open access

Vol 6, No 2 (2021)
Original article
Published online: 2021-05-19
Get Citation

MC4R polymorphism in rs17782313 influences on insulin resistance

Wioletta Szywacz1, Sylwia Mielcarska1, Małgorzata Poręba1, Agata Macionga1, Kamila Stopińska1, Nikola Szweda-Gandor, Władysław Grzeszczak1
·
Medical Research Journal 2021;6(2):94-98.
Affiliations
  1. Department of Internal Medicine, Diabetology and Nephrology in Zabrze, Medical University of Silesia in Katowice, Poland

open access

Vol 6, No 2 (2021)
ORIGINAL ARTICLES
Published online: 2021-05-19

Abstract

Introduction: There are many factors responsible for the development of metabolic syndrome – mainly associated with lifestyle, but also genetic ones. MC4R (melanocortin 4 receptor) genes variants have been associated with the risk of developing obesity, type 2 diabetes mellitus and coronary artery disease.

Aim of the study: To investigate the association between MC4R rs17782313 polymorphism and concentrations of glucose, insulin, HOMA-IR and QUICKI values in the whole study group.

Materials and methods: Study group consisted of 294 patients (136 men and 158 women). Collected venous blood samples were stored at -700C until the study group was completed. In the laboratory of Clinical Hospital 1 in Zabrze, the DNA materials were isolated, proper concentration of the DNA (15 ng/μL) were prepared and quality and quantity were checked by spectrophotometry. Allelic discrimination was performed with the use of fluorescent-labelled TaqMan Pre-designed SNP Genotyping Assay probes.

Results: No statistically significant differences in concentrations of cholesterol, HDL, LDL, TG between genotypes in women and men were observed. In the whole group of patients, glucose and insulin levels did not differ significantly between TT, CT and CC carriers. Significant differences in values of HOMA-IR and QUICKI between TT, CT and CC carriers as well as between TT carriers and CT+CC carriers were found. CC+TT carriers have a significantly lower value of HOMA-IR and higher QUICKI value than TT carriers.

Conclusions: MC4R polymorphism in rs17782313 may be associated with insulin resistance. Further studies are necessary to completely assess the association between investigated polymorphism, insulin resistance and risk of diabetes mellitus development.

Abstract

Introduction: There are many factors responsible for the development of metabolic syndrome – mainly associated with lifestyle, but also genetic ones. MC4R (melanocortin 4 receptor) genes variants have been associated with the risk of developing obesity, type 2 diabetes mellitus and coronary artery disease.

Aim of the study: To investigate the association between MC4R rs17782313 polymorphism and concentrations of glucose, insulin, HOMA-IR and QUICKI values in the whole study group.

Materials and methods: Study group consisted of 294 patients (136 men and 158 women). Collected venous blood samples were stored at -700C until the study group was completed. In the laboratory of Clinical Hospital 1 in Zabrze, the DNA materials were isolated, proper concentration of the DNA (15 ng/μL) were prepared and quality and quantity were checked by spectrophotometry. Allelic discrimination was performed with the use of fluorescent-labelled TaqMan Pre-designed SNP Genotyping Assay probes.

Results: No statistically significant differences in concentrations of cholesterol, HDL, LDL, TG between genotypes in women and men were observed. In the whole group of patients, glucose and insulin levels did not differ significantly between TT, CT and CC carriers. Significant differences in values of HOMA-IR and QUICKI between TT, CT and CC carriers as well as between TT carriers and CT+CC carriers were found. CC+TT carriers have a significantly lower value of HOMA-IR and higher QUICKI value than TT carriers.

Conclusions: MC4R polymorphism in rs17782313 may be associated with insulin resistance. Further studies are necessary to completely assess the association between investigated polymorphism, insulin resistance and risk of diabetes mellitus development.

Get Citation

Keywords

melanocortin 4 receptor, insulin resistance, diabetes mellitus, single nucleotide polymorphism, QUICKI, HOMA-IR

About this article
Title

MC4R polymorphism in rs17782313 influences on insulin resistance

Journal

Medical Research Journal

Issue

Vol 6, No 2 (2021)

Article type

Original article

Pages

94-98

Published online

2021-05-19

Page views

544

Article views/downloads

595

DOI

10.5603/MRJ.a2021.0023

Bibliographic record

Medical Research Journal 2021;6(2):94-98.

