Abstract

The overall purpose of this research project is to understand why individuals with infections receiving nutritional support develop hyperglycemia, and to determine what can be done to prevent this from occurring. The investigator uses a chronically catheterized conscious dog model, receiving continuous nutritional support. Infection is induced by implantation of a fibrinogen clot into the peritoneal cavity. There are three goals to this proposal: (1) to determine the impact of infection on hepatic glucose uptake and the influence of the route of nutrient delivery on this metabolism. (2) To determine the mechanism for the hyperglucagonemia and the role that excess glucagon and nitric oxide play in the metabolic response to nutrient support during infection. (3) To examine the influence of non glucose nutrients which may either exacerbate or correct the impairment in hepatic glucose disposal.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
5R01DK043748-08
Application #
2905447
Study Section
Nutrition Study Section (NTN)
Program Officer
Laughlin, Maren R
Project Start
1992-02-01
Project End
2001-04-30
Budget Start
1999-05-01
Budget End
2000-04-30
Support Year
8
Fiscal Year
1999
Total Cost
Indirect Cost

  Institution

Name
Vanderbilt University Medical Center
Department
Physiology
Type
Schools of Medicine
DUNS #
004413456
City
Nashville
State
TN
Country
United States
Zip Code
37212

  Publications

Rossi, Mario; Zhu, Lu; McMillin, Sara M et al. (2018) Hepatic Gi signaling regulates whole-body glucose homeostasis. J Clin Invest 128:746-759
Boortz, Kayla A; Syring, Kristen E; Pound, Lynley D et al. (2017) Effects of G6pc2 deletion on body weight and cholesterol in mice. J Mol Endocrinol 58:127-139
Boortz, Kayla A; Syring, Kristen E; Dai, Chunhua et al. (2016) G6PC2 Modulates Fasting Blood Glucose In Male Mice in Response to Stress. Endocrinology 157:3002-8
Syring, Kristen E; Boortz, Kayla A; Oeser, James K et al. (2016) Combined Deletion of Slc30a7 and Slc30a8 Unmasks a Critical Role for ZnT8 in Glucose-Stimulated Insulin Secretion. Endocrinology 157:4534-4541
Dooley, James; Garcia-Perez, Josselyn E; Sreenivasan, Jayasree et al. (2016) The microRNA-29 Family Dictates the Balance Between Homeostatic and Pathological Glucose Handling in Diabetes and Obesity. Diabetes 65:53-61
Boortz, Kayla A; Syring, Kristen E; Lee, Rebecca A et al. (2016) G6PC2 Modulates the Effects of Dexamethasone on Fasting Blood Glucose and Glucose Tolerance. Endocrinology 157:4133-4145
Otero, Yolanda F; Mulligan, Kimberly X; Barnes, Tammy M et al. (2016) Enhanced Glucose Transport, but not Phosphorylation Capacity, Ameliorates Lipopolysaccharide-Induced Impairments in Insulin-Stimulated Muscle Glucose Uptake. Shock 45:677-85
House 2nd, Lawrence M; Morris, Robert T; Barnes, Tammy M et al. (2015) Tissue inflammation and nitric oxide-mediated alterations in cardiovascular function are major determinants of endotoxin-induced insulin resistance. Cardiovasc Diabetol 14:56
Kolumam, Ganesh; Chen, Mark Z; Tong, Raymond et al. (2015) Sustained Brown Fat Stimulation and Insulin Sensitization by a Humanized Bispecific Antibody Agonist for Fibroblast Growth Factor Receptor 1/?Klotho Complex. EBioMedicine 2:730-43
Cyphert, Travis J; Morris, Robert T; House, Lawrence M et al. (2015) NF-?B-dependent airway inflammation triggers systemic insulin resistance. Am J Physiol Regul Integr Comp Physiol 309:R1144-52

Showing the most recent 10 out of 24 publications