Functional Polymorphism in the Neuropeptide Y Gene Promoter (rs16147) Is Associated with Serum Leptin Levels and Waist-Hip Ratio in Women

Mutschler, Jochen; Abbruzzese, Elvira; Wiedemann, Klaus; Goltz, Christoph von der; Dinter, Christina; Mobascher, Arian; Thiele, Holger; Díaz-Lacava, Amalia; Dahmen, Norbert; Gallinat, Jürgen; Majić, Tomislav; Petrovsky, Nadine; Thuerauf, Norbert; Kornhuber, Johannes; Gründer, Gerhard; Rademacher, Lena; Brinkmeyer, Jürgen; Wienker, Thomas F.; Wagner, Michael; Winterer, Georg; Kiefer, Falk

doi:10.1159/000346799

Cited by 18 publications

(17 citation statements)

References 88 publications

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“…Human and animal studies suggest that adiposity-induced leptin increase and subsequent leptin resistance would affect these transmitters, causing or worsening asthma symptoms. This relates both to orexigenic neuropeptides such as neuropeptide Y (114)(115)(116)(117)(118)(119)(120) , endocannabinoids (121,122) , endogenous opioids (123)(124)(125)(126) ; and anorexigenic neuropeptides such as tachykinins and its most studied members substance P (127)(128)(129)(130)(131)(132) , α-melanocyte-stimulating hormone (133)(134)(135) , corticotropin-releasing factor (136)(137)(138)(139)(140)(141) and serotonin (142)(143)(144)(145)(146)(147)(148)(149)(150) . Altogether, it suggests that these peptides can modulate asthmatic inflammation among obese patients.…”

Section: Possible Linksmentioning

confidence: 99%

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

2016

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Obesity is a risk factor for asthma, and obese asthmatics have lower disease control and increased symptom severity. Several putative links have been proposed, including genetics, mechanical restriction of the chest and the intake of corticosteroids. The most consistent evidence, however, comes from studies of cytokines produced by the adipose tissue called adipokines. Adipokine imbalance is associated with both proinflammatory status and asthma. Although reverse causation has been proposed, it is now acknowledged that obesity precedes asthma symptoms. Nevertheless, prenatal origins of both conditions complicate the search for causality. There is a confirmed role of neuro-immune cross-talk mediating obesityinduced asthma, with leptin playing a key role in these processes. Obesity-induced asthma is now considered a distinct asthma phenotype. In fact, it is one of the most important determinants of asthma phenotypes. Two main subphenotypes have been distinguished. The first phenotype, which affects adult women, is characterised by later onset and is more likely to be non-atopic. The childhood obesity-induced asthma phenotype is characterised by primary and predominantly atopic asthma. In obesity-induced asthma, the immune responses are shifted towards T helper (Th) 1 polarisation rather than the typical atopic Th2 immunological profile. Moreover, obese asthmatics might respond differently to environmental triggers. The high cost of treatment of obesity-related asthma, and the burden it causes for the patients and their families call for urgent intervention. Phenotype-specific approaches seem to be crucial for the success of prevention and treatment.

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Section: Possible Linksmentioning

confidence: 99%

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

2016

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“…Olza et al [21] found similar results concerning rs16147 in a pediatric population. Moreover, no significant associations were reported by other authors in adult populations [19,22]. …”

Section: Discussionmentioning

confidence: 67%

“…Mutschler et al [19] have shown that the rs16147 SNP is significantly associated with waist-to-hip ratio and serum leptin levels only in females. These results demonstrate that the NPY gene also accounts for the body fat mass distribution measured as waist-to-hip ratio, and they also reveal a gene-by-sex interaction.…”

Section: Discussionmentioning

confidence: 99%

“…These results demonstrate that the NPY gene also accounts for the body fat mass distribution measured as waist-to-hip ratio, and they also reveal a gene-by-sex interaction. Mutschler et al [19] reported an interaction of this SNP with leptin levels in females, too. Our study reported this relationship in males, as an increased leptin level was observed in males with the GG genotype.…”

Section: Discussionmentioning

confidence: 99%

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Association of Neuropeptide Y Gene rs16147 Polymorphism with Cardiovascular Risk Factors, Adipokines, and Metabolic Syndrome in Patients with Obesity

