Key result
Adipose tissue insulin resistance and postprandial adiponectin independently predicted liver histology and altered cardiometabolic parameters in nonobese, nondiabetic patients with NAFLD.
Why the study?
Do adipose tissue dysfunction and response to fat ingestion differ between patients with NASH, simple steatosis, and healthy subjects?
Cross-Sectional (n=80)
Do adipose tissue dysfunction and response to fat ingestion differ between patients with NASH, simple steatosis, and healthy subjects?
Adipose tissue dysfunction and a maladaptive adipokine response to fat ingestion modulate liver injury and cardiometabolic risk in NAFLD, with NASH showing greater impairment than simple steatosis.
Answers are grounded in this paper and cite their sources.
Adipose IR assessment may refine nonobese NAFLD risk stratification; hypothesis-generating for targeted interventions pending prospective trials.
UNLABELLED: Nonalcoholic fatty liver disease (NAFLD) ranges from simple steatosis (SS) to nonalcoholic steatohepatitis (NASH). Though liver-related risk seems confined to NASH, it is currently unclear whether NASH has a higher risk of cardiovascular disease (CVD) and diabetes than SS as a result of the coexistence of obesity and other cardiometabolic confounders. Adipose tissue is an emerging modulator of liver disease in NAFLD and of cardiometabolic disease in the general population. We evaluated in SS and NASH (1) glucose homeostasis and cardiovascular risk profile and (2) the effect of adipose tissue dysfunction, assessed in fasting conditions and postprandially, on liver injury, glucose and lipoprotein metabolism, and markers of early atherosclerosis. Forty nonobese, nondiabetic, normolipidemic biopsy-proven NAFLD patients (20 with SS and 20 with NASH) and 40 healthy subjects, matched for overall/abdominal adiposity and metabolic syndrome, underwent an oral fat load test, with measurement of plasma triglyceride-rich lipoproteins, oxidized low-density lipoproteins, adipokines, and cytokeratin-18 fragments, and an oral glucose tolerance test with minimal model analysis to yield glucose homeostasis parameters. Circulating endothelial adhesion molecules were measured, and adipose tissue insulin resistance (adipose IR) index and visceral adiposity index were calculated. Despite similar fasting values, compared to SS, NASH showed a more atherogenic postprandial lipoprotein profile, an altered adipokine response (i.e., higher resistin increase and an adiponectin fall), and hepatocyte apoptosis activation after fat ingestion. Adipose IR index, endothelial adhesion molecules, and hepatic insulin resistance progressively increased across NAFLD stages. NASH, but not SS, showed an impaired pancreatic β-cell function. On multiple regression analysis, adipose IR index and postprandial adiponectin independently predicted liver histology and altered cardiometabolic parameters. CONCLUSION: Adipose tissue dysfunction, including a maladaptive adipokine response to fat ingestion, modulates liver injury and cardiometabolic risk in NAFLD.
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Musso et al. (2012) conducted a cross-sectional in Nonalcoholic fatty liver disease (NAFLD) (n=80). Nonalcoholic steatohepatitis (NASH) and adipose tissue dysfunction vs. Simple steatosis (SS) and healthy controls was evaluated on Glucose homeostasis, cardiovascular risk profile, and markers of early atherosclerosis. Adipose tissue insulin resistance and postprandial adiponectin independently predicted liver histology and altered cardiometabolic parameters in nonobese, nondiabetic patients with NAFLD.
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