Peripancreatic adipose tissue (PAT) is an understudied visceral fat depot that surrounds pancreas and is in touch with spleen and liver. Recent previous studies suggest that obesity-associated PAT inflammation accelerates pancreatic neoplasia in KrasG12D mice and that PAT conditioned-medium from pre-diabetic rats (9 weeks on high-fat diet; HFD) stimulates insulin secretion, proliferation and apoptosis in INS-1 cells. In this study, we aimed to better characterize PAT functionality in the context of HFD-induced obesity. PAT is a very small depot (0,5 ±0,04 mg) with a relatively high number of small adipocytes in unchallenged mice on chow, and we found that PAT expansion is less pronounced at early stages of HFD-feeding compared to the expansion of inguinal (IWAT), gonadal (GWAT) and mesenteric adipose tissues (MWAT). After 8-weeks HFD feeding the expansion of PAT was however comparable to the other three fat depots, but still PAT was more protected against the deleterious effects of HFD on adipose tissue inflammation and insulin resistance as judged by gene expression analysis (adiponectin, insulin receptor and inflammation markers). Feeding after 16-weeks HFD reduced the glucose and lipid uptake in all fat depots however, it was less pronounced in PAT; both fatty acid and glucose oxidation rates were higher in PAT compared to IWAT, GWAT and MWAT. Moreover, we noted that PAT is the only fat depot where the tissue weight correlates positively with liver weight in HFD-induced obese mice, and surgical removal of PAT followed by 16-week-HFD-feeding was associated with increased hepatic triglyceride content and accumulation of more and larger lipid droplets. PAT did not regenerate during this 16-week HFD time course suggesting that its precursor cells reside within the depot. Taken all data together, we propose that PAT, although it is located in the visceral compartment, can be considered as a metabolically/immunologically healthy fat depot that protects against hepatic steatosis in advanced obesity.


B. Chanclón: None. P. Micallef: None. E. Banke Nordbeck: None. Y. Wu: None. B. Wilder: None. J. Kanerva: None. P. Rorsman: None. I. Wernstedt Asterholm: None.

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