| First Author | Coelho M | Year | 2015 |
| Journal | J Diabetes Res | Volume | 2015 |
| Pages | 542029 | PubMed ID | 26236747 |
| Mgi Jnum | J:330617 | Mgi Id | MGI:7380460 |
| Doi | 10.1155/2015/542029 | Citation | Coelho M, et al. (2015) Effect of Global ATGL Knockout on Murine Fasting Glucose Kinetics. J Diabetes Res 2015:542029 |
| abstractText | 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 mumol/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. |
