Endocrinology, Vol 135, 409-415, Copyright © 1994 by Endocrine Society

ARTICLES

The effects of severe maternal diabetes on glucose transport in the fetal rat

V Atkins, AS Flozak, ES Ogata and RA Simmons
Department of Pediatrics, Northwestern University Medical School, Chicago, Illinois.

We mimicked the condition of severe maternal diabetes by administering high doses of streptozotocin (STZ) to the pregnant rat to determine the effects of increased glucose availability on fetal glucose transport and to assess whether a relationship might exist between glucose transport and altered fetal growth. Fetuses of STZ-treated pregnant rats were growth retarded (3.86 +/- 0.13 vs. 5.29 +/- 0.06 g), hyperglycemic (30.0 +/- 1.0 vs. 5.5 +/- 0.5 mM/liter), and hyperinsulinemic (1263.8 +/- 138.3 vs. 817.9 +/- 116.7 pM/liter). Glucose uptake, Glut 1 messenger RNA (mRNA), and Glut 1 protein were greater in STZ-treated fetal brain than in controls (50%, 83%, and 50%, respectively; P < 0.05). Glut 3 mRNA levels in STZ-treated and control fetal brain were equivalent and significantly less than levels of Glut 1. Glucose uptake in muscle of STZ fetuses was 70% greater than control values (P < 0.05). Glut 1 mRNA levels were increased by 93% in STZ fetal muscle (P < 0.05). Neither Glut 3 nor Glut 4 mRNA could be detected in STZ-treated and control fetal muscle. Glut 1 protein levels were increased by 70% in STZ-treated fetal muscle compared to control muscle (P < 0.05). These observations indicate that altered glucose transport per se does not directly contribute to fetal growth retardation with maternal STZ diabetes. Perturbations in other physiological and metabolic factors may contribute to the pathogenesis of fetal growth retardation in STZ-induced diabetes during pregnancy.

This article has been cited by other articles:

				J. Han, J. Xu, Y. S. Long, P. N. Epstein, and Y. Q. Liu Rat maternal diabetes impairs pancreatic beta-cell function in the offspring Am J Physiol Endocrinol Metab, July 1, 2007; 293(1): E228 - E236. [Abstract] [Full Text] [PDF]

				M. Thamotharan, R. A. McKnight, S. Thamotharan, D. J. Kao, and S. U. Devaskar Aberrant insulin-induced GLUT4 translocation predicts glucose intolerance in the offspring of a diabetic mother Am J Physiol Endocrinol Metab, May 1, 2003; 284(5): E901 - E914. [Abstract] [Full Text] [PDF]

				M. S. Anderson, J. Flowers-Ziegler, U. G. Das, W. W. Hay Jr., and S. U. Devaskar Glucose transporter protein responses to selective hyperglycemia or hyperinsulinemia in fetal sheep Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2001; 281(5): R1545 - R1552. [Abstract] [Full Text] [PDF]

				B. S. Singh, T. C. Westfall, and S. U. Devaskar Maternal Diabetes-Induced Hyperglycemia and Acute Intracerebral Hyperinsulinism Suppress Fetal Brain Neuropeptide Y Concentrations Endocrinology, March 1, 1997; 138(3): 963 - 969. [Abstract] [Full Text] [PDF]