We demonstrated previously that offspring born to pregnant mice lacking the endothelial nitric oxide synthase (eNOS+/-) gene have hypertension (HTN) as adults and, when fed a high-fat diet (HFD), develop a metabolic syndrome (MS) phenotype.
Leptin promotes adequate caloric intake and glycemia in healthy lean individuals, harnessing the benefits of the ideal therapy against metabolic syndrome.
The adipokines DPP-4 and leptin in the serum can influence the body fat distribution of patients with T2MD; there is an important association of DPP-4, leptin and ADPN levels with MS, which may be used as therapeutic targets for multiple metabolism disorders of T2MD.
Low vitamin D level was associated with metabolic syndrome and high leptin level in subjects with nonalcoholic fatty liver disease: a community-based study.
The addition of leptin and adiponectin to the regression models did not substantially change the impact of thyroid hormones on components of MS. Our data suggest that, even within the euthyroid range, excess of truncal adipose tissue is associated with variations in FT4.
We previously found that blood C-reactive protein (CRP), interleukin-6 (IL-6), and leptin levels were predictors of current metabolic syndrome in schizophrenia.
The 8-week individualized training program decreased glucose, triglycerides, total cholesterol, low-density lipoprotein cholesterol and leptin in obese subjects with and without MS.
We aimed to explore the association of <i>LEPR</i> polymorphisms with obesity, metabolic syndrome (MetS), and leptin levels in Afro-Caribbean nondiabetic subjects.
The aim of this study was to determine whether MetS has an impact on the global DNA methylation pattern and the DNA methylation of several genes related to adipogenesis (PPARG, PPARA), lipid metabolism (RXRA, SREBF2, SREBF1, SCD, LPL, LXRb), and inflammation (LRP1 C3, LEP and TNF) in visceral adipose tissue.
Moreover, the circulating miRNA profiles were associated with the plasma leptin level in metabolic syndrome, and miRNAs were found to be involved in hypothalamic leptin sensitivity.
Understanding the inflammatory effects of leptin on the pulmonary system provides opportunities to develop strategies against lung injury related to metabolic syndrome or obesity.
Our results indicate that activation of the miR-34a/SIRT1:AMPK pathway leads to mitochondrial dynamics dysfunction in skeletal muscle of human and experimental NAFLD, representing an appealing prospective target in metabolic syndrome.
The synovium and IPFP in the MetS-OA group secreted more leptin and less adiponectin than those in the non-MetS-OA group (Leptin: 5.32 vs. 1.28 in synovium, respectively; <i>p</i>= 0.028; 6.44 vs. 0.88 in IPFP, respectively; <i>p</i>= 0.017.
<b>Conclusions:</b> Overall, we have found that curcumin intake among patients with metabolic syndrome and related disorders was correlated with a significant reduction in BMI, weight, WC, and leptin, and a significant increase in adiponectin levels, but did not affect HR.
High plasma leptin in early adulthood, a risk factor for cardio-metabolic syndrome, was associated with low weight at age two years (correlation coefficient controlled for adult weight = -0.21, p<0.01).
The finding that metabolic syndrome is associated with worse cognition only in the presence of the eNOS-786C allele may clarify extant inconsistencies in the literature.
The ARR correlated with the number of variables of MetS (r = 0.191, P = 0.002), body mass index (BMI; r = 0.136, P = 0.026), systolic blood pressure (r = 0.183, P = 0.002), diastolic blood pressure (r = 0.1917, P = 0.0014), potassium excreted fraction (r = 0.174, P = 0.004), low-density lipoprotein (r = 0.156, P = 0.01), plasminogen activator inhibitor type 1 (r = 0.158, P = 0.009), microalbuminuria (r = 0.136, P = 0.029), and leptin (r = 0.142, P = 0.019).
Significant increases were observed in blood pressure, HOMA-IR, leptin, triglycerides, insulin, intra-abdominal fat, and number of fat cells per field (<i>p</i> = 0.001) and in advanced glycosylation products, adipocyte area, LPL, HSL activities and/or expression (<i>p</i> ≤ 0.01) in the MS groups progressively from the third month onward.
Linear regression confirmed an independent association of both leptin and hs-CRP with VFth in women, also after adjustment for age and MetS (<i>p</i> = 0.012 and 0.007, respectively).
Finally, we demonstrated that EF-sir2 could significantly improve the metabolic index of mammalian cells through insulin resistanced model in vitro and metabolic syndrome rat model in vivo.