Unique Genetic and Histological Signatures of Mouse Pericardial Adipose Tissue.
A Al-DibouniRenato Simões GasparS IgeS BoatengFelino Ramon CagampangJonathan M GibbinsR D CoxD SellayahPublished in: Nutrients (2020)
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.
Keyphrases
- adipose tissue
- insulin resistance
- high fat diet
- gene expression
- high fat diet induced
- cardiovascular disease
- type diabetes
- glycemic control
- mouse model
- oxidative stress
- metabolic syndrome
- transcription factor
- skeletal muscle
- genome wide
- single cell
- endothelial cells
- high glucose
- heat shock protein
- weight gain
- copy number
- nitric oxide
- binding protein