2015
DOI: 10.1139/bcb-2014-0064
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Associations between visceral fat and liver fat with insulin sensitivity and metabolic risk in obese adolescents

Abstract: We examined the joint and independent associations between VAT and LF with insulin sensitivity (IS) and lipids in seventy-one obese adolescents (BMI ≥ 95th, 14.9 ± 1.8 years). VAT was assessed by magnetic resonance imaging, and LF was quantified by proton magnetic resonance spectroscopy. IS was evaluated by a 3 -h hyperinsulinemic (80 mU·m(-2)·min(-1)) euglycemic clamp. Independent associations between VAT and LF on metabolic variables were assessed in mutually adjusted multivariate models. The joint associati… Show more

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Cited by 6 publications
(6 citation statements)
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“…The insulin levels were maintained at 86.5 (68.5–106.2)  μ U/mL. Peripheral insulin sensitivity ( M value) was calculated by dividing the insulin-stimulated glucose disposal rate by the steady-state plasma insulin concentration during the last 30 minutes of the clamp [14]. …”
Section: Methodsmentioning
confidence: 99%
“…The insulin levels were maintained at 86.5 (68.5–106.2)  μ U/mL. Peripheral insulin sensitivity ( M value) was calculated by dividing the insulin-stimulated glucose disposal rate by the steady-state plasma insulin concentration during the last 30 minutes of the clamp [14]. …”
Section: Methodsmentioning
confidence: 99%
“…Nonalcoholic fatty liver disease (NAFLD) is common among obese children and adolescents (Lavine and Schwimmer 2004) and is strongly linked to insulin resistance, hypertension, and dyslipidemia (Perseghin et al 2006;Schwimmer et al 2008;Kim et al 2012;Wicklow et al 2012;Brown et al 2015). NAFLD ranges from simple steatosis (triglyceride accumulation within hepatocytes) to more advanced form of nonalcoholic steatohepatitis, which includes inflammation and liver cell injury (Lavine and Schwimmer 2004).…”
Section: Introductionmentioning
confidence: 99%
“…VAT is seen as particularly detrimental 59 as it is more insulin‐resistant and has greater capacity to uptake glucose than SAT adipocytes 60 . Moreover, excessively deposited visceral fat will secrete numerous adipokines and inflammatory mediators, such as interleukin (IL)‐6, tumour necrosis factor‐α (TNF‐α), and macrophage chemoattractant protein‐1 (MCP‐1), inducing insulin resistance and accelerating the development of diabetes 61,62 . These mechanisms suggest that interventions to prevent diabetes should give priority to decreasing the accumulation of central adiposity, especially the amount of VAT, in obese individuals.…”
Section: Discussionmentioning
confidence: 99%