Extended Data Fig. 8: Chronic glucagon treatment reverses nonalcoholic fatty liver disease and glucose intolerance in wild-type, but not Insp3r1-knockout, mice.
From: Glucagon stimulates gluconeogenesis by INSP3R1-mediated hepatic lipolysis
a, Body weight (n = 10 wild type − glucagon, 11 wild type + glucagon, 8 knockout − glucagon and 8 knockout + glucagon). b, c, Food and water intake. In b–g, n = 8 wild type − glucagon, 9 wild type + glucagon, 7 knockout − glucagon and 8 knockout + glucagon. d, Energy expenditure. e, f, Oxygen consumption and carbon dioxide production. g, Activity. h, Plasma NEFA. In h–j, n = 10 wild type − glucagon, 11 wild type + glucagon, 8 knockout − glucagon and 8 knockout + glucagon. i, j, Glucose and insulin area under the curve during an intraperitoneal glucose tolerance test. In all panels, mean ± s.e.m. is shown. Statistical comparisons were performed using a two-tailed unpaired Student’s t-test. If no statistical comparison is denoted, the groups were not significantly different. All n values refer to numbers of mice.
