Core--Phenotyping, Physiology, And Metabolism Core
Rexford S Ahima, Associate Professor
University Of Pennsylvania 3451 Walnut Street Philadelphia, Pa 19104
Grant 2P30DK019525-269011 from National Institute Of Diabetes And Digestive And Kidney Diseases IRG: ZDK1
Abstract: Diabetes is highly prevalent in the United States and is associated with increased morbidity from cardiovascular, renal, neurological and other complications. Our understanding of the pathogenesis of diabetes has benefited immensely from pharmacological, dietary and genetic manipulations in mice and other rodents. Despite the rapid increase in the use of gene targeting methodology to elucidate the molecular mechanisms mediating diabetes in mice, such efforts are often hampered by the absence of a clear phenotype. Failure to demonstrate a phenotype is attributable in part to the lack of expertise and/or facilities for evaluating physiologic and metabolic features in mice. We propose to establish a Mouse Phenotyping, Physiology and Metabolism Core, with the objective of providing investigators of the Penn Diabetes Center with state-of-the-art, timely and cost-effective diagnostic studies in mice. The core will offer services for analyzing glucose homeostasis, feeding behavior and energy balance, body composition, blood chemistry and hemodynamics. Activities of the core will be carried out by 2 technicians under the direction of Dr. Rex Ahima. The Phenotyping Core will maintain a databank of physiological, hormonal and metabolic measurements in mouse models of diabetes and obesity, and offer advice and training on various aspects of mouse physiology. Activities of the core will be coordinated with other core laboratories, Le Islet Cell Biology (Franz Matschinsky), Radioimmunoassay (Bryan Wolf), Transgenic and Chimeric (Nancy Cooke and Functional Genomics (Klaus Kaestner). These efforts will result in optimum data acquisition in diabetic mouse models, and facilitate the translation of ideas from the bench to mice and ultimately to humans.
Keywords: bioenergetics, biomedical facility, diabetes mellitus, glucose metabolism, phenotype, blood chemistry, blood glucose, body composition, hemodynamics, insulin, obesity, glucose clamp technique, glucose tolerance test, laboratory mouse, scintillation counter, telemetry, tissue /cell culture, transgenic animal
Project start date: 1977-03-01
Project end date: 2007-02-28
Sponsored Links Excellgen http://Excellgen.com
Grants awarded to Rexford S Ahima
CNS ACTION OF APPETITE SUPPRESSANT AMINOSTEROL
Rexford S Ahima, Assoc Professor A
University Of Pennsylvania, 3451 Walnut Street, Philadelphia, Pa 19104
Grant 3R01DK062348-06S1 from National Institute Of Diabetes And Digestive And Kidney Diseases
Abstract: This award is issued in response to Notice OD-09-060, Recovery Act Administrative Supplements Providing Summer Research Experiences for Students and Science Educators. The obesity epidemic has been linked to increasing incidence of diabetes, cardiovascular disease and other complications. Diet and exercise are essential to weight management; however, it is obvious that many patients would require drug treatment to achieve and maintain weight reduction. The goal of this grant is to understand the actions of a novel aminosterol, which we have found to potently decrease body weight. During the past 3 years, we have shown that the anti-obesity effect of MSI-1436 is mediated through inhibition of food intake as well as increased metabolic rate. Unlike other anorectics, a