Metabolic and hormonal consequencies of the "obesity risk" MC4R variant (rs12970134) in Czech women
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
26680479
DOI
10.33549/physiolres.933119
PII: 933119
Knihovny.cz E-resources
- MeSH
- Adult MeSH
- Genetic Predisposition to Disease epidemiology genetics MeSH
- Genetic Variation genetics MeSH
- Cohort Studies MeSH
- Middle Aged MeSH
- Humans MeSH
- Obesity blood epidemiology genetics MeSH
- Receptor, Melanocortin, Type 4 genetics MeSH
- Risk Factors MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Geographicals
- Czech Republic epidemiology MeSH
- Names of Substances
- MC4R protein, human MeSH Browser
- Receptor, Melanocortin, Type 4 MeSH
Although the mutations in MC4R gene became known as the most common genetic cause of human obesity, the effect of rs12970134 A/G near MC4R gene on insulin resistance has been described. The aim of this study was to determine the effect of rs12970134 on obesity, hormone levels, and glucose metabolism in a cohort of women varying in glucose tolerance: 850 normoglycemic women, 423 diagnosed with polycystic ovary syndrome (PCOS), 402 gestational diabetics (GDM), and 250 type 2 diabetic (T2D) women. We did not confirm the explicit effect of rs12970134 on obesity. However, the influence of the A-allele on body adiposity index was observed in a cohort of women diagnosed with PCOS. In normoglycemic women, the A-allele carriership was associated with lower fasting levels of glucose, insulin, C-peptide, and index of insulin resistance. Furthermore, higher levels of growth hormone, leptin and SHBG, and lower levels of fT3, testosterone, and androstenedione were recorded in normoglycemic A-allele carriers. In conclusion, the study presents the evidence of the impact of rs12970134 on complex hypothalamic regulations.
References provided by Crossref.org
Melanocortin pathways: suppressed and stimulated melanocortin-4 receptor (MC4R)