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M. A. Gillman; R. Sandyk
South African Brain Research Institute Suite 9 Highlands House (NBS Centre) 173 Louis Botha Ave Orange Grove 2192 Johannesburg, South Africa

Arch Gen Psychiatry. 1986;43(2):192-193.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

We read with interest the letter by Mukherjee et al¹ in which an increased incidence of a high fasting blood sugar (FBS) level was found among subjects with tardive dyskinesia (TD). We would like to add that an impaired FBS level has been observed in other exprapyramidal disorders in which dopamine has been shown to play a pathogenetic role, namely, chorea² and Parkinson's disease.³

As early as 1960, Gates and Hyman⁴ reported on the efficacy of oral tolbutamide in diabetic subjects with PD, and in 1961 Barbeau⁵ found decreased glucose tolerance in 50% of subjects with PD. Van Woert and Mueller⁶ found increased FBS and decreased plasma insulin levels in 24 subjects with PD. These findings were attributed to a decreased release of pancreatic insulin in PD. Indeed, dopamine has been shown to stimulate insulin secretion (a βadrenergic—mediated mechanism)⁷ and . . . [Full Text PDF of this Article]

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