JCI - Probing cell type–specific functions of Gi in vivo identifies GPCR regulators of insulin secretion

Probing cell type–specific functions of G_i in vivo identifies GPCR regulators of insulin secretion

Jean B. Regard, Hiroshi Kataoka, David A. Cano, Eric Camerer, Liya Yin, Yao-Wu Zheng, Thomas S. Scanlan, Matthias Hebrok, Shaun R. Coughlin

Published in Volume 117, Issue 12

J Clin Invest. 2007; 117(12):4034–4043 doi:10.1172/JCI32994

Abstract | Full text | PDF | Supplemental material

Options: View larger image (or click on image)

Figure 3

RIP-PTX mice show improved glucose tolerance and resistance to high-fat diet–induced hyperglycemia.

(A) IPGTT in 8- to 10-week-old male RIP-PTX mice, littermate controls, and age-matched, background-matched RIP-cre mice. Glucose (2 mg/g) was administered i.p. at time 0, and plasma glucose was measured at the indicated time points. Note the lower glucose levels in RIP-PTX mice compared with controls (n = 9–10; **P < 0.0001). (B) GSIS. Glucose was administered at 3 mg/g i.p. to mice as in A, and plasma insulin levels were measured at the indicated times. Note the 6.5-fold increase over already elevated basal levels in RIP-PTX mice compared with a 3-fold increase in controls (inset) (n = 7–8; **P < 0.0001). (C) IPGTT in RIP-PTX mice and littermate controls fed a normal or high-fat diet for 30 weeks. RIP-PTX mice fed a high-fat diet had glucose levels significantly lower than controls on a high-fat diet (n = 8–11; P < 0.0001) and lower than controls on a normal diet (n = 8–10; P = 0.007).