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      • SCOPUSKCI등재

        다낭성 난소 증후군 환자에서 비만군과 비비만군에서의 인슐린 저항성

        임영구,이병석,조은정,차동현,박원일,박기현,조동제,이국,송찬호,이은직,Lim, Y.K.,Lee, B.S.,Cho, E.J.,Cha, D.H.,Park, W.I.,Park, K.H.,Cho, D.J.,Lee, K.,Song, C.H.,Lee, E.J. 대한생식의학회 1994 Clinical and Experimental Reproductive Medicine Vol.21 No.1

        This study was designed to investigate the relationship between insulin resistance and obesity in the pathogenesis of polycystic ovarian syndrome(PCO). Twenty-two women with PCO, of whom thirteen were non-obese with body mass index(BMI, kg/$m^2$) of <25 and nine were obese with BMI${\geq}$25 were studied. Eight non-obese control women and seven obese control women were studied. Serum concentrations of testosterone, lutenizing hormone(LH)/follicle-stimulating hormone(FSH) ratio, and insulin-like growth factor I (IGF-I) were found to be significantly higher(P<0.05) in PCO women compared with control women, which clearly is not related to obesity. Serum glucose, insulin, and C-peptide levels were measured during a 2-hour oral glucose tolerance test(OGTT). Non-obese and obese women with PCO both(P<0.05) compared with control women demonstrated significant hyperinsulinemia after OGTT. The degree of hyperinsulinemia was found to be significantly higher in the obese women with PCO compared with the non-obese women with PCO. We concluded that obesity may contribute to hyperinsulinemia, however may not playa central role in the pathogenesis of PCO.

      • KCI등재후보

        말단비대증 환자의 뇌하수체 종양조직에서 H - ras 유전자 변이의 가능성

        임승길(S . K . Lim),권이현(Y . H . Kwon),정윤석(Y . S . Chung),안광진(K . J . Ahn),이은직(E . J . Lee),김경래(K . R . Kim),이현철(H . C . Lee),허갑범(K . B . Huh),김태승(T . S . Kim) 대한내과학회 1993 대한내과학회지 Vol.45 No.3

        N/A Backround: Little is known about the mechanism of tumorigenesis in pituitary adenomas. An important finding in somatotroph adenomas is that a somatic mutation may convert a G protein, Gs(α) into a putative oncogene termed gsp via point mutations at two critcal sites. The ras protooncogenes are structurally related to the G-protein family and are involved in cell proliferation and differentiation. Although ras oncogene mutations have been indentified in a wide variety of human neoplasm, only one case was reported as containting single point mutation in a patient with invasive prolactinoma, In this report we used oligonucleotide-specific hybridization to screen ras mutations in 13 acromegalic tumors. Methods: Pituitary tissue samples were derived from a central portion of the paraffin embedded pituitary tumor to minimize the possibility of contamination with normal tissue. Genomic DNA was isolated and purified from tumor tissue and amplified by the standard PCR method. Amplified DNAs from each of the region of H-ras genes (12/13 and 61) were analyzed for potential ras mutations using oligonucleotide-specific hybridization as described previously. Results: Wild type radiolabelled oligoncleotides were hybridized to the amplified DNAs from the patients' tumor and to the positive specimens. They were, however, easily striped out at 68℃ by nonstringent washing procedures except control (wild type) specimens. All radiolabelled mutant oligonucleotides could be easily striped out of 13 specimens except a control mutant specimen by the same procedure. Conclusion: We could not find any H-ras mutation that might not be frequently found in acromegalic patients, and that gsp (Gsa mutation) or mutations in the PKA system-related proteins might be the main oncogene in acromegalic patients. However further efforts to find the other somatic mutations including K-ras and N-ras should be given to these patients for more precise understanding of pathogenesis and for planning of the better treatment.

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