Increased visceral adipocyte lipolysis--a pathogenic role in nonalcoholic fatty liver disease?

Obesity is a major risk factor for nonalcoholic fatty liver disease, but the primary pathophysiological mechanisms remain unclear.

The aim was to study the relative role of visceral and sc in vitro lipolysis for liver fat accumulation.

Eighteen morbidly obese women participated in the study.

Hepatic triglyceride accumulation and abdominal visceral and sc fat area were assessed by computer tomography. Biopsies were taken from abdominal sc and visceral fat tissue. Basal and maximal lipolysis was measured using various lipolytic drugs acting at different steps in the lipolytic cascade.

No difference in total body, visceral, or sc fat mass was found between patients with high, intermediate, or low amounts of liver fat. In patients with high liver fat content, there was an approximately 2-fold increase in visceral adipocyte maximal glycerol release induced by the different lipolytic agents (P = 0.002 to 0.01). Noradrenaline-mediated free fatty acid release from visceral adipocytes was also about twice as high in patients with high liver fat (P = 0.004). In contrast, in sc adipocytes, no relationship between liver fat content and either glycerol or free fatty acid release was found.

We suggest a pathogenic role of visceral, but not sc, adipocyte lipolytic function in nonalcoholic fatty liver disease, independent of total body fat as well as abdominal fat distribution.