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- 저자 : Olefsky, Jerrold M (검색결과 4 건)
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Lim, T. J.,Upadhyay, A. K.,Moossa, A. R.,Kassir, A. A.,Olefsky, J. M. 啓明大學校 醫科大學 1991 계명의대학술지 Vol.10 No.1
Peptide의 일종인 IAPP (islet associated polypoptide)의 gloucose metabolism에 대한 영향을 관찰하기 위해 8마리의 성숙한 잡종개를 사용 동물실험을 하여 다음과 같은 결론을 얻었다. 의식이 있는 개에서 5-50pmol/kg/mim의 IAPP의 infusion으로 순환 IAPP치가 basal보다 12-50배 상승을 보였다. 실험중 IAPP치가 glucose 또는 insulin homeostasis에 대해서는 영향을 미치지 않았다. IAPP의 정맥주사로 혈장 칼슘농도는 신속한 감소를 보였다. In this study we have administered constant intravenous infusions of IAPP, to conscious dogs during the euglycemic glucose clamp setting. The doses of IAPP used (5 and 50 pmol/kg/min) raised the circulating IAPP levels approxomately 12-fold and 50-fold above basal, respectively. Studies were conducted at two differnet insulin infusion rates, resulting in steady state plasma insulin levels of ∼610 and 2600 pmol. our results showed that the IAPP infusions did not lead to any measurable change in the insulin stimulated glucose disposal rate, at either insulin infusion rate. Additionally, no effect of IAPP on hepatic glucose production was observed. Intravenous glucose tolerance tests were also performed with and without a concomitant IAPP infusion and we found that IAPP had no influence on the glucose profile. Aithough we could not observe any effect of IAPP on any of the measured aspects of glucose or insulin metabolism, we did find a consistent hypocalcemic effect of this perptide. Shortly after the onset if IAPP on any of the measured aspects of glucose or insulin metabolism, we did find a consistent hypocalcemic effect of this peptide. Shortly after the onset of IAPP infusion. serum calcium levels fell by 10-15% and remained at these levels throughout the coures of the IAPP infusion. In summary: (1) infusion of IAPP at doses of 5 or 50 pmol/kg/min in conscious dogs raises the circulating IAPP level 12-to 50-fold above basal (2) During these infusion studies, no effect of IAPP was observed on any of the measured aspectes of glucose or insulin homeostasis. (3) IAPP leads to a prompt reduction in plasma calcium concentrations upon intravenous administration.
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Suppression of Egr-1 transcription through targeting of the serum response factor by oncogenic H-Ras
Shin, Soon Young,Bahk, Young Yil,Ko, Jesang,Chung, Il-Yup,Lee, Young Seek,Downward, Julian,Eibel, Hermann,Sharma, Prem M,Olefsky, Jerrold M,Kim, Young-Ho,Lee, Bonghee,Lee, Young Han Wiley (John WileySons) 2006 The EMBO journal Vol.25 No.5
<P>The transcription factor Egr-1 functions as a key regulator in cellular growth, differentiation, and apoptosis. The loss of Egr-1 expression is closely associated with tumor development, although the molecular mechanism behind the suppression of Egr-1 is largely unknown. In this report, we show that growth factor-induced transcriptional activation of Egr-1 gene is downregulated by chronic expression of oncogenic H-Ras in NIH3T3 fibroblasts. Our results demonstrate that phosphoinositide 3-kinase (PI3K) signaling is necessary for oncogenic H-Ras-mediated reduction of Egr-1 gene expression. Aberrant activation of PI3K signaling by oncogenic Ras decreased the level of serum response factor (SRF) protein through the acceleration of proteolysis, which resulted in decreased SRF binding to the serum response element (SRE) sites within the Egr-1 promoter, leading to the suppression of Egr-1 transcription. Inhibition of PI3K signaling restored the downregulation of SRF and Egr-1 expression caused by oncogenic Ras. Our findings suggest a novel signaling mechanism by which prolonged activation of oncogenic H-Ras can trigger the loss of tumor suppressor Egr-1 through the PI3K pathway in NIH3T3 fibroblast model cell lines.</P>
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Inflammation Is Necessary for Long-Term but Not Short-Term High-Fat Diet–Induced Insulin Resistance
Lee, Yun Sok,Li, Pingping,Huh, Jin Young,Hwang, In Jae,Lu, Min,Kim, Jong In,Ham, Mira,Talukdar, Saswata,Chen, Ai,Lu, Wendell J.,Bandyopadhyay, Guatam K.,Schwendener, Reto,Olefsky, Jerrold,Kim, Jae Bum American Diabetes Association 2011 Diabetes Vol.60 No.10
<P><B>OBJECTIVE</B></P><P>Tissue inflammation is a key factor underlying insulin resistance in established obesity. Several models of immuno-compromised mice are protected from obesity-induced insulin resistance. However, it is unanswered whether inflammation triggers systemic insulin resistance or vice versa in obesity. The purpose of this study was to assess these questions.</P><P><B>RESEARCH DESIGN AND METHODS</B></P><P>We fed a high-fat diet (HFD) to wild-type mice and three different immuno-compromised mouse models (lymphocyte-deficient Rag1 knockout, macrophage-depleted, and hematopoietic cell-specific Jun NH<SUB>2</SUB>-terminal kinase–deficient mice) and measured the time course of changes in macrophage content, inflammatory markers, and lipid accumulation in adipose tissue, liver, and skeletal muscle along with systemic insulin sensitivity.</P><P><B>RESULTS</B></P><P>In wild-type mice, body weight and adipose tissue mass, as well as insulin resistance, were clearly increased by 3 days of HFD. Concurrently, in the short-term HFD period inflammation was selectively elevated in adipose tissue. Interestingly, however, all three immuno-compromised mouse models were not protected from insulin resistance induced by the short-term HFD. On the other hand, lipid content was markedly increased in liver and skeletal muscle at day 3 of HFD.</P><P><B>CONCLUSIONS</B></P><P>These data suggest that the initial stage of HFD-induced insulin resistance is independent of inflammation, whereas the more chronic state of insulin resistance in established obesity is largely mediated by macrophage-induced proinflammatory actions. The early-onset insulin resistance during HFD feeding is more likely related to acute tissue lipid overload.</P>
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