The Vanderbilt Mouse Metabolic Phenotyping Center (VMMPC) was founded in 2001 to advance medical and biological research by providing the scientific community with standardized, high quality phenotyping services for mouse models of diabetes, diabetic complications, and obesity. The VMMPC consists of five cores. The Administrative Core provides scientific, financial, and administrative leadership. This Core also oversees service requests, data management, and tracks mice studied at the VMMPC. The Administrative Core is also responsible for the VMMPC educational program. The Animal Health and Welfare Core evaluates mice submitted to the VMMPC, oversees the health and welfare of the colony, and ensures compliance with regulatory bodies and MMPC guidelines. Services provided by the Metabolic Pathophysiology Core (MPC) emphasize methodology to study energy balance, insulin action, hormone secretion, and metabolism in the conscious, unstressed mouse. The MPC also has the capacity to assess organ or islet function in isolation and can apply state-of-the-art imaging techniques. The Cardiovascular Pathophysiology and Complications Core has a range of tests to study cardiovascular disease and other complications of diabetes. The Analytical Resources Core receives samples generated from VMMPC testing and from experiments conducted outside the VMMPC. Analyses performed by this core are specific to the mouse and are scaled to accommodate small sample volumes. The VMMPC exists because of the insight of leadership at the NIDDK, a generous commitment of space and resources from VUMC, and a well-conceived infrastructure. But the main reason the VMMPC works as well as it does is the people that comprise it. This NIDDK experiment in mouse phenotyping requires a faculty that is willing to make technology that is part of their research lifeline available to the scientific community for no more than the recovery of costs and the knowledge that they are working for a greater good. It requires a staff that is so skilled and committed that scientists are willing to entrust their mice, their research lifelines, with them.
Brown, Judy J; Short, Sarah P; Stencel-Baerenwald, Jennifer et al. (2018) Reovirus-Induced Apoptosis in the Intestine Limits Establishment of Enteric Infection. J Virol 92: |
Schlegel, Cameron; Lapierre, Lynne A; Weis, Victoria G et al. (2018) Reversible deficits in apical transporter trafficking associated with deficiency in diacylglycerol acyltransferase. Traffic 19:879-892 |
McClatchey, Penn Mason; Mignemi, Nicholas A; Xu, Zhengang et al. (2018) Automated quantification of microvascular perfusion. Microcirculation :e12482 |
Williams, Ian M; McClatchey, P Mason; Bracy, Deanna P et al. (2018) Acute Nitric Oxide Synthase Inhibition Accelerates Transendothelial Insulin Efflux In Vivo. Diabetes 67:1962-1975 |
Moore, Mary Courtney; Smith, Marta S; Farmer, Ben et al. (2018) Morning Hyperinsulinemia Primes the Liver for Glucose Uptake and Glycogen Storage Later in the Day. Diabetes 67:1237-1245 |
Cooke, Allison L; Morris, Jamie; Melchior, John T et al. (2018) A thumbwheel mechanism for APOA1 activation of LCAT activity in HDL. J Lipid Res 59:1244-1255 |
Moore, Mary Courtney; Kelley, David E; Camacho, Raul C et al. (2018) Superior Glycemic Control With a Glucose-Responsive Insulin Analog: Hepatic and Nonhepatic Impacts. Diabetes 67:1173-1181 |
Funkhouser-Jones, Lisa J; van Opstal, Edward J; Sharma, Ananya et al. (2018) The Maternal Effect Gene Wds Controls Wolbachia Titer in Nasonia. Curr Biol 28:1692-1702.e6 |
Wasserman, David H; Wang, Thomas J; Brown, Nancy J (2018) The Vasculature in Prediabetes. Circ Res 122:1135-1150 |
Huynh, Frank K; Hu, Xiaoke; Lin, Zhihong et al. (2018) Loss of sirtuin 4 leads to elevated glucose- and leucine-stimulated insulin levels and accelerated age-induced insulin resistance in multiple murine genetic backgrounds. J Inherit Metab Dis 41:59-72 |
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