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Effects of growth hormone on insulin resistance and atherosclerotic risk factors in obese type 2 diabetic patients with poor glycaemic control

DC Field Value Language
dc.contributor.author강은석-
dc.contributor.author김경래-
dc.contributor.author박종숙-
dc.contributor.author안철우-
dc.contributor.author이현철-
dc.contributor.author임승길-
dc.contributor.author차봉수-
dc.date.accessioned2015-06-10T11:54:19Z-
dc.date.available2015-06-10T11:54:19Z-
dc.date.issued2006-
dc.identifier.issn0300-0664-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/108833-
dc.description.abstractOBJECTIVE: We aimed to evaluate the combined effects of GH treatment and diet restriction on lipolysis and anabolism, insulin resistance and atherosclerotic risk factors in obese patients with type 2 diabetes mellitus (T2DM). SUBJECTS: This randomized, double-blind, placebo-controlled study included 24 obese T2DM patients (male : female = 12 : 12, mean age 53.7 +/- 7.2 years) with poor glycaemic control (fasting plasma glucose 10.673 +/- 1.121 mmol/l, HbA(1C) 9.9 +/- 2.3%). Sixteen of these patients were treated with recombinant human GH (1-1.5 units/day, 5 days/week) while undergoing diet restriction and exercise for 12 weeks. METHODS: Anthropometric and bioelectrical impedance measurements were undertaken to determine the lean body mass and total body fat. Computed tomography (CT) was performed to estimate visceral and subcutaneous fat distribution at the umbilicus level and the muscle area of the midthigh. Insulin resistance was measured by the insulin tolerance test (ITT) and by the homeostasis model assessment of insulin resistance (HOMA-IR). RESULTS: The ratios VSR (visceral fat area/subcutaneous fat area) and VMR (visceral fat area/thigh muscle area) were significantly decreased in the GH-treated group compared to the control group. An increase in lean body mass was observed in the GH-treated group. Levels of total cholesterol, triglyceride, free fatty acid (FFA), fibrinogen, and plasminogen activator inhibitor-1 (PAI-1) were significantly decreased after GH treatment. Fasting glucose levels decreased similarly (P < 0.05 anova) in both groups during the treatment period. Fasting C-peptide levels significantly increased, whereas insulin levels significantly decreased, in the GH-treated group, but no changes were observed in the control group. The insulin sensitivity index (ISI) was significantly increased in the GH-treated group (1.3 +/- 1.4 vs. 1.9 +/- 1.0%/min, P < 0.05). CONCLUSIONS: GH treatment in obese T2DM patients with poor glycaemic control is beneficial in decreasing the amount of visceral fats, and may therefore result in improvements in insulin resistance, atherosclerotic risk factors and dyslipidaemia.-
dc.description.statementOfResponsibilityopen-
dc.format.extent444~449-
dc.relation.isPartOfCLINICAL ENDOCRINOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnalysis of Variance-
dc.subject.MESHAtherosclerosis/prevention & control-
dc.subject.MESHDiabetes Mellitus, Type 2/blood-
dc.subject.MESHDiabetes Mellitus, Type 2/drug therapy*-
dc.subject.MESHDiabetes Mellitus, Type 2/pathology-
dc.subject.MESHDouble-Blind Method-
dc.subject.MESHFemale-
dc.subject.MESHHormone Replacement Therapy*-
dc.subject.MESHHuman Growth Hormone/therapeutic use*-
dc.subject.MESHHumans-
dc.subject.MESHInsulin Resistance*-
dc.subject.MESHIntra-Abdominal Fat/pathology-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHObesity/blood-
dc.subject.MESHObesity/drug therapy*-
dc.subject.MESHObesity/pathology-
dc.subject.MESHRisk Factors-
dc.subject.MESHStatistics, Nonparametric-
dc.subject.MESHSubcutaneous Fat/pathology-
dc.titleEffects of growth hormone on insulin resistance and atherosclerotic risk factors in obese type 2 diabetic patients with poor glycaemic control-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorChul Woo Ahn-
dc.contributor.googleauthorChul Sik Kim-
dc.contributor.googleauthorJae Hyun Nam-
dc.contributor.googleauthorHai Jin Kim-
dc.contributor.googleauthorJi Sun Nam-
dc.contributor.googleauthorJong Suk Park-
dc.contributor.googleauthorEun Seok Kang-
dc.contributor.googleauthorBong Soo Cha-
dc.contributor.googleauthorSung Kil Lim-
dc.contributor.googleauthorKyung Rae Kim-
dc.contributor.googleauthorHyun Chul Lee-
dc.contributor.googleauthorKap Bum Huh-
dc.identifier.doi10.1111/j.1365-2265.2006.02490.x-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00068-
dc.contributor.localIdA00294-
dc.contributor.localIdA02270-
dc.contributor.localIdA03301-
dc.contributor.localIdA03375-
dc.contributor.localIdA03996-
dc.contributor.localIdA01660-
dc.relation.journalcodeJ00571-
dc.identifier.eissn1365-2265-
dc.identifier.pmid16584518-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1111/j.1365-2265.2006.02490.x/abstract-
dc.contributor.alternativeNameKang, Eun Seok-
dc.contributor.alternativeNameKim, Kyung Rae-
dc.contributor.alternativeNamePark, Jong Suk-
dc.contributor.alternativeNameAhn, Chul Woo-
dc.contributor.alternativeNameLee, Hyun Chul-
dc.contributor.alternativeNameLim, Sung Kil-
dc.contributor.alternativeNameCha, Bong Soo-
dc.contributor.affiliatedAuthorKang, Eun Seok-
dc.contributor.affiliatedAuthorKim, Kyung Rae-
dc.contributor.affiliatedAuthorAhn, Chul Woo-
dc.contributor.affiliatedAuthorLee, Hyun Chul-
dc.contributor.affiliatedAuthorLim, Sung Kil-
dc.contributor.affiliatedAuthorCha, Bong Soo-
dc.contributor.affiliatedAuthorPark, Jong Suk-
dc.rights.accessRightsnot free-
dc.citation.volume64-
dc.citation.number4-
dc.citation.startPage444-
dc.citation.endPage449-
dc.identifier.bibliographicCitationCLINICAL ENDOCRINOLOGY, Vol.64(4) : 444-449, 2006-
dc.identifier.rimsid49905-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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