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Non-esterified fatty acid concentrations are independently associated with hepatic steatosis in obese subjects
Non-esterified fatty acid concentrations are independently associated with hepatic steatosis in obese subjects
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Non-esterified fatty acid concentrations are independently associated with hepatic steatosis in obese subjects
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Non-esterified fatty acid concentrations are independently associated with hepatic steatosis in obese subjects
Non-esterified fatty acid concentrations are independently associated with hepatic steatosis in obese subjects

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Non-esterified fatty acid concentrations are independently associated with hepatic steatosis in obese subjects
Non-esterified fatty acid concentrations are independently associated with hepatic steatosis in obese subjects
Journal Article

Non-esterified fatty acid concentrations are independently associated with hepatic steatosis in obese subjects

2006
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Overview
Aims/hypothesis We tested the hypothesis that NEFA concentrations are higher in obese subjects with fatty liver than in obese subjects without fatty liver. Materials and methods We recruited 22 obese (BMI>30 kg/m²) men aged 42-64 years, in whom liver fat was assessed by ultrasound and classified into categories of no, mild to moderate and severe fatty liver by two independent radiologists. Regional and visceral abdominal fat were assessed by dual-energy X-ray absorptiometry and magnetic resonance imaging, and endogenous glucose production, whole-body glucose disposal during an insulin clamp, and NEFA concentrations were measured, along with NEFA suppression (percent (%) suppression and insulin sensitivity index for NEFA during an OGTT). Results Seven subjects had no evidence of fatty liver, nine had mild or moderate fatty liver and six had severe fatty liver. The amount of visceral fat was not associated with the degree of fatty liver. Whole-body glucose disposal was inversely associated with fatty liver (38.4, 26.5 and 23.9 μmol kg-¹ min-¹ for the groups with no fatty liver, mild to moderate fatty liver and severe fatty liver, respectively, p=0.004). NEFA suppression during the OGTT was decreased (62.5, 50.8 and 41%, p=0.03, for no, mild to moderate, and severe fatty liver, respectively) and the insulin sensitivity index for NEFA was decreased (0.80, 0.40 and 0.34, p<0.0001). Regression modelling suggested that NEFA concentrations were associated with fatty liver independently of whole-body glucose production and disposal measurements. Conclusions/interpretation In obese men, NEFA concentrations during an OGTT are associated with fatty liver independently of classic measures of insulin sensitivity determined by the hyperinsulinaemic clamp. The contribution to this association by factors regulating NEFA concentrations requires further study.