17 patients with obesity-causing MC4R mutations (BMI: 35.5 ± 7.6) and 35 matched control participants with common obesity (BMI: 34.3 ± 7.1) underwent a DEXA scan for assessment of bone mineral density (BMD), bone mineral apparent density [BMAD = (BMD/√(bone area)], and bone turnover markers (BTMs).
The MC4Rp.Ile269Asn mutation accounted for a population attributable risk of 1.28% and 0.68% for childhood and adult obesity, respectively, in the Mexican population.
First, rapid and differential changes in the gut microbiota in obese-prone (OP) and obese-resistant (OR) mice fed on a high-fat diet (HFD) might cause differential efficiencies in fatty acid harvesting leading to changes in systemic fatty acid concentrations that in turn affect POMC expression and processing.
In this situation, fatty acids cause inflammation via TLR4 (toll like receptor 4) and the nuclei become less responsive to the hormones leptin and insulin, contributing to the development of obesity.
We analyzed associations of these polymorphisms with anthropometric parameters, lipid profile, as well as adiponectin, leptin and soluble leptin receptor (sOB-R) levels in prepubertal healthy children, to search for their possible role in the risk of obesity and obesity-related disorders.
Human and animal studies point to leptin as a link between infertility and obesity, a suggestion that is corroborated by findings of low sperm count, increased sperm abnormalities, oxidative stress, and increased leptin levels in obese men.
Herein, we review some findings on sperm function in obese subfertile or infertile men and those from animal studies following leptin treatment, and discuss the possible link between leptin and reproductive dysfunction in obese men.
The therapy-induced changes in BAI both in the entire tested group and in patients with class I and II obesity correlated well with the percentage of drop in body weight, body mass index (BMI), subcutaneous fat thickness, waist-to-height ratio (WHtR), and leptin concentration.
Indeed, pathological remodelling of white adipose tissue and increased levels of fat-specific cytokines (mainly leptin), as a consequence of the obesity condition, have been associated with several hallmarks of breast cancer, such as sustained proliferative signaling, cellular energetics, inflammation, angiogenesis, activating invasion and metastasis.
A high-fat diet induces hypothalamic inflammation in rodents which, in turn, contributes to the development of obesity by eliciting both insulin and leptin resistance.
Fasted plasma NEFA concentrations were lower in children with obesity than in their normal weight counterparts, despite leptin, insulin resistance indices, RBP4, retinol, and RBP4/retinol (an index of free-RBP4) being higher.
Leptin deficiency is considered a significant cause of monogenic obesity in Egyptian children with early-onset obesity as the diagnosis of these patients would be a perfect target for recombinant leptin therapy.
Since leptin resistance is considered a primary factor underlying obesity, understanding the regulation of leptin signaling could lead to therapeutic tools and provide insights into the causality of obesity.
We report a 47-year-old patient, treated with the anti-programmed cell death (PD)1 antibody pembrolizumab for a metastatic melanoma, who developed severe lipodystrophy after 10 months of treatment, characterized by the loss of subcutaneous fat tissue, central obesity and insulin resistance with a decreased leptin level.
In this study, we tested the hypotheses that 1) obesity has an influence on the ex vivo constitutive expression of vitamin D-hydroxylase genes in hMSCs, and 2) recombinant human (rh) Leptin regulates the D-hydroxylases and promotes osteoblastogenesis in hMSCs.
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.
Fat mass and leptin increased during pregnancy in the HW (p < 0.01) but not in the OB group. sOB-R increased during pregnancy in both groups (p < 0.001).
Leptin level in plasma, independent of BMI and BMI plus waist-to-hip ratio, was shown to be inversely associated with CoTh, but not trabecular BMD, suggesting that hyperleptinemia resulting from obesity might contribute to cortical porosis in patients with type 2 diabetes mellitus.