Keywords

melanocortin 4 receptor
insulin resistance
diabetes mellitus
single nucleotide polymorphism
QUICKI
HOMA-IR

Authors

Wioletta Szywacz
Sylwia Mielcarska
Małgorzata Poręba
Agata Macionga
Kamila Stopińska
Nikola Szweda-Gandor
Władysław Grzeszczak

References (15)
  1. Wang HH, Lee DKi, Liu M, et al. Novel Insights into the Pathogenesis and Management of the Metabolic Syndrome. Pediatr Gastroenterol Hepatol Nutr. 2020; 23(3): 189–230.
  2. Janszky I, Vatten L, Romundstad P, et al. Metabolic syndrome in Poland - the PONS Study. Ann Agric Environ Med. 2011; 18(2): 270–272.
  3. Farooqi IS, O'Rahilly S. Mutations in ligands and receptors of the leptin-melanocortin pathway that lead to obesity. Nat Clin Pract Endocrinol Metab. 2008; 4(10): 569–577.
  4. Lotta LA, Mokrosinski J, Mendes de Oliveira E, et al. Human gain-of-function MC4R variants show signaling bias and protect against obesity. Yearbook of Paediatric Endocrinology. 2020.
  5. Qin Li, Tiwari AK, Zai CC, et al. Regulation of melanocortin-4-receptor (MC4R) expression by SNP rs17066842 is dependent on glucose concentration. Eur Neuropsychopharmacol. 2020; 37: 39–48.
  6. Wei BL, Yin RX, Liu CX, et al. The MC4R SNPs, their haplotypes and gene-environment interactions on the risk of obesity. Mol Med. 2020; 26(1): 77.
  7. Gierach MA, Junik R. Insulin resistance in metabolic syndrome depending on the occurrence of its components. Endokrynologia Polska. ; 2021.
  8. Brodowski J, Szkup M, Jurczak A, et al. Searching for the relationship between the parameters of metabolic syndrome and the rs17782313 (TC) polymorphism of the MC4R gene in postmenopausal women. Clin Interv Aging. 2017; 12: 549–55.
  9. Małgorzata S, Jacek B, Jerzy OA, et al. Searching for Factors Raising the Incidence of Metabolic Syndrome Among 45-60-Year-Old Women. Aging Dis. 2018; 9(5): 831–842.
  10. Yarizadeh H, Mirzababaei A, Ghodoosi N, et al. The interaction between the dietary inflammatory index and MC4R gene variants on cardiovascular risk factors. Clin Nutr. 2021; 40(2): 488–495.
  11. Rotter I, Skonieczna-Żydecka K, Kosik-Bogacka D, et al. Relationships between rs9939609, rs17782313, and rs1801282 polymorphisms and the occurrence of selected metabolic and hormonal disorders in middle-aged and elderly men - a preliminary study. Clin Interv Aging. 2016; 11: 1723–1732.
  12. Dušátková L, Zamrazilová H, Sedláčková B, et al. Association of obesity susceptibility gene variants with metabolic syndrome and related traits in 1,443 Czech adolescents. Folia Biol (Praha). 2013; 59(3): 123–133.
  13. Rana S, Sultana A, Bhatti AA. Association of rs6265 and rs17782313 with metabolic syndrome in Pakistanis. J Biosci. 2019; 44(4).
  14. Lazopoulou N, Gkioka E, Ntalla I, et al. The combined effect of MC4R and FTO risk alleles on childhood obesity in Greece. Hormones (Athens). 2015; 14(1): 126–133.
  15. Voiculescu VM, Solomon I, Popa A, et al. Gene polymorphisms of TNF-238G/A, TNF-308G/A, IL10-1082G/A, TNFAIP3, and MC4R and comorbidity occurrence in a Romanian population with psoriasis. J Med Life. 2018; 11: 69–74.

Regulations

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

By VM Media Group sp. z o.o., ul. Świętokrzyska 73, 80–180 Gdańsk, Poland
tel.:+48 58 320 94 94, fax:+48 58 320 94 60, e-mail: viamedica@viamedica.pl