We aimed to assess in obese youths the relationships between interleukin-6 (IL-6), fat meal-induced endotoxemia and glucose homeostasis. Twenty obese children/adolescents (9-17 years old, 11 boys) underwent a standard oral glucose tolerance test and, 7-14 days later, a 5-h fat meal test (fat=69% of energy, saturated/monounsaturated/polyunsaturated fatty acids=31.5%/35%/33.5%), with serial measures of IL-6 and two markers of lipopolysaccharide (LPS) exposure and translocation, LPS-binding protein (LBP) and soluble CD14 (sCD14). IL-6 correlated not only with basal (homeostatic model assessment-insulin resistance) but also with post-prandial (Matsuda index) insulin sensitivity (r=0.61 (0.24-0.82), P=0.005, r=-0.53 (0.12-0.78), P=0.03, respectively). IL-6 did not change after the meal whereas LBP and sCD14 decreased significantly, indicating LPS translocation. Neither basal sCD14 and LBP nor their incremental concentrations correlated with IL-6 or glucose homeostasis. In our sample, IL-6 was associated with insulin sensitivity but not with LPS exposure, suggesting that meals with a balanced content of saturated/monounsaturated/polyunsaturated fatty acids may not be associated with LPS-induced inflammation and metabolic impairment.

High-fat meal, systemic inflammation and glucose homeostasis in obese children and adolescents

Morandi, A;Fornari, E;Opri, Francesca;Corradi, M;Tommasi, M;Maffeis, C
2017-01-01

Abstract

We aimed to assess in obese youths the relationships between interleukin-6 (IL-6), fat meal-induced endotoxemia and glucose homeostasis. Twenty obese children/adolescents (9-17 years old, 11 boys) underwent a standard oral glucose tolerance test and, 7-14 days later, a 5-h fat meal test (fat=69% of energy, saturated/monounsaturated/polyunsaturated fatty acids=31.5%/35%/33.5%), with serial measures of IL-6 and two markers of lipopolysaccharide (LPS) exposure and translocation, LPS-binding protein (LBP) and soluble CD14 (sCD14). IL-6 correlated not only with basal (homeostatic model assessment-insulin resistance) but also with post-prandial (Matsuda index) insulin sensitivity (r=0.61 (0.24-0.82), P=0.005, r=-0.53 (0.12-0.78), P=0.03, respectively). IL-6 did not change after the meal whereas LBP and sCD14 decreased significantly, indicating LPS translocation. Neither basal sCD14 and LBP nor their incremental concentrations correlated with IL-6 or glucose homeostasis. In our sample, IL-6 was associated with insulin sensitivity but not with LPS exposure, suggesting that meals with a balanced content of saturated/monounsaturated/polyunsaturated fatty acids may not be associated with LPS-induced inflammation and metabolic impairment.
2017
obesity - children - fat meal - inflammation - glucose metabolism
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/972868
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