Previously known as the Mouse Phenotyping Core of the Washington University DRTC, the Diabetes Models Phenotyping Core of the DRC provides specialzed technical services and expertise to DRC members in order to enhance their productivity, increase their efficiency, and promote interactive multidisciplinary research. The Core pursues three overarching objectives: 1) To provide phenotyping services to DRC members to facilitate NIH funded diabetes /metabolism-related research and enhance the cost-effectiveness of that research;2) To train DRC investigators in the maintenance and manipulation of mouse colonies relevant to diabetes and metabolic research;3) To develop new research capabilities to enhance the ability of DRC members to perform diabetes and metabolic research. The Core has been extremely successful at achieving these objectives. During the previous period of support by NIH, 33 different diabetes-related laboratories utilized Core services. In terms of the three services in most demand by our members, the Core performed more than 32,000 biochemical analyses of mouse serum, more than 2,700 body compositions in mice, and more than 3,200 biochemical analyses of tissues. Training is critical to the mission of the Core, and more than 100 clock hours of consultation were provided to members of 15 different DRC laboratories during the previous period of support. Core services evolve based on DRC needs, and we are in the process of establishing in vivo imaging of living mice as a new core service. Since 2007, this Core has supported high impact research relevant to type 1 diabetes, type 2 diabetes, cardiovascular complications of diabetes, lipid mediators of the pathophysiology of diabetes syndromes, and microbiota impacting diabetes phenotypes. Several of these observations have provided the conceptual framework for translational studies in humans with the potential to treat diabetes and its complications.
Diabetes is one of the most serious public health problems in America, both type 1 and type 2 diabetes are increasing in prevalence, and therapeutic options for diabetes and its complications are limited. This Core provides services with the potential to identify novel strategies with the potential to lead to new diabetes treatments.
|Burman, Blaire E; Bacchetti, Peter; Khalili, Mandana (2016) Moderate Alcohol Use and Insulin Action in Chronic Hepatitis C Infection. Dig Dis Sci 61:2417-25|
|Chondronikola, M; Harris, L L S; Klein, S (2016) Bariatric surgery and type 2 diabetes: are there weight loss-independent therapeutic effects of upper gastrointestinal bypass? J Intern Med 280:476-486|
|Rhee, Julie S; Saben, Jessica L; Mayer, Allyson L et al. (2016) Diet-induced obesity impairs endometrial stromal cell decidualization: a potential role for impaired autophagy. Hum Reprod 31:1315-26|
|Siller, Alejandro F; Lugar, Heather; Rutlin, Jerrel et al. (2016) Severity of clinical presentation in youth with type 1 diabetes is associated with differences in brain structure. Pediatr Diabetes :|
|Lin, Jonathan B; Kubota, Shunsuke; Ban, Norimitsu et al. (2016) NAMPT-Mediated NAD(+) Biosynthesis Is Essential for Vision In Mice. Cell Rep 17:69-85|
|Jarad, George; Knutsen, Russell H; Mecham, Robert P et al. (2016) Albumin contributes to kidney disease progression in Alport syndrome. Am J Physiol Renal Physiol 311:F120-30|
|Westbroek, Wendy; Nguyen, Matthew; Siebert, Marina et al. (2016) A new glucocerebrosidase-deficient neuronal cell model provides a tool to probe pathophysiology and therapeutics for Gaucher disease. Dis Model Mech 9:769-78|
|Merriwether, Ericka N; Hastings, Mary K; Bohnert, Kathryn L et al. (2016) Impact of foot progression angle modification on plantar loading in individuals with diabetes mellitus and peripheral neuropathy. Edorium J Disabil Rehabil 2:15-23|
|Chowdhury, Sara; Wang, Songyan; Dunai, Judit et al. (2016) Hormonal Responses to Cholinergic Input Are Different in Humans with and without Type 2 Diabetes Mellitus. PLoS One 11:e0156852|
|Zou, Wei; Rohatgi, Nidhi; Chen, Timothy Hung-Po et al. (2016) PPAR-Î³ regulates pharmacological but not physiological or pathological osteoclast formation. Nat Med 22:1203-1205|
Showing the most recent 10 out of 487 publications