RRC ID 81272
著者 Nakagawa T, Horiuchi K, Kagami K, Kondo S, Isaji M, Matsuhashi Y, Kitamura K, Adachi T, Chiba K.
タイトル The alteration of LBX1 expression is associated with changes in parameters related to energy metabolism in mice.
ジャーナル PLoS One
Abstract The LBX1 gene is located near a single nucleotide polymorphism that is highly associated with susceptibility to adolescent idiopathic scoliosis and is considered one of the strongest candidate genes involved in the pathogenesis of this condition. We have previously found that loss of LBX1 from skeletal muscle results not only in spinal deformity but also in lean body mass, suggesting a potential role for LBX1 in energy metabolism. The purpose of the present study was to test this hypothesis by analyzing the phenotype of mice lacking LBX1 in skeletal muscle with a focus on energy metabolism. We found that loss of LBX1 rendered mice more resistant to high-fat diet-induced obesity, despite comparable food intake between mutant and control mice. Notably, the mutant mice exhibited improved glucose tolerance, increased maximal aerobic capacity, and higher core body temperature compared to control mice. In addition, we found that overexpression of LBX1 decreased glucose uptake in cultured cells. Taken together, our data show that LBX1 functions as a negative regulator of energy metabolism and that loss of LBX1 from skeletal muscle increases systemic energy expenditure resulting in lean body mass. The present study thus suggests a potential association between LBX1 dysfunction and lean body mass in patients with adolescent idiopathic scoliosis.
巻・号 19(8)
ページ e0308445
公開日 2024-1-1
DOI 10.1371/journal.pone.0308445
PII PONE-D-24-20291
PMID 39110747
PMC PMC11305531
MeSH Animals Diet, High-Fat / adverse effects Energy Metabolism* Glucose / metabolism Homeodomain Proteins / genetics Homeodomain Proteins / metabolism Humans Male Mice Mice, Inbred C57BL Mice, Knockout Muscle, Skeletal* / metabolism Obesity / genetics Obesity / metabolism Scoliosis / genetics Scoliosis / metabolism
IF 2.74
リソース情報
ヒト・動物細胞 NIH/3T3(RCB2767)