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Hypovitaminosis D is associated with insulin resistance and ß cell dysfunction

Centre for Diabetes and Metabolic Medicine
Barts and the London NHS Trust
Queen Mary School of Medicine and Dentistry
University of London
London
United Kingdom
E-mail: bboucher{at}doctors.org.uk

W Garry John

Norfolk & Norwich University Hospital
Norwich
United Kingdom

Kate Noonan

Barts and the London NHS Trust
London
United Kingdom

Dear Sir:

It was interesting to see the elegant explanation by Chiu et al (1) of associations between hypovitaminosis D and both insulin resistance and ß cell dysfunction in several different ethic groups, which supports the idea of hypovitaminosis vitamin D as a risk factor for the metabolic syndrome, including Type 2 diabetes (2). Their findings are of particular interest because their subjects were normoglycemic, whereas our earlier data, quoted by Chiu et al, came from dysglycemic subjects (3, 4). The additional finding of adverse effects of hypovitaminosis D on the fasting lipid profile is also important in view of the reports of increased risk of ischemic heart disease with vitamin D deficiency in cross-sectional studies in communities where vitamin D deficiency is common (5, 6). In 146 healthy, nondiabetic British subjects originally from an area of Bangladesh (Sylhet) where both soluble C-reactive protein concentrations and plasma metalloproteinase 9 concentrations were inversely related to vitamin D status (7), we now find on univariate analysis (unpublished data) that serum 25-hydroxyvitamin D concentration relates directly to total and LDL cholesterol and to both apolipoproteins A1 (apo A1) and B (apo B) (Table 1). However, when we examined these data by using the same variables as in the study by Chiu et al, except ethnicity, we found serum 25-hydroxyvitamin D concentrations to relate directly to both total and HDL cholesterol and to apo A1 and apo B but to relate inversely to triacylglycerol. On reexamination that includes additional variables such as smoking, however, serum 25-hydroxyvitamin D concentrations appear to be an independent predictor of increases in apo A1 alone.

In the report of Chiu et al, ethnicity was not a predictor of any of the lipid profile variables assessed, although it was a predictor for vitamin D status (1). In view of our findings, however, we wonder whether there may be any variation in the relations of serum 25(OH)D concentration to elements of the fasting lipid profile between the ethnic groups examined.

REFERENCES

1. Chiu KC, Chu A, Go VLW, Saad MF. Hypovitaminosis D is associated with insulin resistance and ß cell dysfunction. Am J Clin Nutr 2004;79:820–5.[Abstract/Free Full Text]
2. Boucher BJ. Inadequate vitamin D status: does it contribute to the disorders comprising ‘syndrome X’? Br J Nutr 1998;79:315–27.[Medline]
3. Boucher BJ, Mannan N, Noonan K, Hales CN, Evans SJW. Glucose intolerance and impairment of insulin secretion in relation to vitamin D deficiency in East London Asians. Diabetology 1995;38:1239–45.
4. Baynes KC, Boucher BJ, Feskens EJ, Kromhout D. Vitamin D, glucose tolerance and insulinaemia in elderly men. Diabetologia 1997;40:344–7.[Medline]
5. Scragg R, Jackson R, Holdaway IM, Lim T, Beaglehold R. Myocardial infarction is inversely related with plasma 25-hydroxyvitamin D levels: a community-based study. Int J Epidemiol 1990;19:559–63.[Abstract/Free Full Text]
6. Grimes DS, Hindle E, Dyer T. Sunlight, cholesterol and coronary heart disease. Q J Med 1996;89:579–89.
7. Timms PM, Mannan N, Hitman GA, et al. Circulating MMP9, vitamin D and variation in the TIMP-1 response with VDR genotype: mechanisms for inflammatory damage in chronic disorders? QJM 2002;95:787–96.[Abstract/Free Full Text]

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