Effect of Trp64Arg mutation of the β3‐adrenergic receptor gene and C161T substitution of the peroxisome proliferator activated receptor γ gene on obesity in Japanese children

Arashiro, Rina; Katsuren, Keisuke; Fukuyama, Shigeru; Ohta, Takao

doi:10.1046/j.1442-200x.2003.01685.x

Cited by 27 publications

(31 citation statements)

References 45 publications

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“…In humans, the beta-3 adrenergic receptor is predominantly expressed in visceral adipose tissue (Krief et al, 1993). Notably, the Arg allele of this SNP has been linked with increased BMI, adiposity and obesity in children (Arashiro et al, 2003;Endo et al, 2000;Erhardt et al, 2005;Ochoa et al, 2004;Park et al, 2005) supporting the evidence in adults Pierola et al, 2007), and the increased risk for obesity at this ADRB3 loci may be driven partly by an interaction effect of the PPARG SNP Pro12Ala Hsueh et al, 2001;Ochoa et al, 2004). Other studies in young children between the ages 4-10 years and in adolescents report no signifi cant effects of Trp64Arg variants on BMI, weight or height when this variant is examined in isolation (Cecil et al, 2007;Haworth et al, 2008a;Hinney et al, 1997;Kurokawa et al, 2003).…”

Section: Adrenergic Receptor Gene Variants -A Role In Polygenic Obesimentioning

confidence: 99%

Obesity and eating behaviour in children and adolescents: Contribution of common gene polymorphisms

Cecil

Dalton

Finlayson

et al. 2012

International Review of Psychiatry

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The prevalence of childhood obesity is increasing in many countries and confers risks for early type 2 diabetes, cardiovascular disease and metabolic syndrome. In the presence of potent ' obesogenic ' environments not all children become obese, indicating the presence of susceptibility and resistance. Taking an energy balance approach, susceptibility could be mediated through a failure of appetite regulation leading to increased energy intake or via diminished energy expenditure. Evidence shows that heritability estimates for BMI and body fat are paralleled by similar coeffi cients for energy intake and preferences for dietary fat. Twin studies implicate weak satiety and enhanced food responsiveness as factors determining an increase in BMI. Single gene mutations, for example in the leptin receptor gene, that lead to extreme obesity appear to operate through appetite regulating mechanisms and the phenotypic response involves overconsumption and a failure to inhibit eating. Investigations of robustly characterized common gene variants of fat mass and obesity associated ( FTO ), peroxisome proliferator-activated receptor ( PPARG ) and melanocortin 4 receptor ( MC4R ) which contribute to variance in BMI also infl uence the variance in appetite factors such as measured energy intake, satiety responsiveness and the intake of palatable energy-dense food. A review of the evidence suggests that susceptibility to childhood obesity involving specifi c allelic variants of certain genes is mediated primarily through food consumption (appetite regulation) rather than through a decrease in activity-related energy expenditure. This conclusion has implications for early detection of susceptibility, and for prevention and management of childhood obesity.

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Section: Adrenergic Receptor Gene Variants -A Role In Polygenic Obesimentioning

confidence: 99%

Obesity and eating behaviour in children and adolescents: Contribution of common gene polymorphisms

Cecil

Dalton

Finlayson

et al. 2012

International Review of Psychiatry

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“…Japon çocuk-larda yapılan bir araştırmada da PPARG C161T varyasyonunun lipid metabolizması, leptin düzey-leri ve obezite ile ilişkili olduğu görülmüş ancak bu çocuklarda PPARG P12A varyantına rastlanmamıştır. 12 Bir başka çalışmada ise, KVH'si olan ve olmayan tip 2 diyabetiklerde PPARG P12A ve C161T varyasyonlarının yüksek BKİ değerleriyle ilişkili olmalarına rağmen KVH gelişimi üzerine etkilerinin olmadığı gözlenmiştir. 19 Buna karşılık, PPARG P12A ve C161T varyasyonları nefropatik diyabet hastalarındaki kardiyovasküler olaylar için belirteç olarak önerilmiş ve PPARG P12A minör Ala alleli ve C161T minör T alleli de kardiyovasküler risk artışından sorumlu olarak bildirilmiştir.…”

Section: Discussionunclassified

“…43 Bu örneklerde görüldüğü üzere, PPAR gen varyasyonlarının HDL-K ve LDL-K düzeylerine olan etkisi lipid metabolizmasıyla ilişkili metabolik ve kardiyovasküler sistem hastalıklarında pek çok toplumda çalışılmıştır. 12,19,[41][42][43] Buna karşılık, lipoprotein alt fraksiyonları üzerine etkisini araştı-ran sınırlı sayıda çalışma bulunmaktadır.…”

