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Background Although several lines of evidence suggest that hypomagnesaemia is a risk factor for developing type 2 diabetes, there are no studies regarding the association between hypomagnesaemia and the risk for developing impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). Our objective was to examine the association between serum magnesium levels and the risk for developing IFG, IGT and type 2 diabetes. Materials and methods A total of 1122 individuals (20–65 years of age) were enrolled between 1996 and 1997, and 817 individuals re-examined about 10 years later. New-onset IFG (5·6–7·0 mmol L−1 fasting glucose), IGT (7·8–11·1 mmol L−1 glucose 2-h postload), and type 2 diabetes were determined from the number of subjects who had these conditions at the second examination without evidence that they were present at the first one. The relative risk of new-onset metabolic glucose disorders and diabetes (dependent variables) was computed using Poisson regression model adjusted for age, sex, family history of diabetes, waist circumference and homeostasis model assessment for insulin resistance index. Serum magnesium levels of < 0·74 mmol L−1 (independent variable) defined the exposed group. Results At baseline, 420 (51·4%) individuals had hypomagnesaemia. New-onset IFG and IGT was identified in 276 (33·8%) individuals. The relative risk for IFG, IGT and IFG + IGT was 1·11 (95% confidence interval, 0·5–5·1), 1·38 (95% confidence interval, 1·1–6·3) and 1·49 (95% confidence interval, 1·1–4·9), respectively. New-onset diabetes was identified in 78 (9·5%) individuals (relative risk 2·54; 95% confidence interval, 1·1–4·1). Conclusions Hypomagnesaemia is independently associated with the development of IGT, IFG + IGT and type 2 diabetes, but not with the development of IFG. [ABSTRACT FROM AUTHOR]

Polymorphisms within the transcription factor 7-like 2 gene ( TCF7L2) have been associated with type 2 diabetes (T2D) in several recent studies. We characterized three of these polymorphisms (rs12255372, rs7903146 and the microsatellite DG10S478) in an admixed sample of 286 patients with T2D and 275 controls from Mexico City. We also analyzed three samples representative of the relevant parental populations: Native Americans from the state of Guerrero (Mexico), Spanish from Valencia and Nigerians (Bini from the Edo region). In order to minimize potential confounding because of the presence of population stratification in the sample, we evaluated the association of the three TCF7L2 polymorphisms with T2D by using the programadmixmap to fit a logistic regression model incorporating individual ancestry, sex, age, body mass index and education. The markers rs12255372, rs7903146 and DG10S478 are in tight disequilibrium in the Mexican sample. We observed a significant association between the single-nucleotide polymorphism (SNP) rs12255372 and the microsatellite DG10S478 with T2D in the Mexican sample [rs12255372, odds ratio (OR) = 1.78, p = 0.017; DG10S478, OR = 1.62, p = 0.041]. The SNP rs7903146 shows similar trends, but its association with T2D is not as strong (OR = 1.39, p = 0.152). Analysis of the parental samples, as well as other available data, indicates that there are substantial population frequency differences for these polymorphisms: The frequencies of the T2D risk factors are more than 20% higher in European and West African populations than in East Asian and Native American populations. [ABSTRACT FROM AUTHOR]