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Insulin resistance in lean and overweight non-diabetic Caucasian adults: Study of its relationship with liver triglyceride content, waist circumference and BMI.

Insulin resistance in lean and overweight non-diabetic Caucasian adults: Study of its relationship with liver triglyceride content, waist circumference and BMI.
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Gonzalez-Cantero J, Martin-Rodriguez JL, Gonzalez-Cantero A, Arrebola JP, Gonzalez-Calvin JL,


Gonzalez-Cantero J, Martin-Rodriguez JL, Gonzalez-Cantero A, Arrebola JP, Gonzalez-Calvin JL, (click to view)

Gonzalez-Cantero J, Martin-Rodriguez JL, Gonzalez-Cantero A, Arrebola JP, Gonzalez-Calvin JL,

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PloS one 2018 02 0913(2) e0192663 doi 10.1371/journal.pone.0192663
Abstract
AIMS
Insulin resistance is the pathophysiological precursor of type 2 diabetes mellitus (DM-2), and its relationship with non-alcoholic fatty liver disease (NAFLD) has been widely studied in patients with obesity or metabolic syndrome using not only ultrasound but also liver biopsies or proton magnetic resonance spectroscopy (H1-MRS) to assess liver fat content. In contrast, there are no studies on insulin resistance and NAFLD in lean or overweight Caucasian individuals using H1-MRS or liver biopsies for the quantification of hepatic triglyceride content. Our objectives were to study the presence of insulin resistance in lean and overweight Caucasian adults and investigate its possible relationship with liver triglyceride content, waist circumference (as proxy of visceral adiposity), BMI, and cardiometabolic risk factors.

METHODS
A cross-sectional study was conducted in 113 non-obese, non-diabetic individuals classified as overweight (BMI 25-29.9 kg/m2) or lean (BMI 19.5-24.9 kg/m2). Hepatic triglyceride content was quantified by 3T H1-MRS. NAFLD was defined as hepatic triglyceride content >5.56%. Insulin resistance (HOMA-IR), serum adiponectin, and tumor necrosis factor (TNF) were determined.

RESULTS
HOMA-IR was significantly correlated with hepatic triglyceride content (r:0.76; p<0.0001). The lean-with-NAFLD group had significantly higher HOMA-IR (p<0.001) and lower serum adiponectin (p<0.05) than the overweight-without-NAFLD group. Insulin resistance was independently associated with NAFLD but not with waist circumference or BMI. Regression analysis showed hepatic triglyceride content to be the most important determinant of insulin resistance (p<0.01). CONCLUSIONS
Our findings suggest that NAFLD, once established, seems to be involved in insulin resistance and cardio-metabolic risk factors above and beyond waist circumference and BMI in non-obese, non-diabetic Caucasian individuals.

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