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  • Title: Saturation of subcutaneous adipose tissue expansion and accumulation of ectopic fat associated with metabolic dysfunction during late and post-pubertal growth.
    Author: Gyllenhammer LE, Alderete TL, Toledo-Corral CM, Weigensberg M, Goran MI.
    Journal: Int J Obes (Lond); 2016 Apr; 40(4):601-6. PubMed ID: 26443340.
    Abstract:
    BACKGROUND/OBJECTIVE: Puberty is a period defined by large changes in adipose tissue accumulation and distribution; however, longitudinal patterns of ectopic fat development have not been shown. We have previously shown significant declines in beta-cell function (BCF) across puberty and hypothesize that accumulation of ectopic fat deposition, particularly hepatic fat, will predict this fall. SUBJECT/METHODS: We conducted a longitudinal study and examined 2-year change in abdominal fat distribution and type 2 diabetes risk markers in 76 Hispanic children and young adults (16.1±0.5 years, 66% obese, 52% male, 51% post-pubertal). Subcutaneous abdominal adipose tissue (SAAT), visceral adipose tissue (VAT), hepatic fat fraction (HFF) and pancreatic fat fraction (PFF) were measured by 3-Tesla magnetic resonance imaging, and markers of type 2 diabetes risk were collected at fasting and during an oral glucose tolerance test (OGTT). RESULTS: Baseline pubertal status significantly moderated the 2-year change in ectopic fat deposition, such that VAT, HFF and PFF increased in individuals during late and post-pubertal growth, whereas children earlier in their pubertal development decreased ectopic accumulation and had less VAT accumulation (VAT: pTanner*time=0.044, 0.31±0.08 l vs 0.03±0.10 l; HFF: pTanner*time=0.007, 1.34±0.87% vs -2.61±1.11%; PFF: pTanner*time<0.001, 1.61±0.39% vs -0.96±0.50%). Independent of pubertal status, the 2-year increase in HFF and VAT significantly associated with a decline in BCF (ß=-1.04, P=0.038; ß=-1.81, P=0.020) and metabolic function, while accumulation of SAAT significantly associated with BCF (ß=1.36, P=0.012) and metabolic improvement. HFF accumulation was the only depot to significantly predict clinical markers of type 2 diabetes risk, fasting glucose and HbA1c, and circulating free fatty acid levels (ß=1.00, P=0.034; ß=1.00, P=0.015; ß=01.01, P=0.024). CONCLUSIONS: The accumulation of SAAT defends against type 2 diabetes risk and potentially ectopic fat accumulation. Intra-abdominal VAT and HFF accumulation both associate with metabolic decline and BCF, while HFF predicts an even greater number of metabolic risk features.
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