single intraperitoneal or intracerebroventricular (i.c.v.) injection of MSI-1436 decreases body weight for several days. Moreover, MSI-1436 stimulates insulin response and prevents steatosis. An intact leptin signaling is not critical to the action of MSI-1436, since this compound is effective in ob/ob and db/db mice, fa/fa rats, and diet-induced obese mice. In contrast, agouti (Ay/a) mice are less responsive to MSI-1436, suggesting that melanocortin (MC)3/4 receptors are crucial its action in the brain. MSI-1436 binds to hypothalamic and other brain areas which mediate energy balance, and strongly induces Fos-immunoreactivity in the paraventricular hypothalamic nucleus and to a lesser extent in the arcuate, ventromedial nuclei, central amygdala and nucleus solitarius. A CNS action of MSI-1436 is further evident by the suppression of agouti-related peptide (AGRP) and neuropeptide Y (NPY) in hypothalamus. Hence, we hypothesize that MSI-1436 regulates energy balance and glucose through similar hypothalamic circuits. Specific Aim 1 will investigate whether treatment with NPY or AGRP can reverse the effect of MSI-1436. Moreover, we will determine whether deletion of NPY, AGRP and MC4 receptor genes block the action of MSI-1436. Specific Aim 2 will investigate the roles of NPY, AGRP and MC4 receptor in mediating the effect of MSI-1436 on glucose. Specific Aim 3 will evaluate the effects of MSI-1436 on hypothalamic enzymes, i.e. AMP kinase and fatty acid synthase, implicated in energy homeostasis. Finally, specific Aim 4 will determine whether activation of hypothalamic AMP kinase is able to prevent the effect of MSI-1436, as has been shown for various anorectics. Understanding of the central neuronal actions MSI-1436 may elucidate novel targets for the treatment of obesity and related diseases
Keywords: ACTH-Releasing Factor; AMP Kinase; ATP-AMP Phosphotransferase; ATP-AMP Transphosphorylase; Adenylokinase; Adipose tissue; Adverse effects; Agonist; Amygdala; Amygdaloid Body; Amygdaloid Nucleus; Amygdaloid structure; Animals; Anorectic Drug; Anorectic agent; Anorectics; Anorexiant; Anorexic Drugs; Anorexient Agent; Anorexient Drug; Anorexigenic Drugs; Apnea, Sleep; Appetite; Appetite Depressants; Appetite Suppressants; Appetite-Depressing Drugs; Appetite-Suppressant Drugs; Applications Grants; Area; Arthritis; Attenuated; Autoregulation; Binding; Binding (Molecular Function); Body Weight decreased; Brain; CRF-41; CRH; Cancers; Cardiovascular Diseases; Cell Communication and Signaling; Cell Nucleus; Cell Signaling; Cholelithiasis; Common Rat Strains; Corticoliberin; Corticotropin-Releasing Factor; Corticotropin-Releasing Factor-41; Corticotropin-Releasing Hormone; Corticotropin-Releasing Hormone-41; D-Glucose; Data; Desire for food; Dextrose; Diabetes Mellitus; Diabetes Mellitus, Adult-Onset; Diabetes Mellitus, Ketosis-Resistant; Diabetes Mellitus, Non-Insulin-Dependent; Diabetes Mellitus, Noninsulin Dependent; Diabetes Mellitus, Slow-Onset; Diabetes Mellitus, Stable; Diabetes Mellitus, Type 2; Diabetes Mellitus, Type II; Diet; Drugs; Dysfunction; EC 2.3.1.85; Eating; Eels, Lamprey; Encephalon; Encephalons; Energy Expenditure; Energy Metabolism; Enzymes; Epidemic; Excess Mortality; FLR; Failure (biologic function); Fatty Acid Synthetase Complex; Fatty Liver; Fatty Tissue; Fatty-acid synthase; Food Intake; Functional disorder; Gallbladder Calculus; Gallbladder Stone; Gallstones; Genetic; Glucose; Goals; Grant; Grant Proposals; Grants, Applications; Heat Production; Hepatic