Of the 86 studied proteins, 4 were found to be independently associated with hypertension: GDF-15, LEP, SORT-1 and FABP-2; 3 with obesity: CEACAM-8, LEP and PRELP; and 4 with diabetes: GDF-15, REN, CXCL-1 and SCF.
We systematically searched MEDLINE, EMBASE, PsycINFO, and ERIC databases for studies which included the search terms "obesity education" AND either "medical students", "residency", or "fellowship" that met PICOS (Population, Interventions, Comparators, Outcomes, Study Design) criteria for articles published in English for obesity education and evaluation of outcomes.
Further, the number of fragmented mitochondria and Drp1(Ser<sup>616</sup>) phosphorylation were trended to reduce/reduced (0.0104, 95% CI [0.0085, 0.0126], P = 0.091 and 0.0085, 95% CI [0.0068, 0.0102], P = 0.05) in myotubes derived from severely obese humans at 7 months after RYGB surgery in comparison with the presurgery state.
In a sample of 135 unrelated subjects, 35 children with obesity (between ages 3 and 13) and 100 healthy controls (between ages 4 and 16), we examined the expression levels of four candidate miRNAs (<i>hsa-miR-4777-3p, hsa-miR-642b-3p, hsa-miR-3671-1, and hsa-miR-551b-</i>2) targeting the <i>PLIN1</i> as measured by real-time polymerase chain reaction in whole blood samples.
Further, the number of fragmented mitochondria and Drp1(Ser<sup>616</sup>) phosphorylation were trended to reduce/reduced (0.0104, 95% CI [0.0085, 0.0126], P = 0.091 and 0.0085, 95% CI [0.0068, 0.0102], P = 0.05) in myotubes derived from severely obese humans at 7 months after RYGB surgery in comparison with the presurgery state.
In a sample of 135 unrelated subjects, 35 children with obesity (between ages 3 and 13) and 100 healthy controls (between ages 4 and 16), we examined the expression levels of four candidate miRNAs (<i>hsa-miR-4777-3p, hsa-miR-642b-3p, hsa-miR-3671-1, and hsa-miR-551b-</i>2) targeting the <i>PLIN1</i> as measured by real-time polymerase chain reaction in whole blood samples.
In summary, the current data support a main role for Nox1-derived O<sub>2</sub><sup>.-</sup> in kidney vascular oxidative stress and renal endothelial dysfunction in obesity, while reduced endothelial Nox4 expression associated to decreased H<sub>2</sub>O<sub>2</sub> generation and H<sub>2</sub>O<sub>2</sub>-mediated vasodilatation might hinder Nox4 protective renal effects thus contributing to kidney injury.
In the entire cohort, overweight/obese were likely to be older (OR = 1.04, p < 0.0001) and to have a mild CFTR genotype (OR = 3.33, p = 0.0003) and modestly elevated triglyceride levels (OR = 1.008, p < 0.0001).
Further, the number of fragmented mitochondria and Drp1(Ser<sup>616</sup>) phosphorylation were trended to reduce/reduced (0.0104, 95% CI [0.0085, 0.0126], P = 0.091 and 0.0085, 95% CI [0.0068, 0.0102], P = 0.05) in myotubes derived from severely obese humans at 7 months after RYGB surgery in comparison with the presurgery state.
In contrast, lower levels of mRNA FOXP3 expression was detected in ATMC from individuals with obesity that correlated with methylation percentage of FOXP3 gene but no association with miR-155 was detected.
These findings indicate that Adora2a-mediated signaling in vascular endothelial cells disrupts the BBB in dietary obesity, and implicate cerebrovascular dysfunction as the underlying mechanism for deficits in synaptic plasticity and cognition with obesity and insulin resistance.<b>SIGNIFICANCE STATEMENT</b> The blood-brain barrier (BBB) restricts the entry of circulating factors into the brain, but obesity promotes BBB breakdown in humans and animal models.
This study aimed to determine the anti-obesity effect of 17-dimethylaminoethylamino-17-demethoxygeldanamycin (17-DMAG), a heat shock protein 90 (Hsp90) inhibitor, and its underlying mechanism in rats with ovariectomy-induced obesity.
These results suggest that MARK4 promotes lipid accumulation in porcine placental trophoblasts and can be considered as a potential regulator of lipotoxicity associated with maternal obesity in the pig placenta.
Thus, this study aimed to provide further understanding of the role of ubiquitin-specific peptidase 19 (USP19) in fat development, obesity and diabetes.
These findings demonstrate that MSS51 modulates skeletal muscle mitochondrial respiration and regulates whole-body glucose and fatty acid metabolism, making it a potential target for obesity and diabetes.