Background: Heterozygous mutations in melanocortin-4 receptor (MC4R) are the most frequent genetic cause of obesity. Bariatric surgery is a successful treatment for severe obesity. The mechanisms of weight loss after bariatric surgery are not well understood.
Methods: Ninety-two patients who had Roux-en-Y gastric bypass (RYGB) surgery were screened for MC4R mutations. We compared percent excess weight loss (%EWL) in the four MC4R mutation carriers with that of two control groups: 8 matched controls and with the remaining 80 patients who underwent RYGB.
Results: Four patients were heterozygous for functionally significant MC4R mutations. In patients with MC4R mutations, the %EWL after RYGB (66% EWL) was not significantly different compared to matched controls (70% EWL) and non-matched controls (60% EWL) after 1 year of follow-up.
Conclusions: This study suggests that patients with heterozygous MC4R mutations also benefit from RYGB and that weight loss may be independent of the presence of such mutations.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3119798 | PMC |
http://dx.doi.org/10.1007/s11695-010-0295-8 | DOI Listing |
NeuroImmune Pharm Ther
September 2024
Cognitive and Neural Science Program, Department of Psychology, Barnwell College, University of South Carolina, Columbia, SC, USA.
Obesity, by any standard, is a global health crisis. Both genetic and dietary contributions to the development and maintenance of obesity were integral factors of our experimental design. As mutations of the melanocortin 4 receptors (MC4R) are the leading monogenetic cause of obesity, MC4R haploinsufficient rats were fed a range of dietary fat (0-12 %) in a longitudinal design.
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 PDFBMC Genomics
December 2024
Institute of Pig Breeding and Agroindustrial Production, National Academy of Agrarian Sciences of Ukraine, 1 Shvedska Mohyla St, Poltava, 36013, Ukraine.
Background: Trends in the development of genetic markers for the purposes of genomic and marker-assisted selection primarily focus on identifying causative polymorphisms. Using these polymorphisms as markers enables a more accurate association between genotype and phenotype. Bioinformatic analysis allows calculating the impact of missense polymorphisms on the structural and functional characteristics of proteins, which makes it promising for identifying causative polymorphisms.
View Article and Find Full Text PDFJ Adv Vet Anim Res
September 2024
Institute of Biology Systems and Genetic Research, Lithuanian University of Health Sciences, Kaunas, Lithuania.
Objective: (DM) is a prevalent endocrine condition found in cats. Recent research has identified a connection between a higher risk of diabetes in cats and genetic factors. This genetic susceptibility to type 2 diabetes is associated with genes that control insulin secretion and function, as well as those that impact factors like obesity.
View Article and Find Full Text PDFbioRxiv
November 2024
Department of Metabolism and Systems Science, University of Birmingham, Birmingham, UK.
The central melanocortin system links nutrition to energy expenditure, with melanocortin-4 receptor (MC4R) controlling appetite and food intake, and MC3R regulating timing of sexual maturation, rate of linear growth and lean mass accumulation. Melanocortin-2 receptor accessory protein-2 (MRAP2) is a single transmembrane protein that interacts with MC4R to potentiate it's signalling, and human mutations in MRAP2 cause obesity. Previous studies have been unable to consistently show whether MRAP2 affects MC3R activity.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!