Rather than bound fructose, the free fructose from the maternal diet contributes to the programming of obesity through the disruption of leptin, ghrelin, and CD36 expression involved in appetite regulation.
Accordingly, mitochondrial expression of FAT/CD36 and plasma membrane fatty acid-binding protein was decreased in both groups of subjects with obesity.
Together, the findings of this study suggest that obesity with and without PCOS should be regarded as separate entities, and that CD36 overexpression in GC of obese patients is one of the mechanisms by which obesity impairs GC function.
In addition, mice with the <i>Val66Met</i> variant in both alleles (BDNF<sup>M/M</sup>) fed a high-fat diet exhibited extreme obesity with increased CD36 gene and protein levels in macrophages.
This is the first established link between physical binding of fatty acids and a function of CD36, and has implications for obesity and atherosclerosis.
The purpose of this study was to evaluate the relationship between the BMIz trajectory versus the percent body fat (%FAT) trajectory, and if BMIz could predict significant changes in %FAT in a sample of obese children and adolescents.
The aim of this study was to investigate the association of selected single nucleotide polymorphisms (SNPs) of cluster of differentiation 36 (CD36) and peroxisome proliferator-activated receptor γ (PPARγ) with VPA-induced weight gain and obesity in epileptic patients.
Overweight involved 3-14% of the participants and obesity was diagnosed in isolated cases (0-3%); both were considerably lower compared to the estimates based on %FAT.
In the past decade, microvesicles (MVs) and CD36 have increasingly been considered as possible biomarkers for obesity, the metabolic syndrome (MetSy), type 2 diabetes mellitus (T2DM).
Compared with the obesity group, HOMA-IR, AUC, intrahepatic FFA, and protein expression, and mRNA levels of hepatic CD36 in the non-therapy group were significantly increased (P < 0.05).
Our study reveals that absence of TIMP4 can impair lipid absorption and the high fat diet-induced obesity in mice possibly by regulating the proteolytic processing of CD36 protein in the intestinal enterocytes.
Increase in plasma membrane FAT/CD36 content in obese rats and failure in lipin-1 export to nucleus with progression of obesity, implying an increase in FA uptake and their different channeling into lipid intermediates synthesis pathway in old fa/fa rats versus FA usage in lean rats of the same age.
The purpose of this investigation was to evaluate if BMI could predict total fat mass (TFM) and percent body fat (%FAT) in a sample of overweight and obese children.
Obesity is associated with altered duodenal expression of FFAR1, FFAR4 and CD36, suggesting altered capacity for the sensing, absorption and metabolism, of dietary lipids.
Together these data suggest that limiting FA uptake and partial inhibition of FA oxidation in the heart via CD36 ablation may be detrimental for the compensated hypertrophic heart in the absence of sufficiently elevated circulating FAs to provide an adequate energy source.<b>NEW & NOTEWORTHY</b> Limiting CD36-mediated fatty acid uptake in the setting of obesity and/or insulin resistance protects the heart from cardiac hypertrophy and dysfunction.
We explored this association further by investigating correlations between sCD36 levels, intrahepatic lipid content and markers of obesity in NAFLD patients and controls.