<i>LEP</i>R gene polymorphisms: associations with overweight, fat mass and response to diet in women

Mammes, Olivier; Aubert, Roberte; Betoulle, D; Péan, Franck; Herbeth, Bernard; Visvikis, Sophie; Siest, Gérard; Fumeron, Frédéric

doi:10.1046/j.1365-2362.2001.00843.x

Cited by 83 publications

(46 citation statements)

References 44 publications

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“…Previous studies illustrated that the association between Ser343Ser and obesity are controversial among different ethical populations. 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.…”

Section: Discussion:-supporting

confidence: 94%

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: 94%

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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“…21 Two other SNPs, Ser343Ser (rs790419) in exon 1 and Lys109arg (rs1137100) in exon 4 of the LEPR gene, have been associated with obesity in women in France. 22 To obtain a better understanding of the association between leptin and colon cancer, we evaluated 2 variants of the LEP gene, the more commonly studied rs7799039 as well as rs2167270 and 1 variant of the LEPR gene, rs6588147 with risk of developing colon cancer. These variants were selected because of previous reports of their reported functional importance 23 and their being in linkage disequilibrium with other common LEP markers such as rs2167270 and rs3828942.…”

mentioning

confidence: 99%

Leptin and leptin receptor genotypes and colon cancer: Gene–gene and gene–lifestyle interactions

Slattery

Wolff

Herrick

et al. 2008

Intl Journal of Cancer

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Leptin may play an important role in colorectal cancer because of its role in energy balance, insulin and inflammation. We evaluated the LEP rs2167270 (19 G > A) and rs7799039 (22548 G > A) poly-morphisms and the leptin receptor, LEPR rs6588147 (located in intron 2), polymorphism with risk of developing colon cancer in a study of 1,567 cases and 1,965 controls. We evaluated the effects of the polymorphisms with body mass index (BMI), recent use of aspirin/NSAIDs and genetic variations in genes related to insulin signaling pathways including insulin-like growth factor 1 (IGF1), insulin-like growth factor binding protein 3 (IGFBP3), and insulin related substrates 1 and 2 (IRS1, IRS2) and the vitamin D receptor (VDR). We observed a slight reduction in colon cancer risk with the AA LEP rs2167270 genotype (OR 0.79 95% CI 0.64, 0.98) and although not reaching statistical significance, with the combined GG LEP rs2167270 and GG LEPR rs6588147 (OR 0.70, 95% CI 0.49, 1.02) genotypes. BMI did not interact with any of these polymorphisms to alter colon cancer risk. However, recent aspirin/NSAID use significantly interacted with both LEP poly-morphisms. Likewise, variants of IGF1 and IRS2 interacted with the LEP rs2167270 polymorphism. VDR polymorphisms interacted with all LEP and LEPR polymorphisms. These data support an association between LEP and colon cancer. They also suggest that the mechanisms linking leptin to colon cancer may be independent of energy balance. ' 2007 Wiley-Liss, Inc. Leptin is a 16 kDa glycolprotein product of the leptin gene (LEP), which is expressed almost exclusively (>95%) by adipo-cytes. 1 Initial interest in leptin focused on its role in obesity but it is rapidly becoming evident that its physiological properties extend beyond those associated with energy homeostasis. In addition to regulation of energy balance, leptin, has been associated with reproductive factors, inflammatory response, insulin signal-ing, bone remodeling and neuroendocrine function. 2 The leptin receptor , a class I pro-inflammatory cytokine, is a member of the cytokine receptor family that includes IL-6. The leptin receptor plays a key role in how leptin functions. When leptin binds to the leptin receptor, Janus kinase (JAK2), a tyrosine kinase is activated to initiate downstream signaling of suppressors of cytokine signal-ing 1 and 3 (SOCS) and signal transducer and activator of transcription -3 (STAT). 2-4 Of particular importance for cancer is the influence of leptin on SOCS which in turn limits insulin signaling; SOCS3 has been shown to limit leptin signaling. Studies have shown that leptin also can stimulate expression of the inflamma-tory marker CRP (C-reactive protein). 5 There is growing evidence that nuclear hormone receptors regulate the action of leptin and other class I cytokines. 6 However, data also suggest that hormone receptors, such as the vitamin D receptor , might play an important role in regulating leptin; vitamin D 3 has been shown to inhibit leptin secretion in human adipose tissue. 7 Leptin has been ...

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“…Furthermore, carriers of a variant C allele in the LEPR gene [Ser (T) 343Ser (C)] have lost more weight in response to a low calorie intake than the noncarriers (26).…”

Section: Genetic Aspect Of Obesitymentioning

confidence: 99%

Obesity: genome and environment interactions

Bašić

Butorac

Jurčević

et al. 2012

Archives of Industrial Hygiene and Toxicology

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Obesity has become one of the major threats for public health in industrialised world among adults, but also among adolescents and children. It is infl uenced by the interaction of genes, nutrition, environment, and lifestyle. Environmental and lifestyle risk factors include foetal and lifelong environment, nutrient quality, chemical and microbial exposure, and psychical stress, all of which are important contributing infl uences. Removing or limiting chemical and pharmaceutical obesogens from human environment could make a difference in the growing epidemic of obesity. Additionally, nutrigenomics describes how modifi cations in individual diets can improve health and prevent chronic diseases, as well as obesity, by understanding the effects of a genetic profi le in the interaction between food and increase in body weight. Furthermore, individual genetic variations in genome represent an individual′s predisposition for obesity. Therefore, the use of individual genetic information, avoiding obesogens, and a healthy lifestyle could help to improve the management of obesity and maintain a healthy weight.

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LEPR gene polymorphisms: associations with overweight, fat mass and response to diet in women

Cited by 83 publications

References 44 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.

Leptin and leptin receptor genotypes and colon cancer: Gene–gene and gene–lifestyle interactions

Obesity: genome and environment interactions

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