不同体重状况青少年瘦素基因片段的测序

Q4 Immunology and Microbiology Acta Biomedica Scientifica Pub Date : 2023-10-03 DOI:10.29413/abs.2023-8.4.10
T. A. Bairova, O. A. Ershova, A. Yu. Sambyalova, E. V. Belyaeva, V. V. Sinkov, L. V. Rychkova
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引用次数: 0

摘要

背景。肥胖是世界人口中一个重要的社会问题。瘦素基因(LEP)目前被认为是影响与超重和肥胖易感性相关的代谢疾病的潜在候选基因。瘦素通过影响食物摄入和能量消耗,维持恒定的能量储存,在体重稳态中发挥重要作用。瘦素基因的缺陷可能是导致肥胖的原因之一,并因此导致各种与肥胖相关的病理。研究的目的。目的探讨不同体重青少年瘦素基因的单核苷酸多态性(SNP)。方法。该研究涉及20名11-17岁的青少年,他们的体重正常,超重/肥胖。研究方法:用人体测量法评价临床状况;Sanger测序定位于该基因内含子的瘦素基因片段- (5 ' - agccttgttcatcatctgga, 3 ' - tgggaggaatcgctctcaga)。我们还对测序结果进行了生物信息学处理。结果。研究结果为上述LEP基因引物对(s16_L891, s16_R891)选择了891 bps瘦素基因区域的最佳扩增条件。根据测序结果,鉴定出45个LEP基因的单核苷酸取代,其中23个单核苷酸取代先前未在GenBank中登记。在超重和肥胖的青少年群体中,在GenBank数据库中发现了14个未注册的LEP基因单核苷酸替换和13个注册的snp。在体重正常的青少年组中,没有发现这些snp。
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Sequencing of a fragment of the leptin gene in adolescents with different weight status
Background . Obesity is a significant social problem among the population of the world. The leptin gene (LEP) is currently considered as a potential candidate gene influencing metabolic disorders associated with predisposition to overweight and obesity. Leptin plays an important role in body weight homeostasis by influencing food intake and energy expenditure and maintaining constant energy stores. A defect in the leptin gene may be one of the causes of obesity and, as a result, of various obesity-associated pathologies. The aim of the study . To search for single-nucleotide polymorphisms (SNP) of the leptin gene in adolescents with different weight status. Methods . The study involved 20 adolescents aged 11–17 years with normal body weight and overweight/obesity. Research methods: assessment of clinical status with anthropometry; Sanger sequencing of the leptin gene fragment localized in the intron of this gene – (5’-AGCCTTGTTTTCATCATCTGGA, 3’-TGGGAGGAATCGCTCTCAGA). We also carried out bioinformatic processing of sequencing results. Results . As a result of the study, the optimal conditions for amplification of the 891 bps leptin gene region were selected for the above mentioned primer pair of the LEP gene (s16_L891, s16_R891). Based on the results of sequencing, 45 single nucleotide substitutions of the LEP gene were identified, including 23 single nucleotide substitutions which were not previously registered in GenBank. In the group of adolescents with overweight and obesity, 14 unregistered single nucleotide substitutions of the LEP gene and 13 registered SNPs were identified in the GenBank database. In the group of adolescents with normal body weight, these SNPs were not found.
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来源期刊
Acta Biomedica Scientifica
Acta Biomedica Scientifica Immunology and Microbiology-General Immunology and Microbiology
CiteScore
0.40
自引率
0.00%
发文量
106
审稿时长
7 weeks
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