Cardiac-derived TGF-ß1 confers resistance to diet-induced obesity through the regulation of adipocyte size and function.
Mol Metab
; 54: 101343, 2021 12.
Article
en En
| MEDLINE
| ID: mdl-34583010
ABSTRACT
Regulation of organismal homeostasis in response to nutrient availability is a vital physiological process that involves inter-organ communication. Understanding the mechanisms controlling systemic cross-talk for the maintenance of metabolic health is critical to counteract diet-induced obesity. Here, we show that cardiac-derived transforming growth factor beta 1 (TGF-ß1) protects against weight gain and glucose intolerance in mice subjected to high-fat diet. Secretion of TGF-ß1 by cardiomyocytes correlates with the bioavailability of this factor in circulation. TGF-ß1 prevents adipose tissue inflammation independent of body mass and glucose metabolism phenotypes, indicating protection from adipocyte dysfunction-driven immune cell recruitment. TGF-ß1 alters the gene expression programs in white adipocytes, favoring their fatty acid oxidation and consequently increasing their mitochondrial oxygen consumption rates. Ultimately, subcutaneous and visceral white adipose tissue from cadiac-specific TGF-ß1 transgenic mice fail to undergo cellular hypertrophy, leading to reduced overall adiposity during high-fat feeding. Thus, TGF-ß1 is a critical mediator of heart-fat communication for the regulation of systemic metabolism.
Palabras clave
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Tejido Adiposo
/
Miocitos Cardíacos
/
Factor de Crecimiento Transformador beta1
/
Dieta Alta en Grasa
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Obesidad
Límite:
Animals
Idioma:
En
Revista:
Mol Metab
Año:
2021
Tipo del documento:
Article
País de afiliación:
Estados Unidos