<b>Results:</b> We showed that serum miR-27a level correlated positively with obesity and insulin resistance in obese children, and that elevated serum miR-27a levels correlated with insulin resistance in leptin receptor-deficient db/db mice, and with obesity and insulin resistance in high-fat diet-fed C57BL/6J mice.
<b>Methods:</b> Initially to investigate the effect of obesity and IR in the analyzed parameters, insulin-sensitive eutrophic volunteers (CON; <i>n</i> = 9) and obese non-insulin (OB; <i>n</i> = 9) and insulin-resistant (OBR; <i>n</i> = 8) were enrolled.
Congenital Leptin receptor (LEPR) deficiency is a rare genetic cause of early-onset morbid obesity characterised by severe early onset obesity, major hyperphagia, hypogonadotropic hypogonadism and immune and neuroendocrine/metabolic dysfunction.
As regards, rs7799039 AA genotype showed significant higher leptin level than other genotypes in the same group with a non-significant difference in genotypes distribution between obese and controls. rs1137101 variant of leptin receptor and fasting leptin level are correlated with overweight and obesity in Saudi children.
The aim this study was to investigate the prevalence of single nucleotide polymorphisms in LEP gene (LEP 3'UTR A/C, -2548 G/A) and LEPR (K109R and Q223R) and their association with Leptin level and obesity.
We investigated the associations between the obesity candidate genes (fat mass and obesity-associated (FTO), melanocortin-4 receptor (MC4R), leptin (LEP) and leptin receptor) and total energy intake and percentage of energy from macronutrients and ultra-processed foods before and during pregnancy.
J Strength Cond Res 32(4): 1036-1044, 2018-Leptin (LEP) and leptin receptor (LEPR) genes have been studied for their potential association with development of human obesity and its related complications.
We obtained higher serum leptin levels in infants with the GG genotype for LeprA668G, with haplotype GG/GG for Lep G2548A/A19G, and with GG/GG-GG (LepG2548A/A19G-LeprA668G); thus, it seems that the genotype GG could be a protector against obesity development in infancy and adulthood.
LEPR has diverse roles in metabolism, appetite and bone formation with obesity linked to both elevated levels of leptin and increased cancer incidence.
Thus, the aim of the present study is to verify the influence of LEPR polymorphism (rs2767485) on serum orexigenic (NPY, MCH and AgRP) and anorexigenic (Leptin and α-MSH) neuropeptides levels among obese adolescents submitted to 1year of multicomponent weight loss therapy.
Unlike therapeutic interventions that target peroxisome proliferator-activated receptor gamma and leptin receptor activity, which yield detrimental side effects including increased fracture risk and altered feeding behavior, respectively, inhibition of IP6K1 maintains insulin sensitivity and prevents obesity while preserving bone integrity.
Expression of IGF-1 and LEPR indicates a relevant role in androgenic features reversion present in PCOS, hormonal equilibrium, body weight regulation, and glucose metabolism, therefore, under phenotype obesity and infertility regulation in this model.
To understand features of human obesity and type 2 diabetes mellitus (T2D) that can be recapitulated in the mouse, we compared C57BL/6J mice fed a Western-style diet (WD) to weight-matched genetically obeseleptin receptor-deficient mice (<i>db/db</i>).
Through phenotyping of the resulting three lines of rats bearing distinct mutations in the Lepr locus, we found that the strains with a frame-shifted or premature stop codon mutation led to obesity and metabolic disorders.
Therefore, we hypothesized that the LEP-rs7799039 and LEPR-rs1137101 SNPs are related to the risk of pre-pregnancy overweight/obesity (body mass index ≥25 kg/m<sup>2</sup>) as well as to excessive gestational weight gain (GWG) and high concentrations of leptin throughout pregnancy.
Dopamine Neuron-Restricted Leptin Receptor Signaling Reduces Some Aspects of Food Reward but Exacerbates the Obesity of Leptin Receptor-Deficient Male Mice.
Here, we focus on leptin receptor nonsense variants causing obesity, namely the human W31X, murine Y333X and rat Y763X mutations, and explored their susceptibilities to aminoglycoside and PTC124 mediated translational read-through in vitro.
Since no elevations in the expression of the leptin receptor gene (<i>LEPR</i>) or fat metabolism-associated genes (<i>PLIN2, SLC27A4</i>) were recorded in blastocysts recovered from obese mice, the role of leptin in mediating the effects of obesity on embryos at the peripheral level is likely lower than expected.
Obesity did not correlate with protein serum levels.We observed that obesity is more frequent in children with LEPR 223 AG+GG and LEPR 1019 GA+AA genotypes.
The aim of this study was to assess the impact of mothers' and newborns' fat mass and obesity-associated gene (FTO) rs9939609 and leptin receptor (LEPR) rs1137101 gene polymorphisms on neonatal anthropometric parameters in order to identify a potential risk for developing obesity.We performed a cross-sectional study on 355 mother-newborn couples in an Obstetrics Gynecology Tertiary Hospital from Romania, evaluated with regard to anthropometric parameters, clinical and laboratory parameters besides 2 genetic polymorphisms (FTO rs9939609 and LEPRrs1137101).Newborns with mothers carrying variant AT or AA genotype for FTO rs9939609 presented lower BMI (P = 0.012) and lower MUAC (P = 0.029).
Few genes such as leptin, leptin receptor encoded by the db (diabetes), pro-opiomelanocortin, AgRP and NPY and melanocortin-4 receptors and insulin-induced gene 2 were linked to obesity.