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Low-dose GH supplementation reduces the TLR2 and TNF-alpha expressions in visceral fat.
Kubota, Yoshitaka; Unoki, Hiroyuki; Bujo, Hideaki; Rikihisa, Naoaki; Udagawa, Akikazu; Yoshimoto, Shinya; Ichinose, Masaharu; Saito, Yasushi.
Afiliação
  • Kubota Y; Department of Plastic and Reconstructive Surgery, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
Biochem Biophys Res Commun ; 368(1): 81-7, 2008 Mar 28.
Article em En | MEDLINE | ID: mdl-18201559
ABSTRACT
The increased population of TLR2/TNF-alpha co-expressing adipocytes is associated with the development of insulin resistance. We have herein shown the significance of low-dose growth hormone (GH) supplementation for the regulation of TLR2 and TNF-alpha expressions in visceral fat using different kinds of mouse models fed with a high-fat diet. Low-dose GH supplementation reduced the increased population of TLR2/TNF-alpha co-expressing adipocytes in high-fat fed mice. The neutralization of IGF-1 abolished the effect of GH supplementation on the TLR2 expression using GH-overexpressing mice. IGF-1, but not GH, inhibited the FFA-induced TLR2 and TNF-alpha expression in 3T3-L1 cells. Finally, low-dose GH supplementation reduced the TLR2 expression without an obvious change in the visceral fat volume in ob/ob mice. These results indicate that low-dose GH supplementation possibly inhibits the high-fat induced change of the adipocytes to TLR2/TNF-alpha co-expressing cells through the action of IGF-1.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Hormônio do Crescimento / Fator de Necrose Tumoral alfa / Gordura Intra-Abdominal / Receptor 2 Toll-Like Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2008 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Hormônio do Crescimento / Fator de Necrose Tumoral alfa / Gordura Intra-Abdominal / Receptor 2 Toll-Like Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2008 Tipo de documento: Article