Disorder; Homeostasis; Humulin R; Hyperlipemia; Hyperlipidemia; Hypothalamic structure; Hypothalamus; Incidence; Injection of therapeutic agent; Injections; Insulin; Insulin (ox), 8A-L-threonine-10A-L-isoleucine-30B-L-threonine-; Insulin, Regular; Intermediary Metabolism; Intracellular Communication and Signaling; Ion Channel; Ionic Channels; Lampreys; Lateral; Leptin; Life; Life Style; Lifestyle; Link; Lipids; Lipolysis; Liver; Liver Steatosis; Liver diseases; MC4 Receptor; METBL; MODY; MSI 1436; MSI1436; Malignant Neoplasms; Malignant Tumor; Mammals, Mice; Mammals, Rats; Mammals, Rodents; Maturity-Onset Diabetes Mellitus; Mediating; Medication; Melanocortin 4 Receptor; Membrane; Membrane Channels; Metabolic; Metabolic Processes; Metabolism; Metabolism, Lipids/Lipoproteins/Membrane Constituents; Mice; Molecular Interaction; Murine; Mus; Muscle; Muscle Tissue; Myokinase; NAFLD; NASH; NIDDM; Nerve Cells; Nerve Unit; Nervous System, Brain; Neural Cell; Neurocyte; Neurons; Neuropeptide Tyrosine; Non-Insulin Dependent Diabetes; Non-Insulin-Dependent Diabetes Mellitus; Non-alcoholic steatohepatitis; Novolin R; Nucleus; Nucleus Tractus Solitarii; Nucleus solitarius; Ob Gene Product; Ob Protein; Obese Gene Product; Obese Mice; Obese Protein; Obesity; Obesity associated disease; Obesity related disease; Paraventricular Hypothalamic Nucleus; Paraventricular Nucleus; Pathway interactions; Patients; Peptides; Peripheral; Petromyzontidae; Pharmaceutic Preparations; Pharmaceutical Preparations; Pheromone; Physiological Homeostasis; Physiopathology; Property; Property, LOINC Axis 2; Rat; Rattus; Receptor Gene; Receptor Protein; Receptor Signaling; Receptor, Melanocortin, Type 4; Risk; Rodent; Rodentia; Rodentias; Role; SHU 9119; SHU9119; Signal Transduction; Signal Transduction Systems; Signaling; Sleep Apnea Syndromes; Sleep Hypopnea; Sleep-Disordered Breathing; Solitary Nucleus; Starvation; Steroid Compound; Steroids; Structure of paraventricular nucleus; Surface; System; System, LOINC Axis 4; T2D; T2DM; Thermogenesis; Treatment Side Effects; Triacylglycerol; Triglycerides; Type 2 diabetes; Type II diabetes; United States; Weight; Weight Loss; Weight Reduction; Xenopus oocyte; adenylate kinase; adipose; adiposity; adult onset diabetes; amygdaloid nuclear complex; anorexic agent; arthritic; biological signal transduction; body system, hepatic; body weight loss; cardiovascular disorder; cholelith; corpulence; corpulency; corpulentia; corticotropin releasing hormone; db/db mouse; diabetes; diet and exercise; drug/agent; energy balance; failure; fat metabolism; fatty acid oxidation; feeding; food consumption; hepatic steatosis; hepatopathy; hypothalamic; immunoreactivity; improved; in vivo; insight; insulin sensitivity; insulin signaling; intraperitoneal; ketosis resistant diabetes; lipid metabolism; liver disorder; malignancy; maturity onset diabetes; membrane structure; neoplasm/cancer; neuronal; neuropeptide Y; non-alcohol fatty liver; non-alcohol induced steatohepatitis; non-alcoholic fatty liver; non-alcoholic steato-hepatitis; nonalcohol fatty liver; nonalcoholic fatty liver; nonalcoholic steato-hepatitis; nonalcoholic steatohepatitis; novel; ob/ob mouse; obese; obese people; obese person; obese population; obesity treatment; organ system, hepatic; paraventricular nucleus; pathophysiology; pathway; prevent; preventing; receptor; reproductive; response; sedentary; side effect; social role; solitary tract nucleus; therapy adverse effect; treatment adverse effect; white adipose tissue; wt-loss; yellow adipose tissue
