Genetic and Environmental Influences on Adiponectin, Leptin, and BMI Among Adolescents in Taiwan: A Multivariate Twin/Sibling Analysis

Liu, Pi-Hua; Yin, Jiuli; Chen, Wei-Jen; Chang, Chiz‐Tzung; Lee, Tso-Ching; Sun, Han; Chuang, Lee‐Ming

doi:10.1375/twin.11.5.495

Cited by 20 publications

(16 citation statements)

References 47 publications

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“…Several studies have revealed a moderate to high estimate of heritability (30–70%) for plasma adiponectin levels, which are influenced by the interplay of several genes [27-30]. A meta-analysis of genome-wide association studies performed in nearly 40000 individuals in order to identify genes associated with adiponectin levels, revealed 8 loci and confirmed other 2 previously reported loci [31].…”

Section: Introductionsupporting

confidence: 66%

Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease?

Fisman

Tenenbaum

2014

Cardiovasc Diabetol

206

157

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Adiponectin is the most abundant peptide secreted by adipocytes, being a key component in the interrelationship between adiposity, insulin resistance and inflammation. Central obesity accompanied by insulin resistance is a key factor in the development of metabolic syndrome (MS) and future macrovascular complications. Moreover, the remarkable correlation between coronary artery disease (CAD) and alterations in glucose metabolism has raised the likelihood that atherosclerosis and type 2 diabetes mellitus (T2DM) may share a common biological background. We summarize here the current knowledge about the influence of adiponectin on insulin sensitivity and endothelial function, discussing its forthcoming prospects and potential role as a therapeutic target for MS, T2DM, and cardiovascular disease. Adiponectin is present in the circulation as a dimer, trimer or protein complex of high molecular weight hexamers, >400 kDa. AdipoR1 and AdipoR2 are its major receptors in vivo mediating the metabolic actions. Adiponectin stimulates phosphorylation and AMP (adenosin mono phosphate) kinase activation, exerting direct effects on vascular endothelium, diminishing the inflammatory response to mechanical injury and enhancing endothelium protection in cases of apolipoprotein E deficiency. Hypoadiponectinemia is consistently associated with obesity, MS, atherosclerosis, CAD, T2DM. Lifestyle correction helps to favorably modify plasma adiponectin levels. Low adiponectinemia in obese patients is raised via continued weight loss programs in both diabetic and nondiabetic individuals and is also accompanied by reductions in pro-inflammatory factors. Diet modifications, like intake of fish, omega-3 supplementation, adherence to a Mediterranean dietary pattern and coffee consumption also increase adiponectin levels. Antidiabetic and cardiovascular pharmacological agents, like glitazones, glimepiride, angiotensin converting enzyme inhibitors and angiotensin receptor blockers are also able to improve adiponectin concentration. Fibric acid derivatives, like bezafibrate and fenofibrate, have been reported to enhance adiponectin levels as well. T-cadherin, a membrane-associated adiponectin-binding protein lacking intracellular domain seems to be a main mediator of the antiatherogenic adiponectin actions. The finding of novel pharmacologic agents proficient to improve adiponectin plasma levels should be target of exhaustive research. Interesting future approaches could be the development of adiponectin-targeted drugs chemically designed to induce the activaton of its receptors and/or postreceptor signaling pathways, or the development of specific adiponectin agonists.

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Section: Introductionsupporting

confidence: 66%

Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease?

Fisman

Tenenbaum

2014

Cardiovasc Diabetol

206

157

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“…A total of 88 independent estimates of BMI heritability from twin studies were identified from 31 papers (Stunkard et al, 1986, 1990; Hewitt et al, 1991; Korkeila et al, 1991; Neale and Cardon, 1992; Carmichael and McGue, 1995; Forbes et al, 1995; Harris et al, 1995; Herskind et al, 1996; Austin et al, 1997; Faith et al, 1999; Knoblauch et al, 1999; Narkiewicz et al, 1999; Pietilainen et al, 1999; Vinck et al, 1999; Baird et al, 2001; Poulsen et al, 2001; Schousboe et al, 2003, 2004; Nelson et al, 2006; Cornes et al, 2007; Hur, 2007; Ordonana et al, 2007; Silventoinen et al, 2007a,b; Souren et al, 2007; Hur et al, 2008; Liu et al, 2008; Wardle et al, 2008; Lajunen et al, 2009; Watson et al, 2010; Table 1; Figure A2 in Appendix). Reported estimates ranged from 0.47 to 0.90 (5th/50th/95th centiles: 0.58/0.75/0.87; Figure 1).…”

Section: Resultsmentioning

confidence: 99%

Variability in the Heritability of Body Mass Index: A Systematic Review and Meta-Regression

Elks¹,

Hoed²,

Zhao³

et al. 2012

Front. Endocrin.

