Molecular endocrinology最新文献_第9页

Six. Change, Interchange, and the First Successful “Translators” 六。变化、交换与第一批成功的“译者”

Molecular endocrinology Pub Date : 2016-01-31 DOI: 10.7312/mend15860-010

Anne Mendelson

引用次数: 0

Three. “Celestials” on Gold Mountain 三。金山上的“天仙”

Molecular endocrinology Pub Date : 2016-01-31 DOI: 10.7312/mend15860-007

Anne Mendelson

引用次数: 0

Four. The Road to Chinatown 四。去唐人街的路

Molecular endocrinology Pub Date : 2016-01-31 DOI: 10.7312/mend15860-008

Anne Mendelson

引用次数: 0

Prologue: A Stroke of the Pen 序言:一笔一挥

Molecular endocrinology Pub Date : 2016-01-31 DOI: 10.7312/mend15860-004

Anne Mendelson

引用次数: 0

Two. The Culinary “Language” Barrier 两个。烹饪“语言”障碍

Molecular endocrinology Pub Date : 2016-01-31 DOI: 10.7312/mend15860-006

Anne Mendelson

引用次数: 0

A Note on Romanization and Terminology 关于罗马化和术语的说明

Molecular endocrinology Pub Date : 2016-01-31 DOI: 10.7312/mend15860-002

Anne Mendelson

引用次数: 0

Loss of Fatty Acid Binding Protein 4/aP2 Reduces Macrophage Inflammation Through Activation of SIRT3. 脂肪酸结合蛋白4/aP2的缺失通过激活SIRT3减少巨噬细胞炎症。

Molecular endocrinology Pub Date : 2016-01-21 DOI: 10.1210/me.2015-1301

Hongliang Xu, A. V. Hertzel, K. Steen, D. Bernlohr

{"title":"Loss of Fatty Acid Binding Protein 4/aP2 Reduces Macrophage Inflammation Through Activation of SIRT3.","authors":"Hongliang Xu, A. V. Hertzel, K. Steen, D. Bernlohr","doi":"10.1210/me.2015-1301","DOIUrl":"https://doi.org/10.1210/me.2015-1301","url":null,"abstract":"Activation of proinflammatory macrophages plays an important role in the pathogenesis of insulin resistance, type 2 diabetes, and atherosclerosis. Previous work using high fat-fed mice has shown that ablation of the adipocyte fatty acid binding protein (FABP4/aP2) in macrophages leads to an antiinflammatory state both in situ and in vivo, and the mechanism is linked, in part, to increased intracellular monounsaturated fatty acids and the up-regulation of uncoupling protein 2. Here, we show that loss of FABP4/aP2 in macrophages additionally induces sirtuin 3 (SIRT3) expression and that monounsaturated fatty acids (C16:1, C18:1) lead to increased SIRT3 protein expression. Increased expression of SirT3 in FABP4/aP2 null macrophages occurs at the protein level with no change in SirT3 mRNA. When compared with controls, silencing of SIRT3 in Raw246.7 macrophages leads to increased expression of inflammatory cytokines, inducible nitric oxide synthase and cyclooxygenase 2. In contrast, loss of SIRT3 in FABP4/aP2-deficient macrophages attenuates the suppressed inflammatory signaling, reduced reactive oxygen species production, lipopolysaccharide-induced mitochondrial dysfunction, and increased fatty acid oxidation. These results suggest that the antiinflammatory phenotype of FABP4/aP2 null mice is mediated by increased intracellular monounsaturated fatty acids leading to the increased expression of both uncoupling protein 2 and SirT3.","PeriodicalId":18812,"journal":{"name":"Molecular endocrinology","volume":"10 1","pages":"325-34"},"PeriodicalIF":0.0,"publicationDate":"2016-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1210/me.2015-1301","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66016519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 50

Puerarin Protects Pancreatic β-Cells in Obese Diabetic Mice via Activation of GLP-1R Signaling. 葛根素通过激活GLP-1R信号通路保护肥胖糖尿病小鼠胰腺β-细胞

Molecular endocrinology Pub Date : 2016-01-21 DOI: 10.1210/me.2015-1213

Lei Yang, D. Yao, Haiyuan Yang, Ying-jie Wei, Yunru Peng, Yongfang Ding, L. Shu

{"title":"Puerarin Protects Pancreatic β-Cells in Obese Diabetic Mice via Activation of GLP-1R Signaling.","authors":"Lei Yang, D. Yao, Haiyuan Yang, Ying-jie Wei, Yunru Peng, Yongfang Ding, L. Shu","doi":"10.1210/me.2015-1213","DOIUrl":"https://doi.org/10.1210/me.2015-1213","url":null,"abstract":"Diabetes is characterized by a loss and dysfunction of the β-cell. Glucagon-like peptide 1 receptor (GLP-1R) signaling plays an important role in β-cell survival and function. It is meaningful to identify promising agents from natural products which might activate GLP-1R signaling. In this study, puerarin, a diet isoflavone, was evaluated its beneficial effects on β-cell survival and GLP-1R pathway. We showed that puerarin reduced the body weight gain, normalized blood glucose, and improved glucose tolerance in high-fat diet-induced and db/db diabetic mice. Most importantly, increased β-cell mass and β-cell proliferation but decreased β-cell apoptosis were observed in puerarin-treated diabetic mice as examined by immunostaining of mice pancreatic sections. The protective effect of puerarin on β-cell survival was confirmed in isolated mouse islets treated with high glucose. Further mechanism studies showed that the circulating level of GLP-1 in mice was unaffected by puerarin. However, puerarin enhanced GLP-1R signaling by up-regulating expressions of GLP-1R and pancreatic and duodenal homeobox 1, which subsequently led to protein kinase B (Akt) activation but forkhead box O1 inactivation, and promoted β-cell survival. The protective effect of puerarin was remarkably suppressed by Exendin(9-39), an antagonist of GLP-1R. Our study demonstrated puerarin improved glucose homeostasis in obese diabetic mice and identified a novel role of puerarin in protecting β-cell survival by mechanisms involving activation of GLP-1R signaling and downstream targets.","PeriodicalId":18812,"journal":{"name":"Molecular endocrinology","volume":"30 3 1","pages":"361-71"},"PeriodicalIF":0.0,"publicationDate":"2016-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1210/me.2015-1213","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66016313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 58

