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Discordance Between Growth Hormone (GH) Responses After GH-Releasing Hormone and Insulin Hypoglycemia in Myotonic Dystrophy^*

Division of Metabolism and Nutrition, International Center for Exchanging Medical Research (Y.O., K.C.) Kobe 650
The Third Division, Department of Medicine (T.K., Y.K., M.S., N.K., H.A., T.F.), Kobe University School of Medicine Kobe 650
The Department of Neurology, National Hyogo Chuo Hospital (K.T.) Sanda 669-13, Japan

Address all correspondence and requests for reprints to: Dr. Kazuo Chihara, Division of Metabolism and Nutrition, International Center for Medical Research, Kobe University School of Medicine 5-1, 7-aChome Kusunoki-cho, Chuo-ku, Kobe 650, Japan.

Plasma GH responses to human GHRH, arginine, L-dopa, and insulin-induced hypoglycemia were determined in seven myotonic dystrophy (MD) patients. An iv bolus injection of GHRH-(1-44)-NH₂ (1 µg/kg BW) only slightly increased plasma GH concentrations in MD patients. The mean peak plasma GH level after GHRH injection [4.2 ± 0.8 (±SE) µg/L] was significantly lower than that in 10 age-matched normal subjects (26.7 ± 4.3 µg/L) or that in 6 patients with progressive muscular dystrophy (22.8 ± 6.6 µg/h) whose nutritional status was similar to that of the MD patients. Even with a larger dose of GHRH (3 /g/kg BW), the plasma GH rises were minimal in the MD patients (mean peak, 5.9 ± 1.8 µg/L). The plasma GH responses to a 30-min iv infusion of arginine (0.5 g/kg BW) and oral ingestion of L-dopa (0.5 g) were attenuated to a similar extent, whereas insulin-induced hypoglycemia caused a significant increase in plasma GH in all seven MD patients [mean peak, 17.4 ± 4.1 (±SE) µg/L]. The plasma TSH responses to TRH and plasma insulin-like growth factor I levels were similar in the MD patients and normal subjects.

These findings suggest that 1) the impaired GH release after GHRH, arginine, and L-dopa administration in MD patients is not due to somatotroph deficiency, since the GH response to hypoglycemia is well preserved; and 2) insulin-induced hypoglycemia may stimulate GH release at least in part via inhibition of somatostatin release.

^* This work was supported in part by research grants from the Japanese Ministry of Health and Welfare; the Japanese Ministry of Education, Science, and Culture; and the Growth Science Foundation for 1984,1985, and 1987.

Received May 5, 1988.

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