SOCS3 inhibits insulin signaling in porcine primary adipocytes.

Mol Cell Biochem

Laboratory of Animal Fat Deposition and Muscle Development, College of Animal Science and Technology, Northwest A&F University, 22 Xinong Road, Yangling, 712100, Shaanxi Province, People's Republic of China.

Published: December 2010

Insulin resistance is a major player in the pathogenesis of type II diabetes, the metabolic syndrome, and obesity. SOCS3 plays an important role in the development of insulin resistance. To investigate the role of SOCS3 in porcine adipocyte insulin signaling, we first detected the effect of insulin on SOCS3 mRNA and protein expression in porcine primary adipocytes by real-time RT-PCR and Western blotting. Then, we constructed a recombinant adenovirus encoding SOCS3 gene (Ad-SOCS3) which was used to infect differentiated porcine primary adipocytes for 3 days. The expression and phosphorylation of main insulin signaling components were detected by Western blotting. The results showed that 100 nM insulin could induce SOCS3 mRNA expression but not protein expression, and overexpression of SOCS3 decreased IRS1 protein level, insulin-stimulated IRS1 tyrosine phosphorylation, PI3K activation, and Akt phosphorylation, but increased IRS1 serine phosphorylation in porcine primary adipocytes. These results indicate that SOCS3 is an important negative regulator of insulin signaling in porcine adipocytes. Thus, SOCS3 may be a novel therapeutic target for the prevention or treatment of insulin resistance and type II diabetes.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s11010-010-0558-7DOI Listing

Publication Analysis

Top Keywords

insulin signaling
16
porcine primary
16
primary adipocytes
16
insulin resistance
12
socs3
9
insulin
9
signaling porcine
8
type diabetes
8
socs3 mrna
8
protein expression
8

Similar Publications

Background: Type 2 diabetes (T2D) is characterized by insulin resistance and defective insulin secretion. Previously, we found that rats fed soft pellets (SPs) on a 3-hour restricted schedule over 14 weeks demonstrated glucose intolerance and insulin resistance with disruption of insulin signaling.

Objective: To determine (1) the time required for an SP diet to induce insulin resistance, and (2) whether the metabolic derangements in rats fed SPs can be reversed by changing to a standard control diet.

View Article and Find Full Text PDF

Timosaponin AⅢ(TAⅢ), derived from the Chinese medicinal herb Anemarrhena asphodeloides Bunge, has been reported to have a range of pharmacological effects including improvement of learning and memory deficits, anti-tumor, hypoglycemic effect and anti-hypertension. This study explored the therapeutic effects and preliminary mechanisms of TAⅢ in improving insulin resistance in ob/ob mice. We found that treatment with 10 mg·kg·d of TAⅢ reduced the expression of SREBPs and alleviated ectopic lipid deposition by decreasing DAG accumulation in liver.

View Article and Find Full Text PDF

Background: The widespread use of gold nanoparticles (AuNPs) in consumer and medical products necessitates investigation into their potential developmental toxicity.

Aim Of The Work: This study investigated the systemic effects of in-utero AuNP exposure on developing male rat offspring, focusing on metabolic, organ-specific, and cellular pathways.

Materials And Methods: Pregnant rats were intravenously administered AuNPs (5, 10, 15, or 20 mg/kg) or saline from gestational day 1 to birth.

View Article and Find Full Text PDF

Insulin dysregulation (ID) is a common metabolic disorder in horses, characterized by hyperinsulinemia and/or peripheral insulin resistance. The critical role of hyperinsulinemia in endocrinopathic laminitis has driven research into the insulinotropic effects of dietary nutrients and the reciprocal impact of ID on nutrient metabolism. The relationship between ID and carbohydrate metabolism has been extensively studied; however, the effects of ID on protein metabolism in horses remain largely unexplored.

View Article and Find Full Text PDF

For the effective growth of malignant tumors, including glioblastoma, the necessary factors involve endoplasmic reticulum (ER) stress, hypoxia, and the availability of nutrients, particularly glucose. The ER degradation enhancing alpha-mannosidase like protein 1 (EDEM1) is involved in ER-associated degradation (ERAD) targeting misfolded glycoproteins for degradation in an N-glycan-independent manner. EDEM1 was also identified as a new modulator of insulin synthesis and secretion.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!