Details

Autor(en) / Beteiligte

• Park, Hea Jin
• Olsen, Erik
• Fang, Xi
• Dagher, Josephine Bou
• Chung, Jaegwon
• Kang, Se Joong
• Lee, Jae‐Kyung

Titel

The Effect of a High‐Fat Diet and Green Tea Extract on Glucose Metabolism and Inflammation in Regulator of G protein Signaling 10 Knockout Mice

Ist Teil von

• The FASEB journal, 2017-04, Vol.31 (S1)

Erscheinungsjahr

2017

Link zum Volltext

Quelle

Wiley Online Library - AutoHoldings Journals

Beschreibungen/Notizen

• Abstract only Regulator of G protein signaling (RGS) family proteins are GTPase‐accelerating proteins that negatively regulate G protein‐coupled receptors signaling. Among RGS family proteins, RGS10 is one of the smallest proteins and abundant in the brain and immune organs. Previously, we have demonstrated its roles in myeloid cells as a negative regulator of inflammation in the context of neurodegenerative diseases including Parkinsons's disease. Interestingly, RGS10 knockout mice display impaired glucose tolerance concurrently with proinflammatory phenotype, suggesting the involvement of RGS10 in the development of metabolic diseases by regulating inflammation. Moreover, epigallocatechin‐3‐gallate, an anti‐diabetic and anti‐inflammatory polyphenol found in green tea has shown to increase the expression of RGS10 in human cancer cells. However, underlying mechanisms by which RGS10 relates to the development of diabetes or obesity has never been studied. Our data shows that the expression of RGS10 protein was strongly induced in lipid filled mature adipocytes differentiated from 3T3‐L1 preadipocytes in vitro . However, green tea extract (GTE) treatment (50 μM) for 24hours had no effect on the expression of RGS10 protein in both preadipocytes and lipid filled mature adipocytes. We are currently conducting an animal study investigating the impact of high‐fat diet and dietary GTE on metabolic profilein RGS10 knockout mice. C57BL/6 wild type mice and RGS10 knockout mice fed alow‐fat diet (LF), high‐fat diet (HF) or high‐fat diet containing GTE at 2%(HF+GTE) for 8 wks. At week 5, the current stage of the study, the body weight gains were not significantly different between WT and KO mice fed LF (p=0.2081) as well as mice fed HF+GTE (p=0.7656). However, KO mice fed HF gained 1.6 times more weight than WT mice fed the same diet (p=0.0003). GTE inhibits the body weight gain in both WT and KO mice otherwise increased by HF. At the end of experimental period, glucose tolerance test and insulin sensitivity test will be conducted and blood and adipose tissue will be collected to measure markers of glucose metabolism and inflammation. The results suggest that RGS10 may play an important role to regulate high fat diet induced weight gain. Completion of current study will address the impact of high‐fat diet and GTE on glucose metabolism and inflammation upon the expression of RGS10. This finding would provide evidence to better understand the regulation of diabetes and inflammation. Support or Funding Information Support provided by Georgia Experimental Agricultural Station, HATCH #GEO00795 and College of Family and Consumer Sciences (HJP) and College of Veterinary Medicine (JKL) at UGA.