Obesity has become a global epidemic and is a known risk factor for several adverse health outcomes. Single Nucleotide Polymorphism (SNP) in leptin receptor genes become interesting candidates as susceptibility genes for obesity and glucose homeostasis. The present study intended to explore the genetic analysis of LEPR gene K109, Q223R, and K656N polymorphisms and their relation to obesity and fasting plasma glucose (FPG) concentration in the Myanmar population. One hundred and fifty diagnosed obese subjects and 150 healthy non-obese controls were included. Fasting plasma glucose (FPG) was measured and LEPR gene K109R, Q223R, and K656N polymorphisms were detected by DNA analysis. Data were analyzed by chi-square and one-way ANOVA tests. Each genotype frequency distribution of LEPR gene (K109R, Q223R, and K656N) polymorphisms was not associated with obesity (p > 0.05), as well as each allele frequency distribution also similar outcome (p > 0.05). FPG levels of the study population showed no significant differences between each genotype of LEPR gene polymorphisms (p > 0.05). The K109R, Q223R, and K656N polymorphisms of the LEPR gene were not linked to obesity or FPG levels in the population of Myanmar, according to our findings. Therefore, it does not seem that these polymorphisms have an equivalently significant role for the people of Myanmar. To completely understand the unique genetic variables that predispose to obesity in humans, an ongoing study of diverse obesity phenotypes and related gene mutations is necessary as our understanding of the genes causing obesity increases as a result of new findings.
Published in | Biochemistry and Molecular Biology (Volume 7, Issue 3) |
DOI | 10.11648/j.bmb.20220703.11 |
Page(s) | 54-60 |
Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
Copyright |
Copyright © The Author(s), 2022. Published by Science Publishing Group |
Obesity, Fasting Plasma Glucose, LEPR Gene K109R SNP, LEPR Gene Q223R SNP, LEPR Gene K656N SNP
[1] | Mantzoros, C. S. (1999). The role of leptin in human obesity and disease: a review of current evidence. Annals of internal medicine, 130 (8), 671-680. |
[2] | Friedman, J. M., & Halaas, J. L. (1998). Leptin and the regulation of body weight in mammals. Nature, 395 (6704), 763-770. |
[3] | Burguera, B., Couce, M. E., Curran, G. L., Jensen, M. D., Lloyd, R. V., Cleary, M. P., & Poduslo, J. F. (2000). Obesity is associated with a decreased leptin transport across the blood-brain barrier in rats. Diabetes, 49 (7), 1219-1223. |
[4] | Odle, A. K., Haney, A., Allensworth-James, M., Akhter, N., & Childs, G. V. (2014). Adipocyte versus pituitary leptin in the regulation of pituitary hormones: somatotropes develop normally in the absence of circulating leptin. Endocrinology, 155 (11), 4316-4328. |
[5] | Ahrén, B., Larsson, H., Wilhelmsson, C., Näsman, B., & Olsson, T. (1997). Regulation of circulating leptin in humans. Endocrine, 7 (1), 1-8. |
[6] | Considine, R. V., Sinha, M. K., Heiman, M. L., Kriauciunas, A., Stephens, T. W., Nyce, M. R.,... & Caro, J. F. (1996). Serum immunoreactive-leptin concentrations in normal-weight and obese humans. New England Journal of Medicine, 334 (5), 292-295. |
[7] | Cirillo, D., Rachiglio, A. M., La Montagna, R., Giordano, A., & Normanno, N. (2008). Leptin signaling in breast cancer: an overview. Journal of cellular biochemistry, 105 (4), 956-964. |
[8] | Lee, S., Lee, A., Kweon, O. K., & Kim, W. H. (2016). Presence and distribution of leptin receptor in the canine gallbladder. |
[9] | Bruce Thompson, D., Ravussin, E., Bennett, P. H., & Bogardus, C. (1997). Structure and sequence variation at the human leptin receptor gene in lean and obese Pima Indians. Human molecular genetics, 6 (5), 675-679. |
[10] | Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L., & Friedman, J. M. (1994). Positional cloning of the mouse obese gene and its human homologue. Nature, 372 (6505), 425-432. |
[11] | Chen, H., Charlat, O., Tartaglia, L. A., Woolf, E. A., Weng, X., Ellis, S. J.,... & Morgenstern, J. P. (1996). Evidence that the diabetes gene encodes the leptin receptor: identification of a mutation in the leptin receptor gene in db/db mice. Cell, 84 (3), 491-495. |
[12] | Clement, K., Vaisse, C., Lahlou, N., Cabrol, S., Pelloux, V., Cassuto, D.,... & Guy-Grand, B. (1998). A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction. Nature, 392 (6674), 398-401. |
[13] | Montague, C. T., Farooqi, I. S., Whitehead, J. P., Soos, M. A., Rau, H., Wareham, N. J.,... & O'Rahilly, S. (1997). Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature, 387 (6636), 903-908. |