Project start date: 2002-07-15
Project end date: 2011-05-31
Budget start date: 23-JUN-2009
Budget end date: 31-MAY-2011
3R01DK062348-06S1 (2009): $18270
5R01DK062348-03 (2004): $262516
3R01DK062348-07S1 (2010): $53158
5R01DK062348-08 (2010): $304169
5R01DK062348-07 (2009): $307242
5R01DK062348-06 (2008): $328725
5R01DK062348-05 (2007): $313512
2R01DK062348-04A1 (2006): $321850
2R56DK062348-04 (2005): $79250
CNS EFFECTS OF ADIPOKINES ON METABOLISM
Rexford S Ahima, Assoc Professor A
University Of Pennsylvania, 3451 Walnut Street, Philadelphia, Pa 19104
Abstract: Obesity has reached epidemic proportions and poses serious public health challenges, in particular type 2 diabetes, cardiovascular disease, sleep apnea, osteoarthritis and cancer. Adipocyte hormones may provide key insights into the pathogenesis of obesity-related diseases. Leptin and adiponectin stimulate fatty acid oxidation, decrease lipid levels and increase insulin sensitivity. In contrast, resistin decreases insulin sensitivity, and increases glucose and lipids. Leptin acts in the CMS to suppress appetite and increase energy expenditure, but also has direct effects on peripheral tissues. Adiponectin and resistin have direct actions on liver and muscle, but recent observations suggest that these adipokines also have central effects. We hypothesize that the divergent effects of these adipocytes on metabolism are mediated, at least in part, through distinct neuronal targets and signaling pathways in the hypothalamus. Specific Aim 1 will compare the effects of CMS administration of leptin, adiponectin and resistin on energy and glucose metabolism. We will examine the regulation of peripheral glucose fluxes using insulin clamp and radioactive tracer kinetics. Based on our preliminary studies showing an attenuation of the CMS effects of leptin and adiponectin in agouti mice, we will determine whether the opposite effects of leptin/adiponectin versus resistin on glucose levels is mediated through melanocortin (MC)4 receptor signaling. Specific Aim 2 will determine the sites of action of these adipocyte hormones in the hypothalamus, using Fos immunohistochemistry and in situ hybridization. Finally, Specific Aim 3 will determine whether the opposing metabolic effects of leptin, adiponectin and resistin occur through AMP-kinase and SOCS-3 in the hypothalamus. We will test the hypothesis that central administration of resistin antagonizes the central effects of leptin and adiponectin on metabolism, through reciprocal regulation of AMPK, SOC-3, or both signaling pathways. Understanding the hypothalamic and signaling pathways that mediate the effects of leptin, adiponctin and resistin will provide novel insights into the pathophysiology of obesity and diabetes that will facilitate novel diagnostic and treatment strategies
Keywords: (hydroxymethylglutaryl-CoA reductase (NADPH)) kinase; 5`-AMP-activated protein kinase; 5-Oxo-L-prolyl-L-histidyl-L-prolinamide; ACRP30 protein; ACTH-Releasing Factor; AMP Kinase; AMP-activated kinase; AMP-activated protein kinase; AMPK enzyme; ATP-AMP Phosphotransferase; ATP-AMP Transphosphorylase; Adenylokinase; Adipocytes; Adipose Cell; Apnea, Sleep; Appetite; Appetite stimulated; Arthritis, Degenerative; Attenuated; Body Tissues; CIS protein; CIS-1 Protein; CISH; CISH Protein; CRF-41; CRH; Cancers; Cardiovascular Diseases; Cell Communication and Signaling; Cell Signaling; Cell/Tissue, Immunohistochemistry; Chemicals; Chemotherapy-Hormones/Steroids; Corticoliberin; Corticotropin-Releasing Factor; Corticotropin-Releasing Factor-41; Corticotropin-Releasing Hormone; Corticotropin-Releasing Hormone-41; Cytokine Inducible SH2-Containing Protein; Cytokine-Inducible Inhibitor of Signaling Type 1B; D-Glucose; Data; Degenerative polyarthritis; Desire for food; Dextrose; Diabetes Mellitus; Diabetes Mellitus, Adult-Onset; Diabetes Mellitus, Ketosis-Resistant; Diabetes Mellitus, Non-Insulin-Dependent; Diabetes Mellitus, Noninsulin Dependent; Diabetes Mellitus, Slow-Onset; Diabetes Mellitus, Stable; Diabetes Mellitus, Type 2; Diabetes Mellitus, Type II; Disease; Disorder; Dysfunction; Endocrine Gland Secretion; Energy Expenditure; Energy Metabolism; Epidemic; Event; Fat Cells; Functional disorder; G18; Genetic; Genetics, in situ Hybridization; Glucose; HMG CoA reductase (NADPH) kinase; HMG CoA reductase kinase; HMG coenzyme A reductase (NADPH) kinase; Heat Production; Hormonal; Hormones; Humulin R; Hypothalamic structure; Hypothalamus; IHC; Immunohistochemistry; Immunohistochemistry Staining Method; In Situ Hybridization; Increased food appetite; Insulin; Insulin (ox), 8A-L-threonine-10A-L-isoleucine-30B-L-threonine-; Insulin Resistance; Insulin, Regular; Intermediary Metabolism; Intracellular Communication and Signaling; Kinetic; Kinetics; Leptin; Link; Lipids; Lipocytes; Lipolysis; Liver; MC4 Receptor; METBL; MODY; Malignant Neoplasms; Malignant Tumor; Mammals, Mice; Mature Lipocyte; Mature fat cell; Maturity-Onset Diabetes Mellitus; Mediating; Melanocortin 4 Receptor; Metabolic; Metabolic Processes; Metabolism; Mice; Morbidity; Morbidity - disease rate; Murine; Mus; Muscle; Muscle Tissue; Myokinase; NIDDM; Nerve Cells; Nerve Unit; Neural Cell; Neurocyte; Neurons; Neuropeptides; Non-Insulin Dependent Diabetes; Non-Insulin-Dependent Diabetes Mellitus; Novolin R; Nutrition; Nutritional Science; Ob Gene Product; Ob Protein; Obese Gene Product; Obese Protein; Obesity; Obesity associated disease; Obesity related disease; Osteoarthritis; Osteoarthrosis; Paraventricular Hypothalamic Nucleus; Paraventricular Nucleus; Pathogenesis; Pathway interactions; Peripheral; Phenotype; Physiopathology; Prevention strategy; Preventive strategy; Proteins; Protirelin; Protyreline; Public Health; Pyr-His-ProNH2; Radioactive Tracers; Receptor Signaling; Receptor, Melanocortin, Type 4; Regulation; SOCS; Science of nutrition; Signal Pathway; Signal Transduction; Signal Transduction Systems; Signaling; Site; Sleep Apnea Syndromes; Sleep Hypopnea; Sleep-Disordered Breathing; Structure of paraventricular nucleus; Suppressor of Cytokine Signaling; T2D; T2DM; TRH; Testing; Therapeutic Hormone; Thermogenesis; Thyroid-Releasing Hormone; Thyrotropin-Releasing Hormone; Tissues; Type 2 diabetes; Type II diabetes; United States; adenylate kinase; adipocyte complement-related protein 30-kDa; adipocyte, C1q and collagen domain containing protein; adipokines; adiponectin; adiposity; adult onset diabetes; apM-1 protein; apM1 (adipose-specific) protein; attenuation; base; biological signal transduction; blood glucose regulation; body system, hepatic; cardiovascular disorder; corpulence; corpulency; corpulentia; corticotropin releasing hormone; degenerative joint disease; diabetes; disease/disorder; energy balance; fatty acid oxidation; feeding; gene product; glucose control; glucose homeostasis; glucose metabolism; glucose regulation; hydroxymethylglutaryl-CoA-reductase kinase; hypertrophic arthritis; hypothalamic; immunoreactivity; in situ Hybridization Staining Method; increased appetite; increased hunger; innovate; innovation; innovative; insight; insulin resistant; insulin sensitivity; ketosis resistant diabetes; malignancy; maturity onset diabetes; neoplasm/cancer; neuronal; new diagnostics; next generation diagnostics; novel; novel diagnostics; nutrition; ob/ob mouse; obese; obese people; obese person; obese population; organ system, hepatic; paraventricular nucleus; pathophysiology; pathway; public health medicine (field); resistin; treatment strategy
Budget start date: 1-SEP-2009
Budget end date: 31-AUG-2010
5P01DK049210-14_0012 (2009): $298301
Sponsored Links Excellgen http://Excellgen.com
MOUSE PHENOTYPING, PHYSIOLOGY, AND METABOLISM CORE
Rexford S Ahima, Assoc Professor A
University Of Pennsylvania, 3451 Walnut Street, Philadelphia, Pa 19104
Abstract: MOUSE PHENOTYPING, PHYSIOLOGY, AND METABOLISM CORE Director - R. Ahima Our understanding of the pathogenesis of diabetes has benefited from the use of gene targeting methodology in mice to elucidate molecular mechanisms. However, such efforts are often hampered by an absence of a clear metabolic phenotype. Failure to identify a phenotype may be due to lack of expertise and/or facilities for evaluating metabolic changes in mice. The Mouse Phenotyping, Physiology and Metabolism Core provides investigators of the Penn Diabetes and Endocrinology Research Center (DERC) with state-of-the-art, timely and cost-effective diagnostic studies in mice. The core offers consultation and experimental design, monitoring of feeding, energy expenditure and locomotor activity using the Comprehensive Laboratory Animal Monitoring System (CLAMS), treadmill exercise using the Oxymax system, and measurement of body composition using dual emission x-ray absorptiometry (DEXA) and carcass chemistry. Glucose homeostasis is assessed by oral or intraperitoneal (i.p.) glucose administration, and whole body insulin sensitivity by i.p. insulin injection. Insulin clamp and radioactive tracers are used to assess glucose fluxes and tissue specific glucose uptake. Studies in the core are performed by two research specialists under the direction of Rex Ahima. Future plans for the core include the use magnetic resonance (MRI) for measurement of water, lean and fat content, assessment of in vivo lipid kinetics, and employment of an additional technician to expedite services. The Mouse Phenotyping, Physiology and Metabolism Core will maintain a databank of metabolic and hormonal parameters in mouse models of diabetes and obesity, and coordinate its activities with other core laboratories, i.e. Islet Cell Biology (Franz Matschinsky), Radioimmunoassay/Biomarkers (Bryan Wolf; Muredach Reilly), Transgenic and Chimeric Mouse (Nancy Cooke), and Genomics and Gene Targeting Cores (Klaus Kaestner). These efforts will result in optimum data acquisition and metabolic phenotyping of mice, and facilitate the translation of ideas from the bench to mice, and ultimately to humans
Keywords: Animals, Laboratory; Arts; Body Composition; Body Tissues; Bone Tissue; Cellular biology; Chemicals; Chemistry; Consult; Consultations; Coupled; D-Glucose; Data; Data Banks; Data Bases; Data Collection; Databank, Electronic; Databanks; Database, Electronic; Databases; Dextrose; Diabetes Mellitus; Diabetic mouse; Diagnostic; Diagnostic Services; Diagnostic tests; Diet; Dose; Employment; Endocrinology; Energy Expenditure; Energy Metabolism; Ensure; Environmental Factor; Environmental Risk Factor; Equipment; Exercise; Exercise, Physical; Experimental Designs; FLR; Failure (biologic function); Fats; Fatty acid glycerol esters; Fee-for-Service Plans; Fees for Service; Funding; Funding Agency; Funding Source; Future; Gene Targeting; Genomics; Glucose; Home; Home environment; Hormonal; Housing; Human; Human Resources; Human, General; Humulin R; Hydrogen Oxide; Immunologic, Radioimmunoassay; Injection of therapeutic agent; Injections; Insulin; Insulin (ox), 8A-L-threonine-10A-L-isoleucine-30B-L-threonine-; Insulin Resistance; Insulin, Regular; Intermediary Metabolism; Intravenous; Investigators; Islet Cell; Kinetic; Kinetics; Knockout Mice; Laboratories; Laboratory Animals; Laboratory mice; Lipids; Locomotor Activity; METBL; MR Imaging; MR Tomography; MRI; Magnetic Resonance; Magnetic Resonance Imaging; Magnetic Resonance Imaging Scan; Mammals, Mice; Man (Taxonomy); Man, Modern; Manpower; Measurement; Measures; Medical Imaging, Magnetic Resonance / Nuclear Magnetic Resonance; Metabolic; Metabolic Processes; Metabolism; Metabolism and Endocrinology; Method LOINC Axis 6; Methodology; Mice; Mice, Knock-out; Mice, Knockout; Mice, Mutant Strains; Mice, Obese; Mission; Molecular; Monitor; Motor Activity; Murine; Mus; Muscle; Muscle Tissue; Mutant Strains Mice; NIH; NMR Imaging; NMR Tomography; National Institutes of Health; National Institutes of Health (U.S.); Neonatal; Novolin R; Nuclear Magnetic Resonance Imaging; Null Mouse; Obese Mice; Obesity; Operation; Operative Procedures; Operative Surgical Procedures; Oral; Oxygen Consumption; Pathogenesis; Pharmacological Treatment; Phenotype; Physiologic; Physiological; Physiology; Procedures; RIA; Radioactive Tracers; Radioimmunoassay; Research; Research Personnel; Researchers; Rest; Science of Chemistry; Screening procedure; Services; Specialist; Surgical; Surgical Interventions; Surgical Procedure; System; System, LOINC Axis 4; Targetings, Gene; Temperature; Testing; Tissues; Transgenic Organisms; Translations; United States National Institutes of Health; Water; Wolves; Zeugmatography; adiposity; biomarker; blood glucose regulation; cell biology; clinical data repository; clinical data warehouse; corpulence; corpulency; corpulentia; cost; data acquisition; data repository; design; designing; diabetes; diagnosis service; drinking; environmental risk; experiment; experimental research; experimental study; failure; feeding; glucose control; glucose homeostasis; glucose regulation; glucose uptake; in vivo; instrument; insulin resistant; insulin sensitivity; insulin tolerance; intraperitoneal; meetings; member; mouse model; mouse model of diabetes; mouse mutant; obese; obese people; obese person; obese population; personnel; phenome; relational database; research study; respiratory; screening; screenings; surgery; transgenic; web site
Budget start date: 1-APR-2010
Budget end date: 31-MAR-2011
5P30DK019525-34_9011 (2010): $218215
5P30DK019525-33_9011 (2009): $294586
MOUSE METABOLIC PHENOTYPING CORE
Rexford S Ahima, Assoc Professor A
University Of Pennsylvania, 3451 Walnut Street, Philadelphia, Pa 19104
Keywords: Abnormal Assessment of Metabolism; Animals, Laboratory; Arts; Atheroscleroses; Atherosclerosis; Atherosclerotic Cardiovascular Disease; Autoregulation; Body Composition; Body Tissues; Cellular biology; Cessation of life; Chemistry; Circadian Rhythms; Coupled; D-Glucose; Data; Data Banks; Data Bases; Data Collection; Databank, Electronic; Databanks; Database, Electronic; Databases; Death; Dextrose; Diabetes Mellitus; Diagnostic Services; Diagnostic tests; Diet; Disease; Disorder; Diurnal Rhythm; Endocrinology; Ensure; Equipment; Evaluation; Exercise; Exercise, Physical; Fatty Acids; Fatty Acids, sterified; Free Fatty Acids; Funding; Gender; Gene Copy Number; Gene Dosage; Gene Targeting; Generalized Growth; Genes; Genetic; Glucose; Growth; Heterozygote; Home; Home environment; Homeostasis; Housing; Human Resources; Humulin R; Hyperglyceridemia; Hypertriglyceridemia; INSR; Immunologic, Radioimmunoassay; Insulin; Insulin (ox), 8A-L-threonine-10A-L-isoleucine-30B-L-threonine-; Insulin Receptor; Insulin Receptor Protein-Tyrosine Kinase; Insulin, Regular; Insulin-Dependent Tyrosine Protein Kinase; Intermediary Metabolism; Investigators; Islet Cell; Knock-out; Knockout; Laboratories; Laboratory Animals; Lipids; Location; Locomotor Activity; METBL; Maintenance; Maintenances; Mammals, Mice; Manpower; Measurement; Metabolic; Metabolic Processes; Metabolic Studies; Metabolism; Metabolism Studies; Metabolism and Endocrinology; Mice; Monitor; Motor Activity; Mouse Strains; Murine; Mus; Muscle; Muscle Tissue; Muscle, Skeletal; Muscle, Voluntary; Neonatal; sterified Fatty Acids; Novolin R; Nutrition; Nutritional Science; Nyctohemeral Rhythm; Obesity; P-30; P-30 Protein; P30; P30 Protein; Pathogenesis; Phenotype; Phosphorylation; Physiologic; Physiological; Physiological Homeostasis; Procedures; Protein Phosphorylation; Quality Control; RIA; Radioimmunoassay; Raised TG; Raised triglycerides; Research; Research Personnel; Research Resources; Researchers; Resources; Salaries; Science of Chemistry; Science of nutrition; Services; Skeletal Muscle Tissue; Skeletal muscle structure; Stress; Study models; System; System, LOINC Axis 4; Targetings, Gene; Technology; Telemetries; Telemetry; Temperature; Tissue Growth; Tissues; Training; Transgenic Organisms; Triglyceride increased; Triglycerides high; Twenty-Four Hour Rhythm; Wages; adiposity; atheromatosis; atherosclerotic vascular disease; blood glucose regulation; cell biology; circadian; circadian process; clinical data repository; clinical data warehouse; corpulence; corpulency; corpulentia; cost; daily biorhythm; data repository; design; designing; diabetes; diagnosis service; disease/disorder; diurnal variation; drinking; elevated tg; elevated triglyceride; energy balance; experiment; experimental research; experimental study; feeding; functional genomics; glucose control; glucose disposal; glucose homeostasis; glucose regulation; glucose tolerance; glucose uptake; in vivo; insulin stimulated glucose disposal; lipoprotein disorder; metabolic abnormality assessment; nutrition; obese; obese people; obese person; obese population; ontogeny; personnel; phenome; ranpirnase; relational database; research study; square foot; transgenic
Budget start date: 1-SEP-2009
Budget end date: 31-AUG-2010
5P01DK049210-14_9004 (2009): $74579
MOUSE PHENOTYPING, PHYSIOLOGY, AND METABOLISM CORE
Rexford S Ahima, Associate Professor
University Of Pennsylvania
3451 Walnut Street
philadelphia, Pa 19104
Grant 5P30DK019525-329011 from National Institute Of Diabetes And Digestive And Kidney Diseases IRG: ZDK1
Keywords: metabolism, physiology
MOUSE METABOLIC PHENOTYPING CORE
Rexford S Ahima, Associate Professor
University Of Pennsylvania
3451 Walnut Street
philadelphia, Pa 19104
Grant 5P01DK049210-129004 from National Institute Of Diabetes And Digestive And Kidney Diseases IRG: ZDK1
Keywords: biomedical facility, metabolism, phenotype laboratory mouse
Project start date: 2007-09-01
Project end date: 2011-08-31