The Interaction between KCNJ11 Gene Polymorphism and Refined Carbohydrates Intake on Obesity in Indonesian Adolescents

Author(s): Emy Huriyati*, Harry Freitag Luglio, Ahmad H. Sadewa, Mohammad Juffrie

Journal Name: Current Nutrition & Food Science

Volume 16 , Issue 2 , 2020


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Abstract:

Background: Obesity has been associated with genetic and environmental factors. Although carbohydrate intake was previously shown to be associated with a high risk of obesity and insulin resistance, some studies reported that genetic factors also have a role in this association. KCNJ11 is a gene involved in protein K-ATP channels of pancreatic beta cells and previously associated with obesity.

Objective: The objective of this study was to determine the interaction between KCNJ11 polymorphism with a high intake of refined carbohydrates in relation to the incidence of obesity in adolescents.

Methods: This was an observational study with a case-control design. The subjects of this study were male and female adolescents from 10 high schools in Yogyakarta. Dietary intake, body weight, and height were collected. KCNJ11 gene polymorphism was detected by polymerase Chain Reaction- Restriction Fragment Length Polymorphism (PCR-RFLP) method.

Results: There is a significant association between KCNJ11 polymorphism with a high intake of refined carbohydrates in the incidence of obesity in adolescents (OR = 2.35, p =0.036).

Conclusion: There is a significant association between the KCNJ11 polymorphism with a high intake of refined carbohydrates in adolescent obesity.

Keywords: Adolescent, high refined carbohydrate intake, KCNJ11 polymorphism, nutrigenetic, nutrigenomic, obesity.