Section: Discussionunclassified

“…10 PPAR'ların dokulardaki dağılımı farklı olup tüm vücuttaki lipid ve glukoz metabolizması üzerinde birbirinden farklı, ancak zaman zaman örtüşen görevler üstlenen alfa, beta/delta ve gama olarak adlandırılmış üç izoformu bulunmaktadır. 10,12,13 PPAR ailesi, uzun zincirli yağ asitlerinden ökozonoidlere çeşitli endojen ligandlarla aktive edilebilmektedir. Bu özellikleri nedeniyle dislipidemi, diyabet, obezite, adiposit farklılaşması, inflamasyon ve kanser gibi çok sayıda hastalığın tedavisine yönelik terapötik amaçlı sentetik PPAR ligandları üretilmiştir.…”

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Study on the Effects of PPARG and PPAR-B/D Gene Variations on Serum LDL Subfractions in Patients with Coronary Heart Disease

Kanca¹,

Tokat²,

Buğra³

et al. 2017

Turkiye Klinikleri J Med Sci

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The allelic and genotypic frequencies of the PPARG P12A (rs1801282) and PPARD +294T/C (rs52016520) variations were not different between the study groups (p>0.05), while PPARG C161T (rs3856806) CC genotype frequency was higher in the CHD patient group (p=0.029). The Serum LDL subfractions were observed to be only affected by the PPARG P12A variation. While PPARG P12A heterozygous ProAla genotype was associated with increased large-buoyant LDL subfractions (p=0.024), homozygous ProPro genotype was associated with high HDL cholesterol levels (p=0.033) in the control group. The PPARG Pro12Ala normal ProPro genotype was associated with increased triacylglycerol and LDL cholesterol levels (p=0.031 and p=0.010, respectively) and PPAR-B/D +294T/C minor C allele was associated with high LDL cholesterol levels (p=0.038) in the CHD group. There was no effect of the PPARG P12A variation on the lipoprotein subfractions in the CHD group. C Co on nc cl lu u--s si io on n: : We observed that the PPARG Pro12Ala normal ProPro genotype and PPAR-B/D +294T/C minor C allele show a detrimental effect on serum LDL-K levels, while they are not effective on the distribution of LDL subfractions in the CHD patients. However, it was observed that the PPARG ProAla genotype contribute the antiatherogenic large-buoyant LDL subfraction in normolipidemic subjects. As a result, it is possible that the effects of genetic variations of the PPARs on lipid and LDL subfractions may have been affected by cardiometabolic circumstances.K Ke ey yw wo or rd ds s:

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“…In the coding region of this AR subtype a common missense mutation resulting in the substitution of arginine for tryptophan at codon 64 (Trp64Arg) has been reported to be significantly associated with whole body obesity, visceral fat accumulation and other metabolic syndrome components or their cluster [54][55][56][57]. Unfortunately, as previously observed in adults' studies, the association between Trp64Arg and BP levels in obese children was found significant in some studies [54,58] and not significant in others [51,53].…”

Section: α-And β-Adrenergic Receptors (Adra and Adrb) Genesmentioning

confidence: 95%

Searching for genes involved in hypertension development in special populations: children and pre-eclamptic women. Where are we standing now?

Danese¹,

Montagnana²,

Fava³

2013

Clinical Chemistry and Laboratory Medicine (CCLM)

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Primary hypertension is a very common disorder particularly in the aging population but hypertensive disorders can appear earlier in life, especially when obesity and unhealthy lifestyle are present. Also pregnant women can be at risk of developing gestational hypertension and/or pre-eclampsia, which causes complications in nearly 7% of pregnancies. These "special" populations could be regarded as natural models suited to reveal mechanisms of hypertension development which are either common to other forms of hypertension, including primary hypertension or specific to these populations. Recent studies in the field of genetics of primary hypertension have used new powerful tools, such as genome-wide association studies (GWAS) and sequencing, but studies about hypertension during childhood and in pregnancy have seldom used high-throughput technologies and the knowledge in this field comes mostly from the candidate gene approach. In this review we summarize some interesting results from genetic studies conducted in childhood and adolescence and during pregnancy and underline the need to apply modern technologies in these potentially very fruitful populations.

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Effect of Trp64Arg mutation of the β3‐adrenergic receptor gene and C161T substitution of the peroxisome proliferator activated receptor γ gene on obesity in Japanese children

Abstract: All of these data suggest that Trp64Arg mutation of the beta3-AR gene might affect obesity and HDL metabolism in obese boys. In contrast, C161T mutation of the PPARgamma gene, by itself, is unlikely to influence obesity, lipid metabolism or plasma leptin levels.

Cited by 27 publications

References 45 publications

Obesity and eating behaviour in children and adolescents: Contribution of common gene polymorphisms

Obesity and eating behaviour in children and adolescents: Contribution of common gene polymorphisms

Study on the Effects of PPARG and PPAR-B/D Gene Variations on Serum LDL Subfractions in Patients with Coronary Heart Disease

Searching for genes involved in hypertension development in special populations: children and pre-eclamptic women. Where are we standing now?

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