Peripancreatic adipose tissue protects against high-fat-diet-induced hepatic steatosis and insulin resistance in mice.

ABSTRACT: BACKGROUND/OBJECTIVES:Visceral adiposity is associated with increased diabetes risk, while expansion of subcutaneous adipose tissue may be protective. However, the visceral compartment contains different fat depots. Peripancreatic adipose tissue (PAT) is an understudied visceral fat depot. Here, we aimed to define PAT functionality in lean and high-fat-diet (HFD)-induced obese mice. SUBJECTS/METHODS:Four adipose tissue depots (inguinal, mesenteric, gonadal, and peripancreatic adipose tissue) from chow- and HFD-fed male mice were compared with respect to adipocyte size (n?=?4-5/group), cellular composition (FACS analysis, n?=?5-6/group), lipogenesis and lipolysis (n?=?3/group), and gene expression (n?=?6-10/group). Radioactive tracers were used to compare lipid and glucose metabolism between these four fat depots in vivo (n?=?5-11/group). To determine the role of PAT in obesity-associated metabolic disturbances, PAT was surgically removed prior to challenging the mice with HFD. PAT-ectomized mice were compared to sham controls with respect to glucose tolerance, basal and glucose-stimulated insulin levels, hepatic and pancreatic steatosis, and gene expression (n?=?8-10/group). RESULTS:We found that PAT is a tiny fat depot (~0.2% of the total fat mass) containing relatively small adipocytes and many "non-adipocytes" such as leukocytes and fibroblasts. PAT was distinguished from the other fat depots by increased glucose uptake and increased fatty acid oxidation in both lean and obese mice. Moreover, PAT was the only fat depot where the tissue weight correlated positively with liver weight in obese mice (R?=?0.65; p?=?0.009). Surgical removal of PAT followed by 16-week HFD feeding was associated with aggravated hepatic steatosis (p?=?0.008) and higher basal (p?

SUBMITTER: Chanclon B 

PROVIDER: S-EPMC7577900 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature