Introduction. This study evaluated the association between obesity and the K109R, Q223R, and K656N polymorphisms of the leptin receptor (LEPR) locus. Such polymorphisms cause changes in the extracellular extreme of the LEPR gene product and appear to be related to signal transduction toward the cell. Subjects and methods. A total of 128 participants between 6 and 17 years of age from a Mexican Mestizo population were included in the study. Individuals were classified as overweight–obese (n = 76) and normal (n = 52), based on anthropomorphic measurements. The K109R, Q223R, and K656N polymorphisms of the LEPR were determined by the size of restriction fragments obtained from polymorphic fragment amplification (polymerase chain reaction-restriction fragment length polymorphism) obtained from genomic DNA. Allele frequency was compared using the chi-square test. Odds ratio was calculated to determine allele obesity risk factor. Results. Variant allele frequency was 109R = 0.35, 223R = 0.49, and 656N = 0.11 for the K109R, Q223R, and K656N polymorphisms, respectively. No statistically significant association with obesity was found in any of the alleles. The N allele of the K656N polymorphism was associated with nonobesity markers, such as high concentrations of high-density lipoproteins, normal body mass index, less thickness of skinfolds, and body perimeters. None of the alleles studied were shown to be obesity risk factors. Conclusions. Our results suggest that there is no association between the K109R, Q223R, and K656N polymorphisms of the LEPR gene with obesity, and none of the alleles of the LEPR gene K109R, Q223R, and K656N polymorphisms are an obesity risk factor.

Background and objectives: Cardiac remodeling in pregnancy and postpartum is poorly understood. The aim of this study was to evaluate changes in cardiac fibrosis (pericardial, perivascular, and interstitial), as well as the expression of matrix metalloproteinases (MMP-1, MMP-2, and MMP-9) and their inhibitors (Tissue inhibitors of metalloproteinases, TIMP-1 and TIMP-4) during late pregnancy and postpartum in rat left ventricle. Materials and Methods: Female Sprague–Dawley rats were used for this study. Rats were divided three groups: non-pregnant, late pregnancy, and postpartum. The heart was weighed and cardiac fibrosis was studied by conventional histological procedures. The expression and transcript level of target proteins were evaluated using immunoblot techniques and quantitative PCR. Results: The experiments showed an increase of perivascular, pericardial, and interstitial fibrosis in heart during pregnancy and its reversion in postpartum. Moreover, in late pregnancy, MMP-1, MMP-2, and MMP-9 metalloproteinases were downregulated and TIMP-1 and TIMP-4 were upregulated in left ventricle. Conclusions: Our data suggest that the metalloproteinases system is involved in the cardiac extracellular matrix remodeling during pregnancy and its reversion in postpartum, this improves the knowledge of the adaptive cardiac remodeling in response to a blood volume overload present during pregnancy.

Background and objectives: Adipose tissue and skeletal muscle secrete adiponectin, a hormone abundantly secreted by adipocytes, that through the adiponectin receptor, regulate glucose and lipid metabolism. Adiponectin appears to protect skeletal muscles from inflammatory damage induced by oxidative stress. It has been suggested that decreased adiponectin levels could be associated with pathologic conditions, including obesity and diabetes. Furthermore, some studies suggest that exercise could have a beneficial effect by increasing adiponectin levels, but this observation remains controversial. It is also unknown if physical exercise modifies adiponectin expression in skeletal muscles. The aim of this study was to investigate the effect of chronic exercise on serum adiponectin and adiponectin expression in slow-twitch (soleus) and fast-twitch (plantaris) muscles in healthy rats. Materials and methods: Two-month-old male Wistar rats were randomly divided into three groups with n = 6 in each group: control (C), moderate-intensity training (MIT), and high-intensity training (HIT). The rats were conditioned to run on a treadmill for the 8-week period. Forty-eight hours after the last session, blood samples were collected for adiponectin measurements and total RNA was isolated from plantaris and soleus muscles to measure by RT-qPCR adiponectin receptor 1 and adiponectin mRNA expression level. Results: MIT and HIT groups had reduced adiponectin protein levels in serum and the plantaris muscle, but not changes in adiponectin protein were observed in the soleus muscle. No significant differences in Adiponectin receptor 1 (AdipoR1) gene expression were observed following intense or moderate exercise in either muscle group studied. Conclusions: Our study shows that decreasing levels of circulating adiponectin is a result of physical exercise and should not be generalized as a predictive marker of disease.

Previous studies have suggested a role of the endocannabinoid system in metabolic diseases, such as diabetes. We investigated the effect of diabetes on cannabinoid receptor type 1 (CB₁) expression and cannabinoid-induced vasorelaxation in rat aorta rings. Aortas from healthy rats and from rats with experimentally induced diabetes were used to compare the vasorelaxant effect of the cannabinoid agonist arachidonylcyclopropylamide (ACPA) and CB₁ expression and localization. After 4–8 weeks of diabetes induction, CB₁ receptor expression and CB₁ phosphorylation were higher in aortic rings, in association with greater vasorelaxation induced by the CB₁ agonist ACPA compared to healthy rats. The vasorelaxant effect observed in healthy rats is similar throughout the study. Further studies are needed to elucidate the implications of CB₁ receptor overexpression in diabetes and its influence on the progression of the cardiovascular complications of this metabolic disease.