We previously reported elevated adipose leptin expression, plasma leptin concentrations, and adrenocortical leptin receptor expression in the long-term hypoxic (LTH) ovine fetus. This study addressed whether leptin antagonist (LA) administration to LTH fetal sheep altered expression of key genes governing cortisol synthesis. Ewes were maintained at high altitude (3,820 meters) from 40 to 130 days gestation (dG), returned to Loma Linda University, and implanted with a maternal tracheal catheter. Reduced Po2 was maintained by nitrogen infusion. On 132 dG, LTH (n = 11) and age-matched, normoxic control (n = 11) fetuses underwent vascular catheter implantation. At 138 dG, fetuses were continuously infused with either saline or the LA (1.5 mg·kg(-1)·day(-1)) for 4 days and samples collected for blood gases, ACTH, and cortisol. Fetal adrenal cortex was collected for determination of steriodogenic acute regulatory protein (StAR), ACTH, and leptin receptor, cholesterol side-chain cleavage (CYP11A1), cytochrome P-450 11β-hydroxylase (CYP11B1), 17α-hydroxylase (CYP17), 21-hydroxylase (CYP21), signal transducer and activator of transcription 3 (STAT3), pSTAT3, and 17β-hydroxysteroid dehydrogenase (HSD3B) expression. In the saline-infused LTH fetuses, StAR, ACTH receptor, CYP11A1, and CYP17 expression was significantly lower compared with control (P < 0.05), whereas levels of CYP11B1, CYP21, and HSD3B mRNA were similar between groups. LA infusion restored expression of StAR, pSTAT3, CYP11A1, and CYP17, but not ACTH receptor, to normal ontogenic levels in the LTH group while having no effect on control fetuses. Neither fetal plasma ACTH nor cortisol concentrations were altered by LA infusion. We speculate that while leptin plays a role in governing expression of key enzymes and StAR in response to LTH, other factors play a role in modulating cortisol synthesis in these fetuses.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3602822 | PMC |
http://dx.doi.org/10.1152/ajpregu.00377.2012 | DOI Listing |
J Diabetes Metab Disord
June 2025
Personalized Medicine Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, No. 10- Jalal -e-Ale-Ahmad Street, Chamran Highway, Tehran, 1411713119 Iran.
Objectives: The gene is a key focus in obesity research, with studies linking its polymorphisms to various diseases like polycystic ovarian syndrome and energy intake disorders. This study aims to investigate the prevalence of the rs2025804 variant within LEPR and its distribution among healthy individuals across diverse ethnic groups in Iran.
Methods: The frequency of the rs2025804 genotype in the gene was analyzed in 1142 healthy adults representing different ethnicities in Iran.
Biochem Biophys Res Commun
December 2024
Yancheng Clinical College, Xuzhou Medical University, Yancheng, 224000, PR China. Electronic address:
Diabetes is one of the most prevalent metabolic disorders, and its incidence has been experiencing a steady annual rise in recent years. Diabetic peripheral neuropathy (DPN) represents the most frequent adverse complication, exerting a profound impact on the quality of life for those suffering from diabetes. The etiology of DPN is complex, including impaired mitochondrial function.
View Article and Find Full Text PDFWorld J Exp Med
December 2024
Department of Internal Medicine, Gayatri Vidya Parishad Institute of Healthcare and Medical Technology, Visakhapatnam 530048, Andhra Pradesh, India.
Obesity is increasingly prevalent worldwide, with genetic factors contributing to its development. The hypothalamic leptin-melanocortin pathway is central to the regulation of appetite and weight; leptin activates the proopiomelanocortin neurons, leading to the production of melanocortin peptides; these in turn act on melanocortin 4 receptors (MC4R) which suppress appetite and increase energy expenditure. MC4R mutations are responsible for syndromic and non-syndromic obesity.
View Article and Find Full Text PDFPediatr Res
December 2024
Division of Molecular Genetics, Department of Pediatrics, Columbia University Irving Medical Center, New York, NY, USA.
Obesity and weight regulation disorders are determined by the combined effects of genetics and environment. Polygenic obesity results from the combination of common variants in several genes which predisposes the individual to obesity and its related complications. In contrast, monogenic obesity results from changes in single genes, especially those in leptin-melanocortin pathway, and presents with early onset severe obesity, with or without other syndromic features.
View Article and Find Full Text PDFNeurosci Lett
December 2024
AdipoBrain, Departamento de Ciencias Farmacéuticas y de la Salud, Facultad de Farmacia, Universidad San Pablo-CEU, CEU Universities, 28660 Madrid, Spain. Electronic address:
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!