[1]
Kementrian Kesehatan RI. Riset Kesehatan Dasar Jakarta: Badan Penelitian dan Pengembangan Kementrian Kesehatan RI 2013.
[2]
Medawati A, Hadi H, Pramantara DP. Hubungan antara asupan energi, asupan lemak, dan obesitas pada remaja siswa-siswi SLTP di Kota Yogyakarta dan di Kabupaten Bantul. J Gizi Klinik Indonesia 2005; 1(3): 119-29.
[http://dx.doi.org/10.22146/ijcn.17467]
[3]
Lin W-T, Huang H-L, Huang M-C, et al. Effects on uric acid, body mass index and blood pressure in adolescents of consuming beverages sweetened with high-fructose corn syrup. Int J Obes 2013; 37(4): 532-9.
[http://dx.doi.org/10.1038/ijo.2012.121] [PMID: 22890489]
[4]
Lyssenko V, Jonsson A, Almgren P, et al. Clinical risk factors, DNA variants, and the development of type 2 diabetes. N Engl J Med 2008; 359(21): 2220-32.
[http://dx.doi.org/10.1056/NEJMoa0801869] [PMID: 19020324]
[5]
Gloyn AL, Braun M, Rorsman P. Type 2 diabetes susceptibility gene TCF7L2 and its role in beta-cell function. Diabetes 2009; 58(4): 800-2.
[http://dx.doi.org/10.2337/db09-0099] [PMID: 19336690]
[6]
Webster RJ, Warrington NM, Beilby JP, Frayling TM, Palmer LJ. The longitudinal association of common susceptibility variants for type 2 diabetes and obesity with fasting glucose level and BMI. BMC Med Genet 2010; 11: 140.
[http://dx.doi.org/10.1186/1471-2350-11-140] [PMID: 20929593]
[7]
Hernandez-Escalante VM, Nava-Gonzalez EJ, Voruganti VS, et al. Replication of obesity and diabetes-related SNP associations in individuals from Yucatán, México. Front Genet 2014; 5: 380.
[http://dx.doi.org/10.3389/fgene.2014.00380] [PMID: 25477898]
[8]
Pan L, Li R, Park S, Galuska DA, Sherry B, Freedman DS. A longitudinal analysis of sugar-sweetened beverage intake in infancy and obesity at 6 years. Pediatrics 2014; 134(Suppl. 1): S29-35.
[http://dx.doi.org/10.1542/peds.2014-0646F] [PMID: 25183752]
[9]
Payab M, Kelishadi R, Qorbani M, et al. Association of junk food consumption with high blood pressure and obesity in Iranian children and adolescents: the CASPIAN-IV Study. J Pediatr (Rio J) 2015; 91(2): 196-205.
[http://dx.doi.org/10.1016/j.jped.2014.07.006] [PMID: 25449791]
[10]
Gulati S, Misra A. Sugar intake, obesity, and diabetes in India. Nutrients 2014; 6(12): 5955-74.
[http://dx.doi.org/10.3390/nu6125955] [PMID: 25533007]
[11]
Wang F, Han XY, Ren Q, et al. Effect of genetic variants in KCNJ11, ABCC8, PPARG and HNF4A loci on the susceptibility of type 2 diabetes in Chinese Han population. Chin Med J (Engl) 2009; 122(20): 2477-82.
[PMID: 20079163]
[12]
Zhou D, Zhang D, Liu Y, et al. The E23K variation in the KCNJ11 gene is associated with type 2 diabetes in Chinese and East Asian population. J Hum Genet 2009; 54(7): 433-5.
[http://dx.doi.org/10.1038/jhg.2009.54] [PMID: 19498446]
[13]
Fischer A, Fisher E, Möhlig M, et al. KCNJ11 E23K affects diabetes risk and is associated with the disposition index: results of two independent German cohorts. Diabetes Care 2008; 31(1): 87-9.
[http://dx.doi.org/10.2337/dc07-1157] [PMID: 17898091]
[14]
Haider S, Antcliff JF, Proks P, Sansom MSP, Ashcroft FM. Focus on Kir6.2: a key component of the ATP-sensitive potassium channel. J Mol Cell Cardiol 2005; 38(6): 927-36.
[http://dx.doi.org/10.1016/j.yjmcc.2005.01.007] [PMID: 15910877]
[15]
Riedel MJ, Boora P, Steckley D, de Vries G, Light PE. Kir6.2 polymorphisms sensitize β-cell ATP-sensitive potassium channels to activation by acyl CoAs: a possible cellular mechanism for increased susceptibility to type 2 diabetes? Diabetes 2003; 52(10): 2630-5.
[http://dx.doi.org/10.2337/diabetes.52.10.2630] [PMID: 14514649]
[16]
Villareal DT, Koster JC, Robertson H, et al. Kir6.2 variant E23K increases ATP-sensitive K+ channel activity and is associated with impaired insulin release and enhanced insulin sensitivity in adults with normal glucose tolerance. Diabetes 2009; 58(8): 1869-78.
[http://dx.doi.org/10.2337/db09-0025] [PMID: 19491206]
[17]
Nielsen E-MD, Hansen L, Carstensen B, et al. The E23K variant of Kir6.2 associates with impaired post-OGTT serum insulin response and increased risk of type 2 diabetes. Diabetes 2003; 52(2): 573-7.
[http://dx.doi.org/10.2337/diabetes.52.2.573] [PMID: 12540638]
[18]
Jiang Y-D, Chuang L-M, Pei D, et al. Genetic Variations in the Kir6.2 subunit (KCNJ11) of pancreatic ATP-sensitive potassium channel gene are associated with insulin response to glucose loading and early onset of type 2 diabetes in childhood and adolescence in Taiwan. Int J Endocrinol 2014; 2014983016
[http://dx.doi.org/10.1155/2014/983016] [PMID: 25309595]
[19]
Schwanstecher C, Meyer U, Schwanstecher MK. (IR)6.2 polymorphism predisposes to type 2 diabetes by inducing overactivity of pancreatic β-cell ATP-sensitive K(+) channels. Diabetes 2002; 51(3): 875-9.
[http://dx.doi.org/10.2337/diabetes.51.3.875] [PMID: 11872696]
[20]
Cheung CYY, Tso AWK, Cheung BMY, et al. The KCNJ11 E23K polymorphism and progression of glycaemia in Southern Chinese: a long-term prospective study. PLoS One 2011; 6(12)e28598
[http://dx.doi.org/10.1371/journal.pone.0028598] [PMID: 22163043]


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Article Details

VOLUME: 16
ISSUE: 2
Year: 2020
Published on: 14 February, 2020
Page: [185 - 189]
Pages: 5
DOI: 10.2174/1573401315666190423101134

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