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,
ROBERT C. COOKSEY,
JIM LEGAN,
EDWARD F. MEYDRECH,
JOHN HILL and
KEN KUBOTA
University of Mississippi Medical School and the Veterans Administration Medical Center Jackson, Mississippi 39216
University of Alabama Medical School and Veterans Administration Medical Center Birmingham, Alabama 35233
National Research Council of Canada, Plant Biotechnology Institute Saskatoon, Sask, 27N0W9
Harvard Medical School and Thorndike Laboratory, Beth Israel Hospital Boston, Massachusettes 02215
Address all correspondence and requests for reprints to: Dr. Eduardo Gaitan, Endocrinology Section (151), Veterans Administration Medical Center, 1500 East Woodrow Wilson Drive, Jackson, Mississippi 39216.
Pearl millet [Pennisetum millet (L.) leeke] is the main source of food energy for the rural poor in many areas of the semiarid tropics. Epidemiological evidence suggests that millet may play a role in the genesis of endemic goiter in these areas, and sparse experimental data in rats support this suspicion. This study was undertaken to determine in vivo in rats and in vitro using porcine thyroid slices and a thyroid peroxidase(TPO) assay the goitrogenic and antithyroid effects of millet diets, extracts of millet, and certain pure compounds contained therein. For use in these studies, whole grain millet was progressively dehulled to yield successively four bran and four flour fractions in which direct analyses revealed progressively lower concentrations of C-glycosylflavones. In vivo feeding of bran fraction 1, that richest in C-glycosylflavones, led to a significant increase in thyroid weight and antithyroid effects. Feeding of bran fraction 2, the next richest in C-glycosylflavones, produced similar, but less marked, changes. In vitro studies of 125I metabolism using porcine thyroid slices indicated that extracts of bran fractions 1 and 2 were most potent, producing changes similar to those produced by methimazole (MMI). At a concentration of 60 µmol/L, glucosylvitexin, the major C-glycosylflavone present in millet, had effects comparable to those of 1 µmol/L MMI. Similarly, in studies of porcine TPO, extracts of bran fraction 1 caused pronounced (85%) inhibition of enzyme activity, and progressively less inhibition was induced by extracts of bran fractions 2, 3, and 4. Overall, the TPO-inhibiting activities of the various millet fractions closely correlated with their Cglycosylflavone concentrations. Three C-glycosylflavones present in millet, glucosylvitexin, glycosylorientin, and vitexin, also inhibited TPO activity. Thus, in vivo and in vitro studies revealed that millet diets rich in C-glycosylflavones produce goitrogenic and antithyroid effects similar to those of certain other antithyroid agents and small doses of MMI. We conclude that in areas of iodine deficiency in which millet is a major component of the diet, its ingestion may contribute to the genesis of endemic goiter.
* Presented in part at the Ninth International Thyroid Congress, Sao Paulo, Brasil, September 1–6, 1985. This work was supported by the Medical Research Service of the V.A., the International Development Research Centre of Canada, and Grants AM-18416 from the NIDDK and the Dana Fund, Inc.
Received March 7, 1988.
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A. Elnour, L. Hambraeus, M. Eltom, M. Dramaix, and P. Bourdoux Endemic goiter with iodine sufficiency: a possible role for the consumption of pearl millet in the etiology of endemic goiter1 Am. J. Clinical Nutrition, January 1, 2000; 71(1): 59 - 66. [Abstract] [Full Text] [PDF] |
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