[14] | Oksanen, L., Kaprio, J., Mustajoki, P., & Kontula, K. (1998). A common pentanucleotide polymorphism of the 3′-untranslated part of the leptin receptor gene generates a putative stem-loop motif in the mRNA and is associated with serum insulin levels in obese individuals. International journal of obesity, 22 (7), 634-640. |
[15] | D’souza, A. M., Neumann, U. H., Glavas, M. M., & Kieffer, T. J. (2017). The glucoregulatory actions of leptin. Molecular Metabolism, 6 (9), 1052–1065. |
[16] | Bains, V., Kaur, H., & Badaruddoza, B. (2020). Association analysis of polymorphisms in LEP (rs7799039 and rs2167270) and LEPR (rs1137101) gene towards the development of type 2 diabetes in North Indian Punjabi population. Gene, 754, 144846. |
[17] | Gotoda, T., Manning, B. S., Goldstone, A. P., Imrie, H., Evans, A. L., Strosberg, A. D.,... & Aitman, T. J. (1997). Leptin receptor gene variation and obesity: lack of association in a white British male population. Human molecular genetics, 6 (6), 869-876. |
[18] | Matsuoka, N., Ogawa, Y., Hosoda, K., Matsuda, J., Masuzaki, H., Miyawaki, T.,... & Nakao, K. (1997). Human leptin receptor gene in obese Japanese subjects: evidence against either obesity-causing mutations or association of sequence variants with obesity. Diabetologia, 40 (10), 1204-1210. |
[19] | Oliveira, R. D., Cerda, A., Genvigir, F. D. V., Sampaio, M. F., Armaganijan, D., Bernik, M. M. S.,... & Hirata, R. D. C. (2013). Leptin receptor gene polymorphisms are associated with adiposity and metabolic alterations in Brazilian individuals. Arquivos Brasileiros de endocrinologia & metabologia, 57, 677-684. |
[20] | Masuo, K., Straznicky, N. E., Lambert, G. W., Katsuya, T., Sugimoto, K., Rakugi, H.,... & Esler, M. D. (2008). Leptin-receptor polymorphisms relate to obesity through blunted leptin-mediated sympathetic nerve activation in a Caucasian male population. Hypertension Research, 31 (6), 1093-1100. |
[21] | Fan, S. H., & Say, Y. H. (2014). Leptin and leptin receptor gene polymorphisms and their association with plasma leptin levels and obesity in a multi-ethnic Malaysian suburban population. Journal of physiological anthropology, 33 (1), 1-10. |
[22] | Murugesan, D., Arunachalam, T., Ramamurthy, V., & Subramanian, S. (2010). Association of polymorphisms in leptin receptor gene with obesity and type 2 diabetes in the local population of Coimbatore. Indian journal of human genetics, 16 (2), 72. |
[23] | Pyrzak, B., Wisniewska, A., Kucharska, A., Wasik, M., & Demkow, U. (2009). No association of LEPR Gln223Arg polymorphism with leptin, obesity or metabolic disturbances in children. European journal of medical research, 14 (4), 1-4. |
[24] | R. C. Weisell. (2002). Body mass index as an indicator of obesity, Asia Pac. J. Clin. Nutr., vol. 11, pp. S681–S684. |
[25] | Kim, J. Y., Lee, H. B., Lim, S. H., Lee, B. W., Baik, H. H., Kim, Y. O.,... & Chung, J. H. (2011). Association between polymorphisms of leptin receptor and hypercholesterolemia, hypertension, and obesity in Korean population. Stress, 19 (2), 155-163. |
[26] | Mărginean, C. O., Mărginean, C., Voidăzan, S., Meliţ, L., Crauciuc, A., Duicu, C., & Bănescu, C. (2016). Correlations between leptin gene polymorphisms 223 A/G, 1019 G/A, 492 G/C, 976 C/A, and anthropometrical and biochemical parameters in children with obesity: a prospective case-control study in a Romanian population—the nutrichild study. Medicine, 95 (12). |
[27] | Lakka, T. A., Rankinen, T., Weisnagel, S. J., Chagnon, Y. C., Lakka, H. M., Ukkola, O.,... & Bouchard, C. (2004). Leptin and leptin receptor gene polymorphisms and changes in glucose homeostasis in response to regular exercise in nondiabetic individuals: the HERITAGE family study. Diabetes, 53 (6), 1603-1608. |
[28] | Yang, Y., & Niu, T. (2018). A meta-analysis of associations of LEPR Q223R and K109R polymorphisms with Type 2 diabetes risk. PloS one, 13 (1), e0189366. |
[29] | Chung, W. K., Power-Kehoe, L., Chua, M., Chu, F., Aronne, L., Huma, Z.,... & Leibel, R. L. (1997). Exonic and intronic sequence variation in the human leptin receptor gene (LEPR). |
APA Style
Mo Mo Than, Yan Naing Soe, Zaw Myo Lwin, Ye Wint Kyaw, Kyaw Thet Paing, et al. (2022). Association of Leptin Receptor Gene Polymorphisms with Blood Glucose Concentration and Obesity. Biochemistry and Molecular Biology, 7(3), 54-60. https://doi.org/10.11648/j.bmb.20220703.11
ACS Style
Mo Mo Than; Yan Naing Soe; Zaw Myo Lwin; Ye Wint Kyaw; Kyaw Thet Paing, et al. Association of Leptin Receptor Gene Polymorphisms with Blood Glucose Concentration and Obesity. Biochem. Mol. Biol. 2022, 7(3), 54-60. doi: 10.11648/j.bmb.20220703.11
