Abstract
Abdominal obesity has been associated with liver fat storage. However, the relationships between other body composition depots and metabolic syndrome features with hepatic fat are still unclear. We examined abdominal and thigh adipose tissue (AT) compartments associations with liver fat in 140 overweight and obese premenopausal Caucasian women. Blood lipids and, proinflammatory and atherothrombotic markers associations with hepatic fat were also analyzed. A larger visceral AT (VAT) was related with liver fat (P < 0.05). Contrarily, thigh subfascial AT was inversely related to liver fat (P < 0.05). Increased fasting insulin, triglycerides, PAI-1 concentrations, and a higher total-cholesterol/HDL-cholesterol ratio were also associated with hepatic fat, even after adjustment for VAT (P < 0.05). Thigh subfascial adiposity was inversely associated with liver fat, suggesting a potential preventive role against ectopic fat storage in overweight and obese women. These results reinforce the contribution of an abdominal obesity phenotype associated with a diabetogenic and atherothrombotic profile to liver lipotoxicity.
Highlights
Obesity-related comorbidities seem to be more closely related to body fat distribution rather than the total amount per se [1]
Abdominal obesity is a relevant predictor of a higher metabolic risk, assuming that insulin resistance (IR) is the common link between visceral adiposity and dyslipidemia [2,3,4], type 2 diabetes mellitus (DM) [5, 6], liver fat storage [7], hypertension [8], and other cardiovascular diseases (CVD) [8,9,10]
According to the “portal hypothesis,” the increased lipolytic activity in visceral adipocytes leads to an augmented release of free fatty acids (FFA) into portal circulation, promoting liver fat storage that is accompanied by hepatic metabolism disturbances and IR [6, 13, 14]
Summary
Obesity-related comorbidities seem to be more closely related to body fat distribution (e.g., upper versus lower, visceral versus subcutaneous, and truncal versus peripheral) rather than the total amount per se [1]. According to the “portal hypothesis,” the increased lipolytic activity in visceral adipocytes leads to an augmented release of free fatty acids (FFA) into portal circulation, promoting liver fat storage that is accompanied by hepatic metabolism disturbances and IR [6, 13, 14]. In this context, abdominal obesity has been associated with ectopic fat storage, defined as fat accumulation outside “classical” depots such as heart, skeletal muscle, pancreas, and liver [15]. This study investigated the associations of liver fat with metabolic, proinflammatory, and atherothrombotic risk factors
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