554

429

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Evidence for a major role of genetic factors in the determination of body mass index (BMI) comes from studies of related individuals. Despite consistent evidence for a heritable component of BMI, estimates of BMI heritability vary widely between studies and the reasons for this remain unclear. While some variation is natural due to differences between populations and settings, study design factors may also explain some of the heterogeneity. We performed a systematic review that identified 88 independent estimates of BMI heritability from twin studies (total 140,525 twins) and 27 estimates from family studies (42,968 family members). BMI heritability estimates from twin studies ranged from 0.47 to 0.90 (5th/50th/95th centiles: 0.58/0.75/0.87) and were generally higher than those from family studies (range: 0.24–0.81; 5th/50th/95th centiles: 0.25/0.46/0.68). Meta-regression of the results from twin studies showed that BMI heritability estimates were 0.07 (P = 0.001) higher in children than in adults; estimates increased with mean age among childhood studies (+0.012/year, P = 0.002), but decreased with mean age in adult studies (−0.002/year, P = 0.002). Heritability estimates derived from AE twin models (which assume no contribution of shared environment) were 0.12 higher than those from ACE models (P < 0.001), whilst lower estimates were associated with self reported versus DNA-based determination of zygosity (−0.04, P = 0.02), and with self reported versus measured BMI (−0.05, P = 0.03). Although the observed differences in heritability according to aspects of study design are relatively small, together, the above factors explained 47% of the heterogeneity in estimates of BMI heritability from twin studies. In summary, while some variation in BMI heritability is expected due to population-level differences, study design factors explained nearly half the heterogeneity reported in twin studies. The genetic contribution to BMI appears to vary with age and may have a greater influence during childhood than adult life.

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“…In addition, we found three twin studies that had pooled information on children at different ages. [27][28][29] We did not limit our search to weight, but except one early twin study, 27 all of these studies had used BMI or relative weight as an indicator of obesity. Two twin studies represented Korean population, 16,19 one Taiwanese population 29 and one had pooled information from four East Asian populations, 30 but otherwise the studies were conducted in the Caucasian populations.…”

Section: Search Strategymentioning

confidence: 99%

The genetic and environmental influences on childhood obesity: a systematic review of twin and adoption studies

et al. 2009

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In this systematic review, we aimed to collect together all previous twin and adoption studies on childhood and adolescent obesity up to the age of 18 years. Using several sources, we identified nine twin and five adoption studies; all of these studies had used relative weight as an indicator of obesity. Except the two twin studies from the Korean population, all studies represented Caucasian populations. In a meta-analysis of these twin studies, we found that genetic factors had a strong effect on the variation of body mass index (BMI) at all ages. The common environmental factors showed a substantial effect in mid-childhood, but this effect disappeared at adolescence. Adoption studies supported the role of family environment in childhood obesity as correlations were found between adoptees and adoptive parents; however, correlations were substantially stronger between parents and their biological offspring, further supporting the importance of genetic factors. In the future, more studies implementing genetic and environmental measures into twin models are needed as they allow estimation of the proportion of total genetic variation explained by candidate genes and analyses of gene-environment interactions. More studies of genetic architecture in non-Caucasian populations, of gene-environment interactions, and of body composition and body fat distribution are needed. IntroductionChildhood obesity is one of the major public health problems in the modern world. In the period [2003][2004][2005][2006], 32% of the US children were classified as obese or overweight, 1 and increasing trends in childhood obesity are seen all over the world. 2 These results are especially alarming as overweight children show a high risk of becoming obese adults. 3,4 Childhood is an important period of life for health interventions as health-related behaviors are just in formation, and it seems possible to intervene for preventing the development of obesity. 5 Thus, it is crucial to further understand the background mechanisms of childhood obesity to find even more effective measures to prevent it before it begins to produce more or less irreversible health damages.Both genetic and environmental factors will probably contribute to childhood obesity. 6 Family studies have shown that obesity runs in families, although more detailed twin, adoption and family studies have shown that genetic differences between individuals explain a major proportion of the within-population variation in body mass index (BMI, kg m À2 ) in adulthood. [7][8][9] It is probable that genetic factors have an important role in childhood obesity also, but their role may be different or they may result from other genes than those that operate in adulthood. 10 The environmental factors shared by family members, such as co-twins in twin studies, have shown only a slight effect on the variation of adult BMI. 7,8 However, they may have a more important role in childhood, where parents and their offspring live together and where siblings obviously have a much greater opportu...

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Genetic and Environmental Influences on Adiponectin, Leptin, and BMI Among Adolescents in Taiwan: A Multivariate Twin/Sibling Analysis

Cited by 20 publications

References 47 publications

Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease?

Adiponectin: a manifold therapeutic target for metabolic syndrome, diabetes, and coronary disease?

Variability in the Heritability of Body Mass Index: A Systematic Review and Meta-Regression

The genetic and environmental influences on childhood obesity: a systematic review of twin and adoption studies

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