| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 The Mary Nell and Ralph B. Rogers Magnetic Resonance Center, Department of Radiology, University of Texas Southwestern Medical Center, Dallas, TX, USA
2 The Mary Nell and Ralph B. Rogers Magnetic Resonance Center, Department of Radiology, University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Chemistry, University of Texas at Dallas, Richardson, TX, USA
3 The Mary Nell and Ralph B. Rogers Magnetic Resonance Center, Department of Radiology, University of Texas Southwestern Medical Center, Dallas, TX, USA; VA North Texas Health Care System, Dallas, TX, USA
* To whom correspondence should be addressed. E-mail: eunsook.jin{at}utsouthwestern.edu.
The metabolic mechanism of hepatic glucose overproduction was investigated in 3,3'-5-triiodo-L-thyronine(T3)-treated rats and Zucker diabetic fatty (ZDF) rats (fa/fa) after a 24 hr fast. 2H2O and [U-13C3]propionate were administered i.p. and [3,4-13C2]glucose was administered as a primed infusion for 90 min under ketamine/xylazine anesthesia. 13C NMR analysis of monoacetone glucose derived from plasma glucose indicated that hepatic glucose production was 2-fold higher in both T3-treated rats and ZDF rats compared to controls yet the sources of glucose overproduction differed significantly in the two models by 2H NMR analysis. In T3-treated rats, the hepatic glycogen content and hence the contribution of glycogenolysis to glucose production was essentially zero; in this case, excess glucose production was due to a dramatic increase in gluconeogenesis from TCA cycle intermediates. 13C NMR analysis also revealed increased PEPCK flux (4x), increased pyruvate cycling flux (4x), and increased TCA flux (5x) in T3-treated animals. ZDF rats had substantial glycogen stores after a 24 hr fast and consequently nearly 50% of plasma glucose originated from glycogenolysis; other fluxes related to the TCA cycle were not different from controls. The differing mechanisms of excess glucose production in these models were easily distinguished by integrated 2H and 13C NMR analysis of plasma glucose.
This article has been cited by other articles:
|
|
 |
|
  S. Kley, M. Hoenig, J. Glushka, E. S. Jin, S. C. Burgess, M. Waldron, E. T. Jordan, J. H. Prestegard, D. C. Ferguson, S. Wu, et al. The impact of obesity, sex, and diet on hepatic glucose production in cats Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2009; 296(4): R936 - R943. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Satapati, T. He, T. Inagaki, M. Potthoff, M. E. Merritt, V. Esser, D. J. Mangelsdorf, S. A. Kliewer, J. D. Browning, and S. C. Burgess Partial Resistance to Peroxisome Proliferator-Activated Receptor-{alpha} Agonists in ZDF Rats Is Associated With Defective Hepatic Mitochondrial Metabolism Diabetes, August 1, 2008; 57(8): 2012 - 2021. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. P. Klieverik, H. P. Sauerwein, M. T. Ackermans, A. Boelen, A. Kalsbeek, and E. Fliers Effects of thyrotoxicosis and selective hepatic autonomic denervation on hepatic glucose metabolism in rats Am J Physiol Endocrinol Metab, March 1, 2008; 294(3): E513 - E520. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. S. Jin, B.-H. Park, A. D. Sherry, and C. R. Malloy Role of Excess Glycogenolysis in Fasting Hyperglycemia Among Pre-Diabetic and Diabetic Zucker (fa/fa) Rats Diabetes, March 1, 2007; 56(3): 777 - 785. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. C. Burgess, F. M. H. Jeffrey, C. Storey, A. Milde, N. Hausler, M. E. Merritt, H. Mulder, C. Holm, A. D. Sherry, and C. R. Malloy Effect of murine strain on metabolic pathways of glucose production after brief or prolonged fasting Am J Physiol Endocrinol Metab, July 1, 2005; 289(1): E53 - E61. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
