The γ→β globin gene switch in humans is normally on a set developmental clock but is delayed in infants of diabetic mothers. We cultured cord blood erythroid progenitors and assayed globin produced in the presence and absence of metabolites that are elevated in such infants. Analogues of butyric acid at supranormal concentrations significantly augmented γ and inhibited β globin expression. The uptake of α-amino-n-butyric acid into colony-derived erythroblasts was increased in the presence of supranormal insulin. These findings suggest that elevated levels of α-amino-n-butyric acid and insulin in the developing fetus delay the globin switch and may offer potential for augmenting γ globin expression in the β globin chain diseases.
|Original language||English (US)|
|Number of pages||7|
|Journal||Biochemical and Biophysical Research Communications|
|State||Published - Oct 29 1987|
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology