Giorgio Bedogni1,2, Amalia Gastaldelli3, Claudio Tiribelli4, Fiorenza Agosti5, Alessandra De Col5, Rezene Fessehatsion6, Alessandro Sartorio5,6. 1. Liver Research Center, AREA Science Park, Building Q, Strada Statale 14 km 163.5, Basovizza, 34012, Trieste, Italy. giorgiobedogni@gmail.com. 2. International Center for the Assessment of Nutritional Status (ICANS), University of Milano, Milan, Italy. giorgiobedogni@gmail.com. 3. Istituto di Fisiologia Clinica, Consiglio Nazionale delle Ricerche (CNR), Pisa, Italy. 4. Liver Research Center, AREA Science Park, Building Q, Strada Statale 14 km 163.5, Basovizza, 34012, Trieste, Italy. 5. Istituto Auxologico Italiano, IRCCS, Experimental Laboratory for Auxo-Endocrinological Research, Milano, Italy. 6. Istituto Auxologico Italiano, IRCCS, Division of Metabolic Diseases, Verbania, Italy.
Abstract
BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is an independent predictor of type 2 diabetes mellitus (T2DM). Insulin resistance and beta-cell dysfunction are involved in the pathogenesis of T2DM. Insulin resistance is associated with NAFLD but little is known about beta-cell dysfunction and NAFLD. AIM: We tested whether NAFLD severity is associated with insulin sensitivity and beta-cell function in morbidly obese women. SUBJECTS AND METHODS: We studied 61 Caucasian women aged 18-60 years without T2DM and with a body mass index ranging from 35.3 to 48.8 kg/m². The insulin sensitivity index (ISI) and the disposition index (DI) from oral glucose tolerance testing were used as measures of insulin sensitivity and beta-cell function, respectively. Fat was measured by dual-energy X-ray absorptiometry. Fatty liver was diagnosed by ultrasonography and ordinally coded as 0 = none, 1 = light, 2 = moderate, 3 = severe. Proportional-odds logistic regression was used to evaluate the association of NAFLD severity with log(e)ISI and log(e)DI with and without correction for total and truncal fat. RESULTS: The odds of more severe vs. less severe NAFLD decreased for increasing log(e)ISI [odds ratio (OR) 0.40, 95 % CI 0.19-0.84, p < 0.05] and log(e)DI (OR 0.80, 95 % CI 0.69-0.92, p < 0.01). Neither total nor truncal fat had any effect on these associations. CONCLUSION: In morbidly obese women, NAFLD severity is inversely associated with insulin sensitivity and beta-cell function. The association of NAFLD severity with beta-cell dysfunction is stronger than that with insulin resistance.
BACKGROUND:Non-alcoholic fatty liver disease (NAFLD) is an independent predictor of type 2 diabetes mellitus (T2DM). Insulin resistance and beta-cell dysfunction are involved in the pathogenesis of T2DM. Insulin resistance is associated with NAFLD but little is known about beta-cell dysfunction and NAFLD. AIM: We tested whether NAFLD severity is associated with insulin sensitivity and beta-cell function in morbidly obesewomen. SUBJECTS AND METHODS: We studied 61 Caucasian women aged 18-60 years without T2DM and with a body mass index ranging from 35.3 to 48.8 kg/m². The insulin sensitivity index (ISI) and the disposition index (DI) from oral glucose tolerance testing were used as measures of insulin sensitivity and beta-cell function, respectively. Fat was measured by dual-energy X-ray absorptiometry. Fatty liver was diagnosed by ultrasonography and ordinally coded as 0 = none, 1 = light, 2 = moderate, 3 = severe. Proportional-odds logistic regression was used to evaluate the association of NAFLD severity with log(e)ISI and log(e)DI with and without correction for total and truncal fat. RESULTS: The odds of more severe vs. less severe NAFLD decreased for increasing log(e)ISI [odds ratio (OR) 0.40, 95 % CI 0.19-0.84, p < 0.05] and log(e)DI (OR 0.80, 95 % CI 0.69-0.92, p < 0.01). Neither total nor truncal fat had any effect on these associations. CONCLUSION: In morbidly obesewomen, NAFLD severity is inversely associated with insulin sensitivity and beta-cell function. The association of NAFLD severity with beta-cell dysfunction is stronger than that with insulin resistance.
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