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Endothelin receptor B-deficient mice are protected from high-fat diet-induced metabolic syndrome.
Feger, Martina; Meier, Leonie; Strotmann, Jörg; Hoene, Miriam; Vogt, Julia; Wisser, Alexandra; Hirschle, Susanna; Kheim, Marie-Jo; Hocher, Berthold; Weigert, Cora; Föller, Michael.
Afiliação
  • Feger M; University of Hohenheim, Department of Physiology, Stuttgart, Germany.
  • Meier L; University of Hohenheim, Department of Physiology, Stuttgart, Germany.
  • Strotmann J; University of Hohenheim, Department of Physiology, Stuttgart, Germany.
  • Hoene M; Institute for Clinical Chemistry and Pathobiochemistry, Department for Diagnostic Laboratory Medicine, University Hospital Tübingen, Tübingen, Germany.
  • Vogt J; University of Hohenheim, Department of Physiology, Stuttgart, Germany.
  • Wisser A; University of Hohenheim, Department of Physiology, Stuttgart, Germany.
  • Hirschle S; University of Hohenheim, Department of Physiology, Stuttgart, Germany.
  • Kheim MJ; University of Hohenheim, Department of Physiology, Stuttgart, Germany.
  • Hocher B; University of Heidelberg, Department of Nephrology, Mannheim, Germany; Institute of Medical Diagnostics, IMD, Berlin, Germany; Clinical Research Center for Reproduction and Genetics in Hunan Province, Reproductive and Genetic Hospital of CITIC-Xiangya, Changsha, Hunan, China.
  • Weigert C; Institute for Clinical Chemistry and Pathobiochemistry, Department for Diagnostic Laboratory Medicine, University Hospital Tübingen, Tübingen, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Zentrum München, University of Tübingen, Tübingen, Germany; German Center fo
  • Föller M; University of Hohenheim, Department of Physiology, Stuttgart, Germany. Electronic address: michael.foeller@uni-hohenheim.de.
Mol Metab ; 80: 101868, 2024 Feb.
Article em En | MEDLINE | ID: mdl-38159882
ABSTRACT

OBJECTIVE:

Endothelin receptor B (ETB) together with ETA mediates cellular effects of endothelin 1 (ET-1), an autocrine and endocrine peptide produced by the endothelium and other cells. It regulates vascular tone and controls kidney function. Metabolic syndrome is due to high caloric intake and is characterized by insulin resistance, dyslipidemia, and white adipose tissue (WAT) accumulation. ETA/ETB antagonism has been demonstrated to favorably influence insulin resistance. Our study explored the role of ETB in metabolic syndrome.

METHODS:

Wild type (etb+/+) and rescued ETB-deficient (etb-/-) mice were fed a high-fat diet, and energy, glucose, and insulin metabolism were analyzed, and hormones and lipids measured in serum and tissues. Cell culture experiments were performed in HepG2 cells.

RESULTS:

Compared to etb+/+ mice, etb-/- mice exhibited better glucose tolerance and insulin sensitivity, less WAT accumulation, lower serum triglycerides, and higher energy expenditure. Protection from metabolic syndrome was paralleled by higher hepatic production of fibroblast growth factor 21 (FGF21) and higher serum levels of free thyroxine (fT4), stimulators of energy expenditure.

CONCLUSIONS:

ETB deficiency confers protection from metabolic syndrome by counteracting glucose intolerance, dyslipidemia, and WAT accumulation due to enhanced energy expenditure, effects at least in part dependent on enhanced production of thyroid hormone/FGF21. ETB antagonism may therefore be a novel therapeutic approach in metabolic syndrome.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Resistência à Insulina / Síndrome Metabólica / Dislipidemias Limite: Animals Idioma: En Revista: Mol Metab Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Alemanha

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Resistência à Insulina / Síndrome Metabólica / Dislipidemias Limite: Animals Idioma: En Revista: Mol Metab Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Alemanha