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Updated: Jul 20, 2026

Assessing Whole-Body Lipid-Handling Capacity in Mice
Published on: November 24, 2020
Serum resistin and hepatic fat content in nondiabetic individuals
Gianluca Perseghin1, Guido Lattuada, Francesco De Cobelli
1Internal Medicine, Section of Nutrition/Metabolism and Unit of Clinical Spectroscopy, San Raffaele Scientific Institute, 20132 Milan, Italy. perseghin.gianluca@hsr.it
Context:
Serum resistin concentration is increased in patients with nonalcoholic fatty liver disease in proportion with the histological severity of the disease, but the relevance of the contribution of fatty liver per se is undetermined.
Objective:
The objective of the study was to assess the relationship between serum resistin and the degree of ectopic fat accumulation in vivo in humans.
Design And Setting:
The hepatic fat (IHF) content, measured quantitatively by means of 1H magnetic resonance spectroscopy, serum resistin, and biochemical and hormonal metabolic correlates of fatty liver and insulin resistance were assessed in 28 affected patients, and 47 individuals with comparable anthropometric features served as controls. Insulin sensitivity was estimated using the computer homeostatic model assessment (HOMA)-2. A subset of volunteers (n = 18) also underwent 1H magnetic resonance spectroscopy of the calf muscles to assess the intramyocellular lipid content (IMCL).
Results:
In patients with fatty liver, the IHF content (13 +/- 8 vs. 2 +/- 1% wet weight; P < 0.0001) and also the soleus IMCL content (P < 0.05) were increased in comparison with the controls. Patients with fatty liver had lower insulin sensitivity (HOMA2 insulin sensitivity: 59 +/- 24 vs. 72 +/- 29%; P < 0.04), serum resistin (3.4 +/- 0.8 vs. 3.9 +/- 1.0 ng/ml; P < 0.02), and adiponectin (P < 0.01) concentrations. Serum resistin was inversely correlated with the IHF content (r = -0.35; P < 0.003) and the soleus IMCL content (r = -0.51; P < 0.05) but not HOMA2 insulin sensitivity.
Conclusion:
This study demonstrates that excessive ectopic fat accumulation in the liver and skeletal muscle of insulin-resistant subjects is associated with lower serum resistin concentration and not with hyperresistinemia.
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