| First Author | Khan JY | Year | 1999 |
| Journal | Pediatr Res | Volume | 45 |
| Issue | 5 Pt 1 | Pages | 718-25 |
| PubMed ID | 10231871 | Mgi Jnum | J:55839 |
| Mgi Id | MGI:1339458 | Doi | 10.1203/00006450-199905010-00019 |
| Citation | Khan JY, et al. (1999) Effect of primary congenital hypothyroidism upon expression of genes mediating murine brain glucose uptake. Pediatr Res 45(5 Pt 1):718-25 |
| abstractText | Using hyt/hyt mice that exhibit naturally occurring primary hypothyroidism (n = 72) and Balb/c controls (n = 66), we examined the mRNA, protein, and activity of brain glucose transporters (Glut 1 and Glut 3) and hexokinase I enzyme at various postnatal ages (d 1, 7, 14, 21, 35, and 60). The hyt/hyt mice showed an age-dependent decline in body weight (p < 0.04) and an increase in serum TSH levels (p < 0.001) at all ages. An age-dependent translational/posttranslational 40% decline in Glut 1 (p = 0.02) with no change in Glut 3 levels was observed. These changes were predominant during the immediate neonatal period (d 1). A posttranslational 70% increase in hexokinase enzyme activity was noted at d 1 alone (p < 0.05) with no concomitant change in brain 2-deoxy-glucose uptake. This was despite a decline in the hyt/hyt glucose production rate. We conclude that primary hypothyroidism causes a decline in brain Glut 1 associated with no change in Glut 3 levels and a compensatory increase in hexokinase enzyme activity. These changes are pronounced only during the immediate neonatal period and disappear in the postweaned stages of development. These hypothyroid-induced compensatory changes in gene products mediating glucose transport and phosphorylation ensure an adequate supply of glucose to the developing brain during transition from fetal to neonatal life. |
