Fig. 1
From: Sirt2 facilitates hepatic glucose uptake by deacetylating glucokinase regulatory protein
NAD+ restoration increases glucose uptake in steatotic hepatocytes. a, b NAD+ (a) and 2-deoxyglucose (2-DG) uptake (b) levels in primary hepatocytes derived from lean control or db/db mice with or without nicotinamide mononucleotide (NMN) (n = 3). c Schematic representation of NAD+ metabolism. d The protein level of glucokinase (GK) in primary hepatocytes derived from lean and db/db mice (n = 3). e, f NAD+ (e) and 2-DG uptake (f) levels in mouse primary hepatocytes treated with siNampt in the presence or absence of NMN (n = 3). g, h NAD + (g) and 2-DG uptake (h) levels in mouse primary hepatocytes treated with gallotannin (GTN) in the presence or absence of NMN (n = 3). i Glucose tolerance testing (1 g/kg) and the area under the curve (AUC) of the glucose tolerance test in normal chow (NC) mice and high-fat diet (HFD) mice treated with or without NMN during continuous dosing with somatostatin (n = 5). j Hyperinsulinemic-hyperglycemic clamping in HFD mice treated with or without NMN, performed as shown in the schematic. k–m 2-DG uptake levels in the liver, white adipose tissue (WAT), and skeletal muscle of HFD mice (n = 6) (k), hepatic G6pc and Gck mRNA expressions (n = 6) (l), and hepatic GK protein expression (m) during hyperinsulinemic-hyperglycemic clamping. *P < 0.05; one-way analysis of variance (ANOVA) with the Fisher’s PLSD post-hoc test (a, b, d–h, i right) and Student’s t-test (k, l), *P < 0.05, compared with NC, #P < 0.05, HFD vs. HFD with NMN in (i) left; one-way ANOVA with the Fisher’s PLSD post -hoc test. Data in d, m are representative of at least three independent experiments. Error bars show the standard error of the mean (s.e.m.)
