Impact of leptin and leptin‐receptor gene polymorphisms on serum lipids in Japanese obese children

Okada, Tomoo; Ohzeki, Takehiko; Nakagawa, Yuichi; Sugihara, Shigetaka; Arisaka, Osamu

doi:10.1111/j.1651-2227.2010.01778.x

Cited by 30 publications

(33 citation statements)

References 30 publications

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“…Our results were in agreement with the finding of (Mammes et al 2001). Similarly, our finding was in accordance with that obtained by (Okada et al 2010)who found that rs1805134 CC showed a significant association with low level of triglyceride. Ser343SerSNP is a synonymous amino acid variation found in the extracellular portion of leptin receptor.…”

Section: Discussion:-supporting

confidence: 83%

Leptin receptor LYS109ARG, GLN223ARG, SER343SER polymorphisms and obesity: Linkage disequilibrium and haplotype block analysis in Jeddah city.

Linjawi¹,

Hussin²,

Alsaid³

et al. 2016

IJAR

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Section: Discussion:-supporting

confidence: 83%

Leptin receptor LYS109ARG, GLN223ARG, SER343SER polymorphisms and obesity: Linkage disequilibrium and haplotype block analysis in Jeddah city.

Linjawi¹,

Hussin²,

Alsaid³

et al. 2016

IJAR

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“…Okada and cols. (37) who studied 136 obese children between 5 and 17 years found no relationship between this polymorphism and serum lipids.…”

Section: Molecular Featuresmentioning

confidence: 99%

Lack of mutations in the leptin receptor gene in severely obese children

Dias

Fernandes

Melo³

et al. 2012

Arq Bras Endocrinol Metab

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Objective: To analyze the LEPR gene in obese children and to investigate the associations between molecular findings and anthropometric and metabolic features. Subjects and methods: Thirty-two patients were evaluated regarding anthropometric characteristics, blood pressure, heart rate, serum glucose, insulin, leptin levels, and lipid profile. The molecular study consisted of the amplification and automatic sequencing of the coding region of LEPR in order to investigate new mutations. Results: We identified a high prevalence of metabolic disorders: impaired fasting glucose in 12.5% of the patients, elevated HOMA-IR in 85.7%, low HDL-cholesterol levels in 46.9%, high triglyceride levels in 40.6%, and hypertension in 58.6% of the patients. The molecular study identified 6 already described allelic variants: rs1137100 (exon-2), rs1137101 (exon-4), rs1805134 (exon-7), rs8179183 (exon-12), rs1805096 (exon-18), and the deletion/insertion of the pentanucleotide CTTTA at 3'untranslated region. Conclusions: The frequency of alleles observed in this cohort is similar to that described in the literature, and was not correlated with any clinical feature. The molecular findings in the analysis of the LEPR did not seem to be implicated in the etiology of obesity in these patients. Arq Bras Endocrinol Metab. 2012;56(3):178-83 Keywords Obesity; childhood obesity; leptin; leptin receptor gene RESUMO Objetivo: Analisar o LEPR em crianças obesas e investigar associações entre achados moleculares e características antropométricas e metabólicas. Sujeitos e métodos: Foram avaliados 32 pacientes quanto às características antropométricas, à pressão arterial, à frequência cardíaca, às dosagens séricas de glicemia, à insulina, à leptina e ao perfil lipídico. O estudo molecular consistiu na amplificação e no sequenciamento automático da região codificadora do LEPR para pesquisar mutações. Resultados: Identificou-se uma alta prevalência de distúrbios metabóli-cos: glicemia de jejum alterada em 12,5%, HOMA-IR elevado em 85,7%, níveis de HDL-colesterol baixos em 46,9%, níveis de triglicérides elevados em 40,6% e hipertensão arterial em 58,6%. O estudo molecular identificou 6 variações alélicas já descritas na literatura: rs1137100 (éxon-2), rs1137101 (éxon-4), rs1805134 (éxon-7), rs8179183 (éxon-12), rs1805096 (éxon-18) e deleção/ inserção do pentanucleotídeo CTTTA na região 3' não traduzida. Conclusões: A frequência das variações alélicas observada é semelhante à descrita na literatura e não se correlacionou com nenhuma característica clínica. Os resultados da análise molecular do LEPR não parecem estar implicados na etiologia da obesidade desses pacientes. Arq Bras Endocrinol Metab. 2012;56(3):178-83 Descritores Obesidade; obesidade infantil; leptina; gene do receptor de leptina