Luis

Izaola²,

Fuente³

et al. 2016

Lifestyle Genomics

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Background and Aims: The NPY gene has 4 exons, and it is located at 7p15.1. The main genetic variant described in this gene is rs16147. The aim of this study was to investigate the relationship of NPY rs16147 with body weight, insulin resistance, serum adipokine levels, and risk of metabolic syndrome (MetS). Methods: A population of 1,005 obese patients was analyzed in a cross-sectional survey. Weight, fat mass, waist circumference, blood pressure, basal glucose, C-reactive protein, insulin, insulin resistance (homeostasis model assessment of insulin resistance [HOMA-IR]), lipid profile, and adipocytokine (leptin, adiponectin, and resistin) levels were measured. The genotype of the NPY gene polymorphism (rs16147) was studied. Results: Body mass index (1.0 ± 0.1; p < 0.05), weight (2.8 ± 0.4 kg; p < 0.05), fat mass (1.8 ± 0.3 kg; p < 0.05), waist circumference (1.9 ± 0.2 cm; p < 0.05), leptin level (15.4 ± 8.2 ng/mL; p < 0.05), insulin level (5.1 ± 1.3 mIU/L; p < 0.05), and HOMA-IR (1.4 ± 0.1 units; p < 0.05) were lower in A allele carriers than in non-A allele carriers in males. Males with an A allele had a lower percentage of MetS (54.8 vs. 69.1%; p < 0.05), central obesity (94.5 vs. 100%; p < 0.05), and hyperglycemia (24.7 vs. 33.8%; p < 0.05) than non-A allele carriers. Logistic regression analysis indicated that male non-A allele carriers had an increased risk of MetS (odds ratio [OR] = 1.26, 95% confidence interval [CI] = 1.17-1.83; p = 0.034), an increased risk of central obesity (OR = 1.08, 95% CI = 1.02-1.11; p = 0.044), and an increased risk of hyperglycemia (OR = 1.20, 95% CI = 1.09-1.79; p = 0.028) after adjusting for age. Conclusions: In obese males, the rs164147 polymorphism of the NPY gene is associated with leptin, insulin level, HOMA-IR, and an increased risk of MetS and its related phenotypes, such as central obesity and hyperglycemia.

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“…Moreover, studies in adults are scarce. For example, Mutschler et al [30] showed that this genetic variant of the NPY gene is significantly associated with the waist-to-hip ratio. However, a lack of association was reported in another adult sample [31].…”

Section: Discussionmentioning

confidence: 99%

Polymorphism rs16147 of the Neuropeptide Y Gene Modifies the Response of Cardiovascular Risk Biomarkers and Adipokines to Two Hypocaloric Diets

Luis

Izaola²,

Primo³

et al. 2017

Lifestyle Genomics

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Aims: Our aim was to evaluate the relationship of weight loss and changes in adipokine levels after two hypocaloric diets in obese subjects with polymorphism rs16147 of the neuropeptide Y gene. Subjects and Methods: A population of 283 obese patients was analyzed. At the basal visit, patients were randomly allocated to one of two diets for a period of 3 months (diet I, low in carbohydrates; diet II, low in fat). Results: With diet I and in both genotype groups (major versus minor allele), body mass index (BMI), weight, fat mass, waist circumference, and leptin decreased. With diet II and in all genotypes, BMI, weight, fat mass, waist circumference, and leptin decreased. With both diets and in subjects with the minor allele, insulin levels (diet I: major allele -1.7 ± 7.8 IU/L versus minor allele -4.2 ± 6.1 IU/L, p = 0.01; diet II: major allele -2.3 ± 6.1 IU/L versus minor allele -4.0 ± 5.2 IU/L, p = 0.02) and insulin resistance (diet I: major allele -0.2 ± 3.1 units versus minor allele -1.7 ± 3.0 units, p = 0.03; diet II: major allele -0.9 ± 2.0 units versus minor allele -1.7 ± 1.3 units, p = 0.01) decreased. Conclusion: The rs16147 genotype affected the reduction in insulin resistance and insulin levels in response to two different hypocaloric diets in obese subjects, with a lack of response in subjects with the major allele.

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Functional Polymorphism in the Neuropeptide Y Gene Promoter (rs16147) Is Associated with Serum Leptin Levels and Waist-Hip Ratio in Women

Cited by 18 publications

References 88 publications

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

Association of Neuropeptide Y Gene rs16147 Polymorphism with Cardiovascular Risk Factors, Adipokines, and Metabolic Syndrome in Patients with Obesity

Polymorphism <b><i>rs16147</i></b> of the <b><i>Neuropeptide Y</i></b> Gene Modifies the Response of Cardiovascular Risk Biomarkers and Adipokines to Two Hypocaloric Diets

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