Nonalcoholic fatty liver disease: a marker of adipose tissue distribution

Abstract

Recent evidence has shifted the paradigm of white adipose tissue from simple energy storage to the body's major endocrine and paracrine organ synthesizing and releasing multiple signaling proteins, collectively termed adipokines. White adipose tissue is distributed in two large depots (subcutaneous and visceral) and many small depots associated with the heart, blood vessels, lymph nodes, ovaries, mammary glands, prostate gland, pancreas. Even in a lean person, adipose tissue represents about 15-20 % of body weight, including external (subcutaneous and visceral) and internal (organ-associated) adipose tissue, the latter being even more important than the former; however the internal fat distribution was beyond the scope of the present study. Nonalcoholic fatty liver disease (NAFLD) is a term used to describe the accumulation of fat in the liver of people in the absence of alcohol consumption or consumption of less than 20 g/day. It is a progressive, low-grade inflammatory disease related to obesity and metabolic syndrome. NAFLD represent a spectrum of disorders ranging from fat accumulation (steatosis) to nonalcoholic steatohepatitis (NASH) that can progress to fibrosis and cirrhosis. The aim of the present study was to evaluate the clinic and metabolic parameters in patients with type 2 diabetes and NAFLD depending on gender and BMI and to assess relation of adipose tissue distribution with insulin resistance. Total of 118 patients (mean age 55.93 years; male, 46, female, 72) with type 2 diabetes evaluated in an outpatient diabetes clinic were diagnosed with NAFLD by ultrasonography and were assessed by weight, body mass index (BMI), waist circumference, fasting plasma glucose, HbAlc, and fasting insulin level. We calculated the HOMA-IR index [FPG (mmol/l) x FI (μU/ml)]:22.5. Body adipose percentage and trunk adipose content were measured using bioelectrical impedance analysis (TANITA BC-418). Overall, the present results suggest that insulin resistance may be considered a pathogenic link between T2DM and NAFLD, also at the level of adipose tissue distribution. Evaluating the distribution of internal, organ-associated adipose tissue remains a challenge for future studies in patients with T2DM and NAFLD. Adipobiology 2012; 4: 97-101.