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“…Leptin (from the Greek leptos = thin) is a key hormone of the physiological system that regulates body weight [3,7,9]. Synthesized and secreted by the adipose tissue, leptin functions as an afferent satiety signal for the hypothalamus [6,10], where it triggers a cascade of neuroendocrine responses that result in the inhibition of orexigenic peptides [7].…”

Section: Introductionmentioning

confidence: 99%

“…In this process, leptin, a 16-kDa and 167-amino-acid protein of the cytokinin family, is synthesized [11,15,16]. The leptin gene promoter is known to be positively regulated by many transcription factors that are important for adipocyte differentiation [3,15,16]. The polymorphism of the promoter region of the ob -2548G>A gene (rs7799039), identified in the 5′ region, is associated with leptin levels in obese and morbidly obese individuals [3,7,11].…”

Section: Introductionmentioning

confidence: 99%

“…On the one hand, governmental agencies were successful in the eradication of famine among the poorest strata of the population; on the other hand, obesity presents itself as a more frequent and more serious problem than malnutrition. Obesity is a risk factor for a series of diseases or disorders, such as arterial hypertension, cardiovascular diseases, diabetes, cancer, osteoarthritis, menstrual disorders/infertility, a reduction in high-density lipoprotein cholesterol (HDL-C), hypercholesterolemia, lipid disorders, increased insulin levels, and glucose intolerance [2,3]. …”

Section: Introductionmentioning

confidence: 99%

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LEP -2548G>A Polymorphism of the Leptin Gene and Its Influence on the Lipid Profile in Obese Individuals

et al. 2014

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Background/Aim: We studied the molecular pathogenesis of obesity, involving complex interactions between environmental and genetic factors, with a focus on the leptin gene. It was our aim to characterize the LEP -2548G>A leptin polymorphism and lipid profile in obese and normal-weight individuals. Methods: A total of 212 individuals were divided into the study group including 136 obese patients (body mass index, BMI ≥30) and the control group with 76 normal-weight individuals (BMI >18.5 and ≤24.9). DNA was amplified by polymerase chain reaction and restriction fragment length polymorphism. The lipid profile was analyzed by enzymatic colorimetric methods. The level of significance was set at p < 0.05. Results: There was a prevalence of the GA genotype in both groups. However, comparative group analysis showed an association of the recessive model (AA+GA) with increased triglycerides (TG) and decreased high-density lipoprotein cholesterol (HDL-C) levels in the study group. Conclusion: This study did not confirm an association between obesity and the LEP -2548G>A polymorphism. However, AA+GA genotypes, in the presence of obesity, seem to contribute to a reduction in HDL-C and an increase in TG compared with normal-weight individuals. This should be confirmed in further studies.

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Impact of leptin and leptin‐receptor gene polymorphisms on serum lipids in Japanese obese children

Abstract: These results suggest that LEPR gene polymorphisms may partly contribute to serum lipid profile in obese children.

Cited by 30 publications

References 30 publications

Leptin receptor LYS109ARG, GLN223ARG, SER343SER polymorphisms and obesity: Linkage disequilibrium and haplotype block analysis in Jeddah city.

Leptin receptor LYS109ARG, GLN223ARG, SER343SER polymorphisms and obesity: Linkage disequilibrium and haplotype block analysis in Jeddah city.

Lack of mutations in the leptin receptor gene in severely obese children

LEP -2548G>A Polymorphism of the Leptin Gene and Its Influence on the Lipid Profile in Obese Individuals

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