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Soluble activin receptor type IIB treatment does not cause fat loss in mice with diet‐induced obesity
Author(s) -
McPherron A. C.,
Guo T.,
Wang Q.,
Portas J.
Publication year - 2012
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2011.01520.x
Subject(s) - endocrinology , medicine , myostatin , adipose tissue , obesity , receptor , weight loss , activin receptor , insulin resistance , lean body mass , biology , chemistry , skeletal muscle , body weight
The growth factor myostatin (MSTN) negatively regulates skeletal muscle mass. Mstn gene deletion in mice causes increased muscle mass, reduced adiposity and resistance to genetic or diet‐induced obesity (DIO). Pharmacologic MSTN inhibition in mice also causes increased muscle mass and resistance to DIO. To test whether MSTN inhibition causes weight loss in mice that are already obese, we inhibited MSTN in mice fed a high‐fat diet (HFD). Mice were fed a diet containing 60% kcal from fat for 12 weeks followed by treatment with a soluble MSTN receptor derived from the activin receptor type IIB extracellular domain. During the next 12 weeks of soluble receptor treatment and HFD feeding, lean mass increased without a loss of adipose mass. Glucose metabolism was also similar between groups. Our results suggest that MSTN inhibition may be ineffective at inducing weight loss in obese patients.