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Articles by D. H. Wasserman
Total Records ( 2 ) for D. H. Wasserman
  O. P McGuinness , J. E Ayala , M. R Laughlin and D. H. Wasserman

This article addresses two topics. We provide an overview of the National Institutes of Health Mouse Metabolic Phenotyping Center (MMPC) Program. We then discuss some observations we have made during the first eight years of the Vanderbilt MMPC regarding common phenotyping practices. We include specific recommendations to improve phenotyping practices for tests of glucose tolerance and insulin action. We recommend that methods for experiments in vivo be described in manuscripts. We make specific recommendations for data presentation, interpretation, and experimental design for each test. To facilitate and maximize the exchange of scientific information, we suggest that guidelines be developed for methods used to assess glucose tolerance and insulin action in vivo.

  E. D Berglund , L Kang , R. S Lee Young , C. M Hasenour , D. G Lustig , S. E Lynes , E. P Donahue , L. L Swift , M. J Charron and D. H. Wasserman

Hepatic glucagon action increases in response to accelerated metabolic demands and is associated with increased whole body substrate availability, including circulating lipids. The hypothesis that increases in hepatic glucagon action stimulate AMP-activated protein kinase (AMPK) signaling and peroxisome proliferator-activated receptor- (PPAR) and fibroblast growth factor 21 (FGF21) expression in a manner modulated by fatty acids was tested in vivo. Wild-type (gcgr+/+) and glucagon receptor-null (gcgr–/–) littermate mice were studied using an 18-h fast, exercise, and hyperglucagonemic-euglycemic clamps plus or minus increased circulating lipids. Fasting and exercise in gcgr+/+, but not gcgr–/– mice, increased hepatic phosphorylated AMPK at threonine 172 (p-AMPKThr172) and PPAR and FGF21 mRNA. Clamp results in gcgr+/+ mice demonstrate that hyperlipidemia does not independently impact or modify glucagon-stimulated increases in hepatic AMP/ATP, p-AMPKThr172, or PPAR and FGF21 mRNA. It blunted glucagon-stimulated acetyl-CoA carboxylase phosphorylation, a downstream target of AMPK, and accentuated PPAR and FGF21 expression. All effects were absent in gcgr–/– mice. These findings demonstrate that glucagon exerts a critical regulatory role in liver to stimulate pathways linked to lipid metabolism in vivo and shows for the first time that effects of glucagon on PPAR and FGF21 expression are amplified by a physiological increase in circulating lipids.

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