- The Changes in Atherosclerotic Markers and Adiopocytokines after Treatment with Growth Hormone for the Patients with Hypopituitarism and Growth Hormone Deficiency.
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Hyun Won Shin, In Kyung Jeong, Goo Yeong Cho, Cheul Young Choi, Jong Yeop Kim, Yeong Je Chae, Min Ho Cho, Byung Wan Lee, Seong Jin Lee, Chul Young Park, Eun Gyoung Hong, Hyeon Kyu Kim, Doo Man Kim, Jae Myung Yu, Sung Hee Ihm, Moon Ki Choi, Hyung Joon Yoo, Sung Woo Park
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J Korean Endocr Soc. 2006;21(6):515-525. Published online December 1, 2006
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DOI: https://doi.org/10.3803/jkes.2006.21.6.515
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- BACKGROUND
It is known that patients with hypopituitarism have a high mortality rate due to the presence of atherosclerosis, cardiovascular diseases and stroke. The aim of this study was the effect of growth hormone (GH) on the atherosclerotic markers and the adipocytokine levels. METHOD: The study was conducted on 13 adult patients with hypopituitarism and growth hormone deficiency (GHD), and they had been stabilized after receiving hormone replacement therapy for other insufficient pituitary hormones, other than GH, for more than one year. Before treatment with GH, we compared the lipid metabolism, glucose metabolism, cardiovascular risk factors and adipocytokine levels, including adiponectin, leptin, TNF-alpha and IL-6, between the GHD patients and 13 healthy adults who were of a similar age and gender distribution. Patients with GHD were treated with 1 U/day of GH for 6 months. We measured insulin-like growth factor-I (IGF-I), blood pressure, body composition, lipid metabolism, glucose metabolism and hs-CRP, cardiac function, adiponectin, leptin, TNF-alpha and IL-6 levels, flow mediated vasodilation (FMD) and nitroglycerin mediated vasodilation (NMD) before and after GH treatment. RESULTS: The patients with hypopituitarism and GHD showed significantly higher levels of total cholesterol (P = 0.002), low-density lipoprotein cholesterol (LDL-C) (P = 0.036), hs-CRP (P = 0.0087) and leptin (P < 0.001) than did the normal healthy adults. However, there was no difference between the normal adults and the patients with GHD for the systolic and diastolic BP, the levels of apoA, apoB, fasting blood glucose(FBG) and HOMA-IR. In the subjects with GHD after treatment with GH, the level of fat mass (P = 0.0017), total cholesterol (P = 0.004), LDL-C (P = 0.001), leptin (P = 0.013), TNF-alpha (P < 0.001) and hs-CRP (P = 0.0001) were significantly reduced, while lean body mass (P = 0.0161), FFA (P = 0.049) and FMD (P = 0.0051) showed a significant increase. However, there was no significant difference in the level of the systolic and diastolic BP, LDL-C, apoA, apoB, LP (a), HOMA-IR, ejection fraction, left ventricular posterior wall, E/A ratio, intraventricular septum, NMD, intima-media thickness, adiponectin, IL-6, FBG and fasting insulin before and after GH treatment. CONCLUSION: The subjects with GHD were vulnerable to cardiovascular disease. GH therapy for 6 months had a positive effect on their various cardiovascular risk factors.
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Citations
Citations to this article as recorded by  - Molecular Biology of Atherosclerosis
In-Kyung Jeong
Endocrinology and Metabolism.2010; 25(3): 166. CrossRef
- 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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Abstract
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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)
- Relationship between the Expression of Growth Hormone-Releasing Hormone Receptor Gene and Endocrinologic Profiles in GH-Secreting Pituitary Adenomas.
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Sung Woon Kim, Jin Woo Kim, Young Seol Kim, Young Kil Choi, Seung Joon Park, In Myoung Yang, Jung Taek Woo, Mi Sook Ryu, Chul Young Park, Sun Woo Kim
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J Korean Endocr Soc. 1999;14(2):241-254. Published online January 1, 2001
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Abstract
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- BACKGROUND
Growth hormone-releasing hormone (GHRH) plays a key role in the regulation of the proliferation and differentiation of somatomammotroph cells as well as secretion of GH. The actions of GHRH are mediated through the GHRH receptor (GHRH-R) that is a G protein coupled receptor with seven transmembrane domains. It has been demonstrated that alternative splicing occurs in the third cytoplasmic domain of rat and human GHRH-R mRNA, However, the clinical significance of the altemative splicing remains to be unsolved. To find an insight into the clinical significance, we investigate the correlation between the GHRH-R gene expression and a variety of clinical clinical and endocrinological findings in 11 acromegalic patients. METHODS: Eleven acromegalic patients (3 males and 8 females, mean age 43.5 years) were included in this study. Six endocrine tests were carried out to evaluate the GH seeretory function of tumors. Invasiveness of tumors were evaluated by preoperative MRI findings on the basis of Hardys classification. Sequence the gsp oncogene and estimate the GHRH-R gene expression by RT-PCR and in vitro transcription. RESULTS: Three different sized cDNA fragments, 250 bp, 700 bp and 810 bp, were found after RT-PCR. The amount of 250 bp fragment was higher than those of the other two fragments. The clinical findings (age, size, GH level, frequency of paradoxical response to TRH or GnRH, octreotide response, hypothalamic somatostatinergic activity) of the group with high expression of the 250 bp fragment did not significantly differ from those of the group with low expression. The GHRH-R gene expression of tumors with gsp oncogene did not significantly differ from that of tumors without gsp oncogene. CONCLUSION: These results suggest that the expression of GHRH-R gene may not be an important determinant for tumor growth, and the lower GH response to GHRH of tumors with gsp oncogene may not be attributed to the lower expression of GHRH-R gene. The expression of GHRH-R is likely to be regulated by a certain property of tumors for GH secretion and growth.
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