Leptin Receptor Lys656Asn Polymorphism Is Associated with Decreased Leptin Response and Weight Loss Secondary to a Lifestyle Modification in Obese Patients

Luis, Daniel Antonio de; Fuente, Rocío Aller de la; Sagrado, M. González; Izaola, Olatz; Conde-Vicente, Rosa

doi:10.1016/j.arcmed.2006.03.009

Cited by 43 publications

(26 citation statements)

References 21 publications

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“…One of them is the SNP on codon 656, this change produce a modification in electric charge with a possibility to be functional. Patients with rs8179183 variant of LEPR gene have a different metabolic response than wild type after weight loss secondary to different diets [5][6][7]. In these previous studies, only leptin levels had a significant decrease in wild group.…”

Section: Introductionmentioning

confidence: 88%

“…Rossum et al [15] did not show relation between Lys656Asn SNP and weight regain in a cohort in The Netherlands. Other study [5] demonstrated the different changes in weight loss and leptin response secondary to a hypocaloric diet with a 25% of calories from fats and with <20% of monounsaturated fats in relation with Lys656Asn SNP. In other design of our group, the weight loss secondary to a high polyunsaturated fatty acid (PUFA) diet produced, in carriers of ASn656 allele, a different change than nonAsn allele carriers, with a lack of improvement in insulin, leptin levels, and HOMA-IR.…”

Section: Discussionmentioning

confidence: 99%

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Effects of a High Protein/Low Carbohydrate Versus a Standard Hypocaloric Diet on Weight and Cardiovascular Risk Factors, Role of a Lys656asn Polymorphism of Leptin Receptor Gene

Luis¹,

Aller²,

Izaola³

et al. 2016

J Metabolic Synd

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Section: Introductionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Effects of a High Protein/Low Carbohydrate Versus a Standard Hypocaloric Diet on Weight and Cardiovascular Risk Factors, Role of a Lys656asn Polymorphism of Leptin Receptor Gene

Luis¹,

Aller²,

Izaola³

et al. 2016

J Metabolic Synd

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“…However, the treatment response was different. It should be remembered that the polymorphism analysed is not associated with changes in leptin levels but rather causes leptin resistance [14]. Atorvastatin may modify this situation and the increase in BMD may be related to an anabolic action of leptin.…”

Section: Discussionmentioning

confidence: 99%

Atorvastatin and BMD in Coronary Syndrome. Role of Lys656Asn Polymorphism of Leptin Receptor Gene

et al. 2009

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Abstract. Objectives. To evaluate the effect of atorvastatin on bone mass and markers of bone remodeling in patients with acute coronary syndrome according to the Lys656Asn leptin receptor gene polymorphism. Methods. Sixty-two patients with acute coronary syndrome were included. Patients were allocated to low and high doses of atorvastatin according to baseline levels of cholesterol and triglycerides and the index of vascular risk and were studied at hospital admission and at 12 months. Cholesterol, triglycerides, total calcium, phosphorus, magnesium, osteocalcin and urinary deoxypyridinoline were determined in all patients at baseline and at 12 months of follow up. Densitometric studies were conducted in the lumbar spine and hip. Patients with a T-score<-2.5 were considered osteoporotic. The Lys656Asn leptin receptor gene polymorphism was determined by PCR. Results. Forty-two patients were Lys/Lys homozygotic and 20 Lys/Asn heterozygotic. The prevalence of osteoporosis was 31% for the Lys/Lys genotype and 27% for the Lys/Asn genotype with no significant differences between groups. There was a significant increase in bone mineral density in the lumbar spine (1.117 ± 0.24 versus 1.135 ± 0.24, P = 0.008) in patients with the Lys/Lys genotype. Conclusion. Atorvastatin increases lumbar spine bone mineral density only in patients with the Lys/Lys genotype of the Lys656Asn polymorphism. . Inflammatory cytokines play an important role in the imbalance between bone formation and resorption that leads to the reduced bone mass seen in osteoporosis [3]. In addition, drugs such as statins are effective in both diseases, diminishing vascular events in patients with atherosclerosis and increasing bone mass in those with high levels of cholesterol [4]. Human leptin is a protein of 167 amino acids manufactured in fat cells which is involved in regulating the ingestion and consumption of energy. It intervenes in the regulation of bone mass by means of a central hypothalamic mechanism, exerting a double antagonistic effect on bone formation and resorption through activation of the sympathetic nervous system and the Cocaine Amphetamine Regulated Transcript (CART) [5]. In addition, studies have shown that hyperleptinemia can exert atherogenic effects [6]. In North American patients, elevated leptin levels have been associated with an increased risk of myocardial infarction in both males (3.16, 95% CI 1.40-7.37) and females (3.95, 95% CI 1.29-12.72) [7].Leptin exerts its biological effect by bonding with a receptor from the cytokine-receptor family. The leptin

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“…In a study of the Lys656Asn variant within LEPR, homozygotes for the Lys656 allele had a considerable loss of body weight, fat mass, waist circumference, and a decrease in body mass index (BMI), systolic blood pressure, and leptin levels, compared to the carriers of the Asn656 allele (27). Some studies have investigated the effect of a polymorphism in the peroxisome proliferator-activated receptor γ (PPARγ) gene, Pro12Ala.…”

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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Leptin Receptor Lys656Asn Polymorphism Is Associated with Decreased Leptin Response and Weight Loss Secondary to a Lifestyle Modification in Obese Patients

Cited by 43 publications

References 21 publications

Effects of a High Protein/Low Carbohydrate Versus a Standard Hypocaloric Diet on Weight and Cardiovascular Risk Factors, Role of a Lys656asn Polymorphism of Leptin Receptor Gene

Effects of a High Protein/Low Carbohydrate Versus a Standard Hypocaloric Diet on Weight and Cardiovascular Risk Factors, Role of a Lys656asn Polymorphism of Leptin Receptor Gene

Atorvastatin and BMD in Coronary Syndrome. Role of Lys656Asn Polymorphism of Leptin Receptor Gene

Obesity: genome and environment interactions

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