Kruppel-like factor 14 ameliorated obesity and related metabolic disorders by promoting adipose tissue browning.

KLF14 adipose browning hepatic steatosis insulin resistance obesity

Journal

American journal of physiology. Endocrinology and metabolism
ISSN: 1522-1555
Titre abrégé: Am J Physiol Endocrinol Metab
Pays: United States
ID NLM: 100901226

Informations de publication

Date de publication:
01 Dec 2023
Historique:
pubmed: 8 11 2023
medline: 8 11 2023
entrez: 8 11 2023
Statut: ppublish

Résumé

Obesity has been identified as a serious and debilitating disease that threatens human health, but the current treatment strategies still have some shortcomings. Exercise and dieting are difficult for many people to adhere to, and a series of surgical risks and pain brought about by volume reduction have made it difficult for the current weight loss effect to meet human expectations. In this study, we first found that mice with overexpression of the transcription factor Kruppel-like factor 14 (KLF14) in subcutaneous adipose tissue gained weight more slowly while consuming a high-fat diet than did control mice, and these mice also showed reduced insulin resistance and liver lipid deposition abnormalities. Mechanistically, the browning of white adipose tissue was promoted in adipose tissue with KLF14 overexpression; therefore, we preliminarily concluded that KLF14 can improve obesity by promoting the browning of white adipose tissue and energy consumption, thus ameliorating obesity and related metabolic disturbances. In summary, our results revealed that KLF14 may promote white adipose tissue browning, thus ameliorating high-fat diet-induced obesity and hepatic steatosis, as well as serum lipid levels and insulin resistance, thereby achieving a positive effect on metabolism.

Identifiants

pubmed: 37938176
doi: 10.1152/ajpendo.00226.2023
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

E744-E754

Subventions

Organisme : MOST | National Natural Science Foundation of China (NSFC)
ID : 82200955

Auteurs

Xiaoxiang Mao (X)

Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Clinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.

Yuanxiang Li (Y)

Department of Oncology, Hubei Cancer Hospital, TongJi Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.

Yi Zhong (Y)

Clinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.

Ru Chen (R)

Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Clinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.

Kun Wang (K)

Department of Geriatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.

Dandan Huang (D)

Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Clinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.

Xi Luo (X)

Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Clinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.

Classifications MeSH