Metabolic dysregulation is central to the pathogenesis of diabetes and obesity. The Metabolic Pathophysiology Core (MPC) provides services to comprehensively phenotype metabolic processes in mouse models. The MPC has three Subcores: Metabolic Regulation, Tissue and In Vivo Imaging and Bariatric Surgery. The Metabolic Regulation Subcore provides tools to accurately assess metabolism in healthy, conscious, unstressed mice. This Subcore uses unique skills in chronically implanting catheters into the carotid artery and jugular vein to perform glucose clamps in the mouse. In addition, it has developed techniques to catheterize the portal vein and stomach to deliver hormones and nutrients by their physiologic routes. This Subcore also provides services to assess the components of energy balance (energy expenditure, food intake, activity, body composition). The MPC provides not only standardized tests for metabolic and endocrine assessments, but is also able to adapt using more sophisticated protocols. Additional services include in vitro organ perfusion techniques (liver, pancreas, hindlimb). It partners with VDRTC Islet Procurement and Analysis Core to provide high quality islets to investigators as well as tools to characterize islet function. The Tissue and In Vivo Imaging Subcore offers novel imaging technology to study metabolic processes in real time at the molecular level. Resources ofthis Subcore include: 1) a multi-photon excitation confocal microscope to visualize real time kinetics of calcium, NAD(P)H, and pH and fluorescent probes in cells and in situ whole organ preparations;and 2) bioluminescence imaging, to assay real-time kinetics of gene expression in intact mice by combining luciferase as a reporter gene with a highly sensitive optical single photon detection system. The Bariatric Surgery Subcore provides mice with restrictive or bypass surgical procedures that recapitulate the surgical procedures performed in humans for weight loss. The MPC, by virtue of its novel subcores, provides state-of-the-art technology to delineate the mechanism for the phenotypic expression of metabolic disorders in mice.
This core provides services to investigators to help them quantify the impact of a genetic or pharmacologic manipulation on metabolic and endocrine processes in mice with the hope of helping them discover how to cure metabolic disease such as obesity and diabetes.
|Gupta, Madhu; Solanki, Malvika H; Chatterjee, Prodyot K et al. (2014) Maternal magnesium deficiency in mice leads to maternal metabolic dysfunction and altered lipid metabolism with fetal growth restriction. Mol Med 20:332-40|
|Kang, Li; Mayes, Wesley H; James, Freyja D et al. (2014) Matrix metalloproteinase 9 opposes diet-induced muscle insulin resistance in mice. Diabetologia 57:603-13|
|Barnes, Tammy M; Otero, Yolanda F; Elliott, Amicia D et al. (2014) Interleukin-6 amplifies glucagon secretion: coordinated control via the brain and pancreas. Am J Physiol Endocrinol Metab 307:E896-905|
|Babaev, Vladimir R; Hebron, Katie E; Wiese, Carrie B et al. (2014) Macrophage deficiency of Akt2 reduces atherosclerosis in Ldlr null mice. J Lipid Res 55:2296-308|
|Patel, Manishkumar; Gleason, Alexa; O'Malley, Stacey et al. (2014) Non-invasive bioluminescence imaging of ?-cell function in obese-hyperglycemic [ob/ob] mice. PLoS One 9:e106693|
|Cordoba-Chacon, Jose; Gahete, Manuel D; McGuinness, Owen P et al. (2014) Differential impact of selective GH deficiency and endogenous GH excess on insulin-mediated actions in muscle and liver of male mice. Am J Physiol Endocrinol Metab 307:E928-34|
|Lee, Stacey; Page-McCaw, Patrick; Gamse, Joshua T (2014) Kctd12 and Ulk2 partner to regulate dendritogenesis and behavior in the habenular nuclei. PLoS One 9:e110280|
|Zhu, Lin; Martinez, Melissa N; Emfinger, Christopher H et al. (2014) Estrogen signaling prevents diet-induced hepatic insulin resistance in male mice with obesity. Am J Physiol Endocrinol Metab 306:E1188-97|
|Huang, Xuan; Hernandez, Ciria C; Hu, Ningning et al. (2014) Three epilepsy-associated GABRG2 missense mutations at the ?+/?- interface disrupt GABAA receptor assembly and trafficking by similar mechanisms but to different extents. Neurobiol Dis 68:167-79|
|Freeman, Megan Culler; Graham, Rachel L; Lu, Xiaotao et al. (2014) Coronavirus replicase-reporter fusions provide quantitative analysis of replication and replication complex formation. J Virol 88:5319-27|
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