Aim:We assessed levels of polyunsaturated fatty acid (PUFA) in serum and red blood cells (RBCs) among groups stratified by generation and its clinical significance in Japanese subjects living in an urban area.
The nutritional environment to which animals are exposed in early life can lead to epigenetic changes in the genome that influence the risk of obesity in later life. Here, we demonstrate that the fibroblast growth factor-21 gene (Fgf21) is subject to peroxisome proliferator-activated receptor (PPAR) α–dependent DNA demethylation in the liver during the postnatal period. Reductions in Fgf21 methylation can be enhanced via pharmacologic activation of PPARα during the suckling period. We also reveal that the DNA methylation status of Fgf21, once established in early life, is relatively stable and persists into adulthood. Reduced DNA methylation is associated with enhanced induction of hepatic FGF21 expression after PPARα activation, which may partly explain the attenuation of diet-induced obesity in adulthood. We propose that Fgf21 methylation represents a form of epigenetic memory that persists into adulthood, and it may have a role in the developmental programming of obesity.
Aims:In obesity, fatty acid composition is altered with reduced docosahexaenoic acid (DHA) levels. Desaturating enzymes, stearoyl-CoA desaturase (SCD), delta-6 desaturase (D6D) and delta-5 desaturase (D5D) modulate fatty acid composition and are thus associated with the development of metabolic syndrome. The aim of this study was to identify the relationships among DHA content, desaturase indices and the components of metabolic syndrome in childhood obesity. Methods: Thirty-two obese children (27 male, 5 female) aged 12.0 2.6 years (mean SD), with a relative body weight greater than 120% of the standard weight for sex, age and height, were recruited. Fatty acid composition of plasma phospholipids was analyzed by gas chromatography, and the desaturase indices were assessed: SCD (
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