SNARE-Mediated Cholesterol Movement to Mitochondria Supports Steroidogenesis in Rodent Cells. snare介导的胆固醇向线粒体的运动支持啮齿动物细胞的甾体生成。

Molecular endocrinology Pub Date : 2016-01-15 DOI: 10.1210/me.2015-1281

Ye Lin, Xiaoming Hou, W. Shen, R. Hanssen, V. Khor, Y. Cortez, A. Roseman, S. Azhar, F. Kraemer

{"title":"SNARE-Mediated Cholesterol Movement to Mitochondria Supports Steroidogenesis in Rodent Cells.","authors":"Ye Lin, Xiaoming Hou, W. Shen, R. Hanssen, V. Khor, Y. Cortez, A. Roseman, S. Azhar, F. Kraemer","doi":"10.1210/me.2015-1281","DOIUrl":"https://doi.org/10.1210/me.2015-1281","url":null,"abstract":"Vesicular transport involving soluble N-ethylmaleimide sensitive factor attachment protein receptor (SNARE) proteins is known to be responsible for many major cellular activities. In steroidogenic tissues, chronic hormone stimulation results in increased expression of proteins involved in the steroidogenic pathway, whereas acute hormone stimulation prompts the rapid transfer of cholesterol to the inner mitochondrial membrane to be utilized as substrate for steroid hormone production. Several different pathways are involved in supplying cholesterol to mitochondria, but mobilization of stored cholesteryl esters appears to initially constitute the preferred source; however, the mechanisms mediating this cholesterol transfer are not fully understood. To study the potential contribution of SNARE proteins in steroidogenesis, we examined the expression levels of various SNARE proteins in response to hormone stimulation in steroidogenic tissues and cells and established an in vitro mitochondria reconstitution assay system to assess the contribution of various SNARE proteins on cholesterol delivery for steroidogenesis. Our results from reconstitution experiments along with knockdown studies in rat primary granulosa cells and in a Leydig cell line show that soluble N-ethylmaleimide sensitive factor attachment protein-α, synaptosomal-associated protein of 25 kDa, syntaxin-5, and syntaxin-17 facilitate the transport of cholesterol to mitochondria. Thus, although StAR is required for efficient cholesterol movement into mitochondria for steroidogenesis, specific SNAREs participate and are necessary to mediate cholesterol movement to mitochondria.","PeriodicalId":18812,"journal":{"name":"Molecular endocrinology","volume":"68 1","pages":"234-47"},"PeriodicalIF":0.0,"publicationDate":"2016-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1210/me.2015-1281","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66016235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 32

Research Resource: Genetic Labeling of Human Islet Alpha Cells. 研究资源:人胰岛α细胞的遗传标记。

Molecular endocrinology Pub Date : 2016-01-08 DOI: 10.1210/me.2015-1220

P. Pauerstein, K. Park, H. Peiris, Jing Wang, Seung K. Kim

{"title":"Research Resource: Genetic Labeling of Human Islet Alpha Cells.","authors":"P. Pauerstein, K. Park, H. Peiris, Jing Wang, Seung K. Kim","doi":"10.1210/me.2015-1220","DOIUrl":"https://doi.org/10.1210/me.2015-1220","url":null,"abstract":"The 2 most abundant human pancreatic islet cell types are insulin-producing β-cells and glucagon-producing α-cells. Defined cis-regulatory elements from rodent Insulin genes have permitted genetic labeling of human islet β-cells, enabling lineage tracing and generation of human β-cell lines, but analogous elements for genetically labeling human α-cells with high specificity do not yet exist. To identify genetic elements that specifically direct reporter expression to human α-cells, we investigated noncoding sequences adjacent to the human GLUCAGON and ARX genes, which are expressed in islet α-cells. Elements with high evolutionary conservation were cloned into lentiviral vectors to direct fluorescent reporter expression in primary human islets. Based on the specificity of reporter expression for α- and β-cells, we found that rat glucagon promoter was not specific for human α-cells but that addition of human GLUCAGON untranslated region sequences substantially enhanced specificity of labeling in both cultured and transplanted islets to a degree not previously reported, to our knowledge. Specific transgene expression from these cis-regulatory sequences in human α-cells should enable targeted genetic modification and lineage tracing.","PeriodicalId":18812,"journal":{"name":"Molecular endocrinology","volume":"30 2 1","pages":"248-53"},"PeriodicalIF":0.0,"publicationDate":"2016-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1210/me.2015-1220","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66016414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6