Skip Navigation LinksHome > June 2012 - Volume 54 - Issue 6 > Increased Pancreatic Fat Fraction Is Present in Obese Adoles...
Journal of Pediatric Gastroenterology & Nutrition:
doi: 10.1097/MPG.0b013e318244a685
Original Articles: Gastroenterology

Increased Pancreatic Fat Fraction Is Present in Obese Adolescents With Metabolic Syndrome

Maggio, Albane B.R.*; Mueller, Pascal; Wacker, Julie; Viallon, Magalie§; Belli, Dominique C.||; Beghetti, Maurice; Farpour-Lambert, Nathalie J.*; McLin, Valérie A.||

Supplemental Author Material
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Abstract

Objectives: Little is known about pancreatic fat accumulation and its possible associations with metabolic syndrome (MetS) and glucose metabolism. The aim of the present study was to quantify pancreatic fat fraction (PFF) in lean and obese adolescents and explore its relation to metabolic parameters.

Methods: We recruited 25 lean and 24 obese adolescents. PFF and visceral adipose tissue (VAT) were determined using magnetic resonance imaging. We measured blood pressure, fasting glucose, insulin, liver enzymes, leptin, and lipid levels. Obese subjects underwent an oral glucose tolerance test.

Results: PFF was significantly higher in obese than in lean subjects (4.8 ± 1.2 vs 3.6 ± 0.9; P < 0.001) and was associated with VAT, γ-glutamyltransferase, triglycerides, high-density lipoprotein cholesterol, leptin concentrations, and MetS (P < 0.05 for all). None of the obese subjects had glucose intolerance, but when adjusted for VAT, the following 3 parameters correlated negatively with PFF: fasting and 30- minute and 120-minute insulin levels. We divided subjects into 3 groups: group I, lean without MetS; group II, obese without MetS; and group III, obese with MetS, and observed that PFF increased gradually among groups (I: 3.56% ± 0.88%; II: 4.70% ± 1.06%; III: 5.34% ± 1.49%; P < 0.001).

Conclusions: Obese adolescents accumulate fat in the pancreas. PFF correlates with the presence of MetS. Even in the absence of glucose intolerance, pancreatic fat deposition is associated with impaired insulin response to glucose overload. This suggests that β-cell dysfunction may already be present in nondiabetic obese adolescents, mirroring what has been shown in adults, and that pancreatic fat accumulation may participate in obesity-associated pancreatic endocrine dysfunction.

Copyright 2012 by ESPGHAN and NASPGHAN

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