Unique Genetic and Histological Signatures of Mouse Pericardial Adipose Tissue

Nutrients

F.R. Cagampang¹  R.D. Cox²  A. Al-Dibouni³  R. Gaspar³  D. Sellayah³  J. Gibbins³  S. Ige³  S. Boateng³ 

[1] Institute of Developmental Sciences, Human Development and Health, School of Medicine, University of Southampton, Southampton SO16 6YD, UK;MRC Harwell Institute, Genetics of Type 2 Diabetes, Mammalian Genetics Unit, Harwell Campus, Oxfordshire OX11 0RD, UK;School of Biological Sciences, University of Reading, Whiteknights, Reading, Berkshire RG6 6AS, UK;

关键词: adipose tissue;    obesity;    metabolism;   

DOI  :  10.3390/nu12061855

来源: DOAJ

【 摘 要 】

Obesity is a major risk factor for a plethora of metabolic disturbances including diabetes and cardiovascular disease. Accumulating evidence is showing that there is an adipose tissue depot-dependent relationship with obesity-induced metabolic dysfunction. While some adipose depots, such as subcutaneous fat, are generally metabolically innocuous, others such as visceral fat, are directly deleterious. A lesser known visceral adipose depot is the pericardial adipose tissue depot. We therefore set out to examine its transcriptional and morphological signature under chow and high-fat fed conditions, in comparison with other adipose depots, using a mouse model. Our results revealed that under chow conditions pericardial adipose tissue has uncoupling-protein 1 gene expression levels which are significantly higher than classical subcutaneous and visceral adipose depots. We also observed that under high-fat diet conditions, the pericardial adipose depot exhibits greatly upregulated transcript levels of inflammatory cytokines. Our results collectively indicate, for the first time, that the pericardial adipose tissue possesses a unique transcriptional and histological signature which has features of both a beige (brown fat-like) but also pro-inflammatory depot, such as visceral fat. This unique profile may be involved in metabolic dysfunction associated with obesity.

【 授权许可】

Unknown