- Effect of Isoproterenol on the Glucose-induced Hypothalamin Somatostatin Release.
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Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, In Myoung Yang, Jung Taek Woo, Chul Young Park, Sun Woo Kim, Jung Hyun Ro, Sang Hwa Kim, Seung Joon Oh, Duk Yoon Kim
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J Korean Endocr Soc. 1999;14(2):255-264. Published online January 1, 2001
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- BACKGROUND
Acute hypoglycemia stimulates somatostatin (SRIH) release from the hypothalamus, and which in turn suppress growth hormone (GH) secretion from the anterior pituitary gland. However, the exact mechanism of glucose increases the hypothalamic SRIH secretion is not well known. Beta-adrenergic pathway is known to stimulate the hypothalamus SRIH release. We, therefore, hypothesized that the glucose-induced SRIH release may be mediated by the stimulation of the central beta-adrenergic system, and investigated to determine whether a beta-adrermgic aganist, isoproterenol, contribute the suppressive effect of glucose on the GHRH-induced GH secretian. METHODS: Ten healthy young men, aged 23 to 26 years, were studied. Four endocrinological tests were carried out. (Test 1) GHRH (Bachem, CA, U.S.A.), 100pg bolus, was given intravenously at 0 minute. (Test 2) Glucose 100 gm dissolved in water, was given orally at -30 minute and GHRH was administered as Test 1. (Test 3) Isoproterenol (Isuprel, Sanofi Winthrop, USA), 0.012 mg/kg, wasinfused continuously between 0 minute and 120 minute, and GHRH was administered as Test 1. (Test 4) Isoproterenol, 0.012 mg kg was infused continuously between 0 minute and 120 minute, and glucose and GHRH were administered as Test 2. RESULTS: Oral glucose ingestion significantly suppressed the GHRH-induced GH secretion. The acute hyperglycemia significantly suppressed GHRH-induced GH secretion. The pretreatments with isoproterenol significantly suppressed the GHRH-induced GH levels. The pretreatment with glucose and isoproterenol suppressed the GHRH-induced GH levels more compared to those induced by glucose in Test 2. The GH levels in Test 4 did not significantly differ from those in Test 3. CONCLUSION: The results of this study suggests that the hypothalamic somatostatinergic activity induced by the oral glucose administeration is not mediated by the beta-adrenergic pathway in normal men. (J Kor Soc Endocrinool 14:255-264, 1999)
- Changes of Bone Turnover Markers after Treatment with Growth Hormone Therapy in Children with Growth Retardation.
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In Myung Yang, Jeong Taek Woo, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, Ki Oak han, Duk Yoon Kim, Hyung In Yang
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J Korean Endocr Soc. 1994;9(4):344-349. Published online November 6, 2019
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- The effects of growth hormone(GH) deficiency and recombinant human GH replacement(0.5IU/kg per week) on bone mineral metabolism in 21GH-deficiency children were studied. All children had significantly reduction of bone density(Z score;-1.4+-0.71). After 1 month of therapy, the levels of serum insulin-like growth factor 1(IGF-1), osteocalcin(OC) and carboxyterminal propeptede of type 1 procollagen(PICP) were significantly elevated. But IGFBP-3 were not shown to change significantly. The changes in serum levels of PICP during the first month of recombinant human GH treatment were positively related to growth velocity, whereas the changes in IGF-1 and OC during the first month of therapy were not. We conclude that the recombinant human GH treatment caused significant modifications of mineral metablism and that the measurement of the changes of biochemical markers of bone metablism espacially PICP may be a useful tool in prediction improved growth velocity during long term GH replacement therpy.
- A clinical study of thyrotoxic periodic paralysis.
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Sung Yi Kang, Sung Hoon Kim, Duk Yoon Kim, Jeong Taek Woo, In Myung Yang, Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Kwang Won Kim, Young Kil Choi
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J Korean Endocr Soc. 1993;8(1):19-26. Published online January 1, 2001
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- No abstract available.
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