Phenotypic and genetic clustering of diabetes and metabolic syndrome in Chinese families with type 2 diabetes mellitus

Li, J K Y; Ng, Maggie; So, Wing Yee; Chiu, Cherry K P; Ozaki, Risa; Tong, Peter C.Y.; Cockram, Clive S.; Chan, Juliana C.N.

doi:10.1002/dmrr.577

Cited by 94 publications

(78 citation statements)

References 34 publications

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“…While previous studies have suggested common underlying factors influencing the endophenotypes related to the metabolic syndrome [10,17], genetic, environmental and phenotypic correlations between groups of endophenotypes estimated from the present study did not entirely support this finding. The correlations between endophenotypes were mostly weak, except moderate correlations between insulin-related endophenotypes and either obesity or lipid endophenotypes.…”

Section: Discussioncontrasting

confidence: 99%

“…These results indicate that phenotypic variation in individual endophenotypes is mostly due to genetic effects and this is consistent with the many univariate analyses published by us and others [9][10][11][12][13]23]. Environmental factors contributing to the variation of the endophenotypes between individuals appear to be mostly experienced by individuals and not shared between family members.…”

Section: Discussionsupporting

confidence: 91%

“…A wide range of heritabilities (mostly moderate to high) have been estimated for obesity traits (mean: 0.55; range: 0.37-0.80) [9][10][11][12][13][14]; insulin-related traits (mean: 0.38; range: 0.08-0.75) [9][10][11][13][14][15][16]; BP (mean: 0.41; range: 0.16-0.76) [9][10][11][12][13] and lipid traits (mean: 0.46; range: 0.20-0.70) [9][10][11][12][13]. However, the underlying mechanism of the clustering of these characteristics in an individual remains unclear [17].…”

Section: Introductionmentioning

confidence: 99%

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Are there common genetic and environmental factors behind the endophenotypes associated with the metabolic syndrome?

et al. 2007

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Aims/hypothesis The cluster of obesity, insulin resistance, dyslipidaemia and hypertension, called the metabolic syndrome, has been suggested as a risk factor for cardiovascular disease and type 2 diabetes. The aim of the present study was to evaluate whether there are common genetic and environmental factors influencing this cluster in a general population of twin pairs. Materials and methods A multivariate genetic analysis was performed on nine endophenotypes associated with the metabolic syndrome from 625 adult twin pairs of the GEMINAKAR study of the Danish Twin Registry.Results All endophenotypes showed moderate to high heritability (0.31-0.69) and small common environmental variance (0.05-0.21). In general, genetic and phenotypic correlations between the endophenotypes were strong only within sets of physiologically similar endophenotypes, but weak to moderate for other pairs of endophenotypes. However, moderate correlations between insulin resistance indices and either obesity-related endophenotypes or triacylglycerol levels indicated that some common genetic backgrounds are shared between those components. Conclusions/interpretation We demonstrated that, in a general population, the endophenotypes associated with the metabolic syndrome apparently do not share a substantial common genetic or familial environmental background.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

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Are there common genetic and environmental factors behind the endophenotypes associated with the metabolic syndrome?

et al. 2007

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“…This is because the 20 loci identified by GWA studies have small λ s values (Table 3), with a λ s value in combination of only about 1.08-1.10. The expected λ s value for type 2 diabetes appears to be somewhere between 1.2 and 6 [96,[117][118][119][120]. Therefore, we must conclude that much of the genetic cause of type 2 diabetes remains unidentified and the GWA results should be seen as complementing, not replacing, the linkage analyses.…”

Section: Discussionmentioning

confidence: 97%

“…This is justified under the assumption that heritable precursors of type 2 diabetes will share the same genetic determinants as type 2 diabetes itself. Diabetes-related QTs are heritable in multiple ethnic groups (for examples, see [94][95][96]), and many also predict the subsequent development of diabetes (for examples, see [97][98][99]). In addition, genetic correlation has been demonstrated between type 2 diabetes and some QTs [100] and between various QTs [14, 37, 96, 100-102].…”

Section: Discussionmentioning

confidence: 99%

Agreement among type 2 diabetes linkage studies but a poor correlation with results from genome-wide association studies

Lillioja

Wilton

2009

Diabetologia

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Aims/hypothesis Little of the genetic basis for type 2 diabetes has been explained, despite numerous genetic linkage studies and the discovery of multiple genes in genome-wide association (GWA) studies. To begin to resolve the genetic component of this disease, we searched for sites at which genetic results had been corroborated in different studies, in the expectation that replication among studies should direct us to the genomic locations of causative genes with more confidence than the results of individual studies. Methods We have mapped the physical location of results from 83 linkage reports (for type 2 diabetes and diabetes precursor quantitative traits [QTs, e.g. plasma insulin levels]) and recent large GWA reports (for type 2 diabetes) onto the same human genome sequence to identify replicated results in diabetes genetic 'hot spots'. Results Genetic linkage has been found at least ten times at 18 different locations, and at least five times in 56 locations. All replication clusters contained study populations from more than one ethnic background and most contained results for both diabetes and QTs. There is no close relationship between the GWA results and linkage clusters, and the nine best replication clusters have no nearby GWA result. Conclusions/interpretation Many of the genes for type 2 diabetes remain unidentified. This analysis identifies the broad location of yet to be identified genes on 6q, 1q, 18p, 2q, 20q, 17pq, 8p, 19q and 9q. The discrepancy between the linkage and GWA studies may be explained by the presence of multiple, uncommon, mildly deleterious polymorphisms scattered throughout the regulatory and coding regions of genes for type 2 diabetes.

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Progression to impaired glucose metabolism in first‐degree relatives of patients with type 2 diabetes in Isfahan, Iran

Janghorbani

Amini

2009

Diabetes Metabolism Res

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Phenotypic and genetic clustering of diabetes and metabolic syndrome in Chinese families with type 2 diabetes mellitus

Abstract: Background The aim of this study was to investigate the familiality and clustering of type 2 diabetes (T2DM) and metabolic syndrome (MES) predominantly in families with young-onset diabetes from the Hong Kong Family Diabetes Study.

Cited by 94 publications

References 34 publications

Are there common genetic and environmental factors behind the endophenotypes associated with the metabolic syndrome?

Are there common genetic and environmental factors behind the endophenotypes associated with the metabolic syndrome?

Agreement among type 2 diabetes linkage studies but a poor correlation with results from genome-wide association studies

Progression to impaired glucose metabolism in first‐degree relatives of patients with type 2 diabetes in Isfahan, Iran

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