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Glucose Tolerance and Erythrocyte Insulin Receptors in Friedreich's Ataxia

Published online by Cambridge University Press:  18 September 2015

P. Draper ,
D. Shapcott ,
A. Larose ,
J. Stankova ,
F. Levesque  and
B. Lemieux
P. Draper
Affiliation:
Le Centre Hospitalier Universitaire de l'Université de Sherbrooke, Sherbrooke, Quebec
D. Shapcott
Affiliation:
Le Centre Hospitalier Universitaire de l'Université de Sherbrooke, Sherbrooke, Quebec
A. Larose
Affiliation:
Le Centre Hospitalier Universitaire de l'Université de Sherbrooke, Sherbrooke, Quebec
J. Stankova
Affiliation:
Le Centre Hospitalier Universitaire de l'Université de Sherbrooke, Sherbrooke, Quebec
F. Levesque
Affiliation:
Le Centre Hospitalier Universitaire de l'Université de Sherbrooke, Sherbrooke, Quebec
B. Lemieux
Affiliation:
Le Centre Hospitalier Universitaire de l'Université de Sherbrooke, Sherbrooke, Quebec
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Detailed in vivo and in vitro studies of glucose and insulin metabolism in Friedreich's ataxia patients and unaffected family members have further defined the extent of the abnormalities in carbohydrate metabolism. The high incidence of glucose intolerance and a hyper-insulinemic response to a glucose challenge in a high percentage of Friedreich's ataxia patients has been confirmed. An increased incidence of glucose intolerance among hétérozygotes is suggested, while the siblings show a more normal distribution of diabetes and a nearly normal insulin response to the glucose tolerance test. Human growth hormone patterns are normal for all groups.

Preliminary studies of insulin binding to erythrocytes suggest a difference in the binding characteristics among diabetic Friedreich's ataxia patients, while the binding in the non-diabetic Friedreich's ataxia group is similar to that of non-diabetic controls. Results from a small group of non-diabetic siblings suggest a normal insulin binding, while a tendency toward increased binding at low insulin concentrations among diabetic family members is noted.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 6 , Issue 2 , May 1979 , pp. 233 - 239
Copyright
Copyright © Canadian Neurological Sciences Federation 1979

References

Andermann, E., Rêmillard, G. M., Goyer, G., Blitzer, L., and Barbeau, A. (1976). Genetic and Family studies in Friedreich's Ataxia. Can. J. Neurol. Sci. 3, 287–301.CrossRefGoogle ScholarPubMed
Bar, R. S., and Roth, J. (1977). Insulin receptor Status in Disease States of Man. Arch. Int. Med., 137, 474–481.CrossRefGoogle ScholarPubMed
Bar, R. S., Levis, W. R., Rechler, M. M., Harrison, L. C.Siebert, C., Podskalny, J., Roth, J., and Muggeo, M. (1978). Extreme insulin resistance in Ataxia Teangiectasia. Defect in affinity of insulin receptors. New England J. Med., 298, 1164–1171.Google Scholar
Barbosa, J., Nuttall, F. Q., Kennedy, W., and Goetz, F. (1974). Plasma Insulin in Patients with Myotonie Dystrophy and their Relatives. Medicine, Vol. 53, 307–323.CrossRefGoogle Scholar
Blecher, M. (1979). Cell-surface receptors in health and disease. Clin. Chem. 25, 11–19.CrossRefGoogle ScholarPubMed
Danowski, T. S., Khurana, R. C., Nolan, S., Stephan, T., Gegick, C. G., Chae, S., and Vidalon, C. (1973). Insulin patterns in equivocal glucose tolerance tests (chemical diabetes). Diabetes, 22, 808–812.CrossRefGoogle ScholarPubMed
Gambhir, K. K., Archer, J. A., and Carter, L. (1977). Insulin radioreceptor for human erythrocytes. Clin. Chem., 23, 1590–1595.CrossRefGoogle ScholarPubMed
Gambhir, K. K., Archer, J. A., and Bradley, C. J. (1978). Characteristics of Human Erythrocyte Insulin Receptors. Diabetes, 27, 701–708.CrossRefGoogle ScholarPubMed
Gonen, B., and Rubenstein, A. H. (1978). Haemoglobin Al and diabetes mellitus. Diabetológia, 15, 1–8.CrossRefGoogle Scholar
Muggeo, M., Bar, R. S., and Roth, J. (1977). Change in affinity of insulin receptors following oral glucose in normal adults. J. Clin. Endocrinol. Metab., 44, 1206–1209.CrossRefGoogle ScholarPubMed
Renold, A. E., Mintz, D. H., Muller, W. A., and Cahill, G. F. Jr. (1978). Diabetes Mellitus.In: The Metabolic Basis of Inherited Disease, 4th edition. (Stanbury, J. B., Wyngaarden, J. B., and Fredrickson, D. S., eds) McGraw-Hill, New York, p80–109.Google Scholar
Shapcott, D., Melancon, S., Butter-Worth, R. F., Khoury, K., Collu, R., Breton, G., Geoffroy, G., Lemieux, B., and Barbeau, A. (1976). Glucose and Insulin metabolism in Friedreich's ataxia. Can. J. Neurol. Sci. 3, 361–364.CrossRefGoogle ScholarPubMed
Sommen, V., Tamborlane, W., De Fronzo, R., Genel, M., and Felig, P., (1978). Insulin binding and insulin sensitivity in Isolated Growth Hormone Deficiency. New Engl. J. Med. 299, 1025–1030.CrossRefGoogle Scholar
Thoren, C. (1978). Note on diabetes mellitus in a prospective study of Friedreich's ataxia.In: Advances in Neurology, vol. 21. The inherited ataxias: biochemical, viral and pathological studies. (Kark, R.A.P., Rosenberg, R.N., and Schut, L. J. eds). Raven Press, New York, pp 391–393.Google Scholar