Orphan receptor small heterodimer partner is an important mediator of glucose homeostasis.

Orphan receptor small heterodimer partner is an important mediator of glucose homeostasis. Research Abstract Details 

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Orphan receptor small heterodimer partner is an important mediator of glucose homeostasis. Abstract Text:

Li Wang,Jiansheng Huang,Pradip Saha,Rohit N Kulkarni,Min Hu,Yongdeuk Kim,Keungyu Park,Lawrence Chan,Arun S Rajan,Inkyu Lee,David D Moore,

The orphan receptor small heterodimer partner (SHP; NROB2) is a transcriptional repressor that inhibits nuclear receptor signaling in diverse metabolic pathways. Here, we report that SHP(-/-) mice exhibited hypoinsulinemia with age, which was associated with increased peripheral insulin sensitivity and increased response of isolated islets to glucose stimulation, yet maintain normal levels of blood glucose. Deficiency in SHP function resulted in up-regulation of glucose transporter 4 mRNA and glucose uptake in muscles, and overexpression of SHP in C2C12 cells inhibited both basal and peroxisomal proliferator-activated receptor gamma (PPARgamma) coactivator-1alpha-stimulated glucose transporter 4 expression and glucose uptake. SHP(-/-) hepatocytes showed markedly decreased basal glucose production in cultures, and SHP(-/-) livers had increased glycogen stores and were more sensitive to insulin inhibition of glucose output, which were concomitant with decreased expression for PPARgamma1, fatty acid translocase, glucose-6-phosphatase, and phosphoenol/pyruvate carboxykinase, and increased mRNAs for glucokinase and pyruvate kinase. In white fat, SHP deficiency resulted in up-regulation of genes involved in insulin sensitizing, including PPARgamma2 and adiponectin. We show that, at the transcriptional level, SHP directly represses adiponectin promoter activity by PPARgamma/liver receptor homolog-1. The results suggest that the increases in insulin sensitivity through multiple signaling pathways in muscle, liver, and fat, with an increase in islet secretory function, represent the complex mechanism whereby SHP deficiency leads to improvement in insulin sensitivity, secretion, and diabetes.

Orphan receptor small heterodimer partner is an important mediator of glucose homeostasis. Publishing Authors By Initials

L Wang,J Huang,P Saha,RN Kulkarni,M Hu,Y Kim,K Park,L Chan,AS Rajan,I Lee,DD Moore,

For similar proteins: receptors, cytoplasmic and nuclear research abstracts see: proteins: receptors, cytoplasmic and nuclear research

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Orphan receptor small heterodimer partner is an important mediator of glucose homeostasis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Molecular endocrinology (Baltimore, Md.)

VOLUME: 20

Page Numbers: 2671-81

Journal Abbreviation: Mol. Endocrinol.

ISSN: 0888-8809

DAY: 27

MONTH: 06

YEAR: 2006

Orphan receptor small heterodimer partner is an important mediator of glucose homeostasis. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8801431

Orphan receptor small heterodimer partner is an important mediator of glucose homeostasis. Keywords Mesh Terms:

KEYWORDS: Receptors, Cytoplasmic and Nuclear

MESH TERMS: physiology

Chemical & Substance for Abstract: Orphan receptor small heterodimer partner is an important mediator of glucose homeostasis. Information

Substance Name: Glucose

Registry Number: 50-99-7

Grant and Affiliation Information for Orphan receptor small heterodimer partner is an important mediator of glucose homeostasis.

AFFILIATION: Department of Medicine, University of Kansas Medical Center, Kansas City, Kansas 66160, USA. lwang2@kumc.edu

Country: United States

AGENCY: United States NHLBI

GRANT: R01 HL51586

ACRONYM: HL

MEDLINETA: Mol Endocrinol

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