient in adipose triglyceride lipase (ATGL(-/-)) present elevated ectopic lipid levels but are paradoxically glucose-tolerant. Measurement of endogenous glucose production (EGP) and Cori cycle activity provide insights into the maintenance of glycemic control in these animals. These parameters were determined in 7 wild-type (ATGL(+/-)) and 6 ATGL(-/-) mice by a primed-infusion of [U-(13)C6]glucose followed by LC-MS/MS targeted mass-isotopomer analysis of blood glucose. EGP was quantified by isotope dilution of [U-(13)C6]glucose while Cori cycling was estimated by analysis of glucose triose (13)C-isotopomers. Fasting plasma free fatty-acids were significantly lower in ATGL(-/-) versus control mice (0.43 ± 0.05 mM versus 0.73 ± 0.11 mM, P < 0.05). Six-hour fasting EGP rates were identical for both ATGL(-/-) and control mice (79 ± 11 versus 71 ± 7 μmol/kg/min, resp.). Peripheral glucose metabolism was dominated by Cori cycling (80 ± 2% and 82 ± 7% of glucose disposal for ATGL(-/-) and control mice, resp.) indicating that peripheral glucose oxidation was not significantly upregulated in ATGL(-/-) mice under these conditions. The glucose (13)C-isotopomer distributions in both ATGL(-/-) and control mice were consistent with extensive hepatic pyruvate recycling. This suggests that gluconeogenic outflow from the Krebs cycle was also well compensated in ATGL(-/-) mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blood Glucose / metabolism*
  • Carbon Isotopes
  • Chromatography, Liquid
  • Citric Acid Cycle*
  • Fatty Acids, Nonesterified / metabolism*
  • Lipase / genetics*
  • Liver / metabolism*
  • Mice
  • Mice, Knockout
  • Oxidation-Reduction
  • Proton Magnetic Resonance Spectroscopy
  • Tandem Mass Spectrometry

Substances

  • Blood Glucose
  • Carbon Isotopes
  • Fatty Acids, Nonesterified
  • Lipase
  • PNPLA2 protein, mouse