Fig. 3
From: Hepatic Sdf2l1 controls feeding-induced ER stress and regulates metabolism
Functions of Sdf2l1 in vivo. Wild-type mice were administered with Ad-Sdf2l1 RNAi intravenously (2.0 × 107 PFU/g BW) to knock down the gene in the liver. a–c ER stress and insulin signaling in the liver (n = 4–5), analyzed by a RT-PCR (n = 4–5), b Western blotting of microsomal fractions (n = 4), and c Western blotting of total lysates (n = 4). d–f Effects of knocking down on glucose metabolism (n = 9–11): d ad libitum-fed plasma glucose, e plasma glucose in insulin tolerance test (ITT), after intraperitoneal injection of human regular insulin (0.75 U/kg BW), f plasma glucose and insulin levels in an oral glucose tolerance test (OGTT), after oral administration of glucose (0.75 g/kg BW), following 16 h of fasting. g–i Results of hyperinsulinemic-euglycemic clamp studies after 3 h of fasting (2.5 mU/kg/min, n = 6–7), in wild-type mice with Sdf2l1 knocked down: g glucose infusion rate (GIR), endogenous glucose production (EGP), and rate of glucose disappearance (Rd); h, i the liver samples after the clamp studies were analyzed by h Western blotting and i RT-PCR. j, k Effects of knocking down on lipid metabolism, analyzed with j triglyceride contents quantification (n = 4–5), and k Oil Red O staining. Values of the data are expressed as mean ± SEM. *P < 0.05, **P < 0.01. Unpaired 2-tailed t-test was used for assessment. Scale bars: 100 μm
