Visceral obesity and gastrointestinal (GI) tract dysfunction play crucial roles in the development of metabolic disturbances associated with obesity. This is due, in part, to their shared use of the portal vein. Inflammation links obesity-associated impairments within visceral adipose tissue (VAT), the GI tract, and liver. We believe that the lymph nodes contribute to this inflammation, due to their central role in immune function. The mesenteric lymph nodes (MLN) are critical for initiating and maintaining immune tolerance and protective inflammatory responses within both the GI tract and VAT. Thus we propose that the MLN are a unifying structure which can influence VAT, GI tract, and liver function.


Male C57BL/6 mice, aged 2-3 months, received either surgical removal of the MLN via cauterization or a sham abdominal surgery. Following 1 week of recovery, mice received either a purified low fat (CH) or high fat diet (HFD) for 10 weeks. At termination, the MLN, jejunum, and VAT were collected for immune cell characterization by flow cytometry. Whereas protein concentration was measured in the liver.


MLN removal resulted in 1) a significant reduction in total immune cell number within the jejunum of both CH and HFD fed mice (60% and 45%—respectively); 2) an increase in visceral adiposity within HFD but not CH fed mice; and 3) an overall reduction in hepatic insulin sensitivity within all groups. Food intake was higher in HFD groups compared with CH groups, however there were no differences seen between surgery groups.


Taken together these data demonstrate that the MLN are central to jejunum immune function and VAT regulation, while also contributing to the regulation of hepatic insulin signaling.