@article{10.11648/j.bmb.20220703.11, author = {Mo Mo Than and Yan Naing Soe and Zaw Myo Lwin and Ye Wint Kyaw and Kyaw Thet Paing and Khine Kyaw Oo and Phyo Thaw Htun and Aung Lin Oo and Min Thein and Ye Myat Kyaw and Zaw Min Htut}, title = {Association of Leptin Receptor Gene Polymorphisms with Blood Glucose Concentration and Obesity}, journal = {Biochemistry and Molecular Biology}, volume = {7}, number = {3}, pages = {54-60}, doi = {10.11648/j.bmb.20220703.11}, url = {https://doi.org/10.11648/j.bmb.20220703.11}, eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.bmb.20220703.11}, abstract = {Obesity has become a global epidemic and is a known risk factor for several adverse health outcomes. Single Nucleotide Polymorphism (SNP) in leptin receptor genes become interesting candidates as susceptibility genes for obesity and glucose homeostasis. The present study intended to explore the genetic analysis of LEPR gene K109, Q223R, and K656N polymorphisms and their relation to obesity and fasting plasma glucose (FPG) concentration in the Myanmar population. One hundred and fifty diagnosed obese subjects and 150 healthy non-obese controls were included. Fasting plasma glucose (FPG) was measured and LEPR gene K109R, Q223R, and K656N polymorphisms were detected by DNA analysis. Data were analyzed by chi-square and one-way ANOVA tests. Each genotype frequency distribution of LEPR gene (K109R, Q223R, and K656N) polymorphisms was not associated with obesity (p > 0.05), as well as each allele frequency distribution also similar outcome (p > 0.05). FPG levels of the study population showed no significant differences between each genotype of LEPR gene polymorphisms (p > 0.05). The K109R, Q223R, and K656N polymorphisms of the LEPR gene were not linked to obesity or FPG levels in the population of Myanmar, according to our findings. Therefore, it does not seem that these polymorphisms have an equivalently significant role for the people of Myanmar. To completely understand the unique genetic variables that predispose to obesity in humans, an ongoing study of diverse obesity phenotypes and related gene mutations is necessary as our understanding of the genes causing obesity increases as a result of new findings.}, year = {2022} }
TY - JOUR T1 - Association of Leptin Receptor Gene Polymorphisms with Blood Glucose Concentration and Obesity AU - Mo Mo Than AU - Yan Naing Soe AU - Zaw Myo Lwin AU - Ye Wint Kyaw AU - Kyaw Thet Paing AU - Khine Kyaw Oo AU - Phyo Thaw Htun AU - Aung Lin Oo AU - Min Thein AU - Ye Myat Kyaw AU - Zaw Min Htut Y1 - 2022/07/18 PY - 2022 N1 - https://doi.org/10.11648/j.bmb.20220703.11 DO - 10.11648/j.bmb.20220703.11 T2 - Biochemistry and Molecular Biology JF - Biochemistry and Molecular Biology JO - Biochemistry and Molecular Biology SP - 54 EP - 60 PB - Science Publishing Group SN - 2575-5048 UR - https://doi.org/10.11648/j.bmb.20220703.11 AB - Obesity has become a global epidemic and is a known risk factor for several adverse health outcomes. Single Nucleotide Polymorphism (SNP) in leptin receptor genes become interesting candidates as susceptibility genes for obesity and glucose homeostasis. The present study intended to explore the genetic analysis of LEPR gene K109, Q223R, and K656N polymorphisms and their relation to obesity and fasting plasma glucose (FPG) concentration in the Myanmar population. One hundred and fifty diagnosed obese subjects and 150 healthy non-obese controls were included. Fasting plasma glucose (FPG) was measured and LEPR gene K109R, Q223R, and K656N polymorphisms were detected by DNA analysis. Data were analyzed by chi-square and one-way ANOVA tests. Each genotype frequency distribution of LEPR gene (K109R, Q223R, and K656N) polymorphisms was not associated with obesity (p > 0.05), as well as each allele frequency distribution also similar outcome (p > 0.05). FPG levels of the study population showed no significant differences between each genotype of LEPR gene polymorphisms (p > 0.05). The K109R, Q223R, and K656N polymorphisms of the LEPR gene were not linked to obesity or FPG levels in the population of Myanmar, according to our findings. Therefore, it does not seem that these polymorphisms have an equivalently significant role for the people of Myanmar. To completely understand the unique genetic variables that predispose to obesity in humans, an ongoing study of diverse obesity phenotypes and related gene mutations is necessary as our understanding of the genes causing obesity increases as a result of new findings. VL - 7 IS - 3 ER -