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During the past funding cycle, the establishment of the services provided by the Cell Biology Core has fostered a large variety of research related to the Core Objectives. Cell Biological Studies related to the DRTC have expanded within the research community as evidenced by publications as well as grant applications from investigatoVs who traditionally do not work in the area of diabetes mellitus and metabolism. The adipose tissue bank and adipose biology expertise and service of the DRTC was transferred to operate under the auspices of the newly funded Mid-Atlantic nutrition and obesity research center (NORC) at the University of Maryland. This ensured a strengthening and continuity of adipose tissue related services to the DRTC community while freeing resources, which were used for innovation and expansion of services through the Cell Biology Core of the Baltimore DRTC. The Cell Biology Core started a local repository of transgenic mouse models of tissue/cell specific transgenic CRE -deleter ordoxycylcine regulatable mice. These well-characterized mice, in the C57BI/6 background, have become a valuable resource for the research community. Responding to investigators' needs as well as to pertinent questions related to metabolism and diabetes mellitus, the Cell Biology has expanded its services and expertise in the area of cellular bioenergetics and mitochondrial biology. This new addition will provide expertise and services to image and quantify mitochondrial content and mitochondrial shape and constellation, to assess mitochondrial dynamics (fusion and division), provide expertise in quantification of mitochondrial gene and protein expression (e.g. uncoupling proteins, complexes of the electron transfer chain) and cellular mitochondrial DNA content. In addition DRC users will gain access to unique genetic mouse models (e.g. floxed Drp1, floxeci Opal mice), which allow conditional tissue specific ablation of proteins involved in mitochondrial fusion and division and in mediating apoptosis in response to oxidative cellular stress.
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Mechanism of Defective Incretin Action in Beta Cells during Type 2 Diabetes Mellitus
Mechanism of Defective Incretin Action in Beta Cells during Type 2 Diabetes Mellitus
Mechanism of Defective Incretin Action in Beta Cells during Type 2 Diabetes Mellitus
In vivo Cell-Specific Exosome Analysis
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支链氨基酸代谢紊乱调控“Adipocytes - Macrophages Crosstalk”诱发2型糖尿病脂肪组织功能和结构障碍的作用及机制