Metabolic and hormonal consequencies of the "obesity risk" MC4R variant (rs12970134) in Czech Women

Title:

Metabolic and hormonal consequencies of the "obesity risk" MC4R variant (rs12970134) in Czech Women

Creator:

Olga Bradnová, Daniela Vejražková, Markéta Vaňková, Petra Lukášová, Josef Včelák, Soňa Stanická, Kateřina Dvořáková, and Běla Bendlová

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:0fbfa9d6-f733-434a-a76f-bbb217a31226
uuid:0fbfa9d6-f733-434a-a76f-bbb217a31226
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, obezita, leptin, růstový hormon, hormony štítné žlázy, obesity, growth hormone, thyroid hormones, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

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., O. Bradnová, D. Vejražková, M. Vaňková, P. Lukášová, J. Včelák, S. stanická, K. Dvořáková, B. Bendlová., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2015 Volume:64 | Number:Suppl 2

Harvested from:

CDK

Metadata only:

false