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World J Diabetes. Aug 15, 2014; 5(4): 511-526
Published online Aug 15, 2014. doi: 10.4239/wjd.v5.i4.511
Published online Aug 15, 2014. doi: 10.4239/wjd.v5.i4.511
SH2B1 regulation of energy balance, body weight, and glucose metabolism
Liangyou Rui, Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI 48109, United States
Author contributions: Rui L contributed to this work.
Supported by The National Institutes of Health (NIH) grants, No. RO1 DK 065122 and No. RO1 DK091591
Correspondence to: Liangyou Rui, PhD, Department of Molecular and Integrative Physiology, University of Michigan Medical School, 1137 Catherine Street, Ann Arbor, MI 48109, United States. ruily@umich.edu
Telephone: +1-734-6157544 Fax: +1-734-6479523
Received: November 25, 2013
Revised: March 6, 2014
Accepted: May 31, 2014
Published online: August 15, 2014
Revised: March 6, 2014
Accepted: May 31, 2014
Published online: August 15, 2014
Core Tip
Core tip: The Src homology 2B (SH2B) family members mediate cell signaling in response to a variety of hormones, cytokines, and growth factors. In the brain, SH2B1 enhances leptin signaling and leptin’s anti-obesity action. In peripheral tissues, SH2B1 cell-autonomously enhances insulin signaling. In pancreatic islets, SH2B1 is required for compensatory β cell expansion in response to insulin resistance and β cell stress. SH2B1-deficiency results in severe leptin resistance, energy imbalance, obesity, and type 2 diabetes. SH2B1 mutations are linked to leptin resistance, insulin resistance, obesity, and type 2 diabetes in humans. Thus, SH2B1 is a critical metabolic regulator in mammals.