Low-dose GH supplementation reduces the TLR2 and TNF-alpha expressions in visceral fat.
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.
Kubota
Yoshitaka
Y
Department of Plastic and Reconstructive Surgery, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
Unoki
Hiroyuki
H
Bujo
Hideaki
H
Rikihisa
Naoaki
N
Udagawa
Akikazu
A
Yoshimoto
Shinya
S
Ichinose
Masaharu
M
Saito
Yasushi
Y
D041721:3T3-L1 Cells; D000821:Animal Feed; D000818:Animals; D005786:Gene Expression Regulation / Q000187:drug effects; D013006:Growth Hormone / Q000494:pharmacology*; D006801:Humans; D050152:Intra-Abdominal Fat / Q000187:drug effects* / Q000378:metabolism*; D051379:Mice; D009765:Obesity / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control; D012333:RNA, Messenger / Q000235:genetics; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*
D012333:RNA, Messenger; C493486:Tlr2 protein, mouse; D051195:Toll-Like Receptor 2; D014409:Tumor Necrosis Factor-alpha; D013006:Growth Hormone