Extended Data Figure 4.
Glucagon acutely stimulates gluconeogenesis by activating intrahepatic, but not white adipose tissue, lipolysis. (a) Liver HSL phosphorylation (n=5). Blots in Figures 1f and 2a, and Extended Data Figures 1b, 1d, 1f, 3f, 3g, and 4a were stripped and re-probed for all proteins of interest. In panels a-c, groups were compared using the 2-tailed unpaired Student’s t-test. (b)-(c) In vitro NEFA and glycerol production from isolated hepatocytes (n=14 WT and 15 KO). (d) Plasma NEFA concentrations in mice treated with somatostatin, replacement basal insulin, and glucagon (n=5 WT and 6 KO). No significant differences were observed between genotypes using the 2-tailed unpaired Student t-test, or before vs. after glucagon using the 2-tailed paired Student’s t-test. (e)-(f) NEFA production and VPC in isolated hepatocytes incubated in the ATGL inhibitor atglistatin (n=6). (g)-(n) NEFA production from isolated hepatocytes treated with ET-18-OCH3 (n=3), U-73122 (n=3), H-89 (n=6), vasopressin (n=3), KN-93 (n=6), 2-APB (n=3), caffeine (n=3), and thapsigargin (n=3). In all panels, *P<0.05, **P<0.01, ***P<0.001 versus the same genotype -glucagon -drug; §P<0.05, §§ P<0.01, §§§ P<0.001 versus the same genotype +glucagon -drug by the 2-tailed unpaired Student’s t-test. If no statistical comparison is denoted, the groups were not significantly different. Error bars represent the S.E.M.