Fig. 1: Kmt5c deficiency impairs hepatocyte gluconeogenesis.
From: Non-catalytic mechanisms of KMT5C regulating hepatic gluconeogenesis

a–d Western blot (top) and densitometry analyses (bottom) were conducted to determine KMT5C and H4K20me3 protein levels in liver tissues. a Eight-week-old male C57BL/6 J mice were sacrificed at fed, 16 h fasting, and 4 h refeeding states (n = 3 for KMT5C, n = 4 for H4K20me3). b Control and ob/ob mice at fed state (2-month-old male mice, n = 5 each group). c Control and db/db mice at fed state (2-month-old male mice, n = 3 for KMT5C, n = 4 for H4K20me3). d Male normal chow and HFD-induced obese mice at fed state. HFD has been fed for 12 weeks. (n = 4 for KMT5C, n = 6 for H4K20me3). e The KMT5C protein level in non-parenchymal cells (NPC) and hepatocytes isolated from male mice livers at the age of 2 months. (n = 2 for each group). f–i Western blot analysis of indicated proteins in primary hepatocytes (f, h) and protein quantifications (g, i). f Cre or control GFP adenovirus-infected primary hepatocytes isolated from 12-week-old male Kmt5cflox/flox mice (n = 4 per group). h primary hepatocytes were isolated from 12-week-old male WT and KO mice and were stimulated with or without 100 nM glucagon for 14 h (n = 3 per group). j, k Glucose production was measured in the culture medium of primary hepatocytes isolated from 12-week-old male WT and KO mice, using pyruvate and lactate (j) (n = 3 per group) or glycerol (k) (n = 4 per group) as substrates. a–d, g, i–k data present mean ± s.e.m. a–e n presents biologically independent animals. f–k, n represents biologically independent cell samples. b–d, g, j, k two-tailed unpaired Student’s t test; a, i one-way ANOVA. All experiments here were repeated independently three times with similar results. Source data are provided as a Source Data file.