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Research | Carayannopoulos LAB
Impaired glucose homeostasis is associated with
pathologic conditions that result in developmental abnormalities,
including diabetes where uncontrolled hyperglycemia during
embryogenesis is associated with increased rates of congenital
malformation and GLUT1 deficiency syndrome (G1DS), a severe
epileptic encephalopathy of childhood associated with
developmental delay, microcephaly and spasticity caused by
impaired glucose transport across the blood brain barrier (BBB).
While these clinical observations suggest that tightly controlled
glucose metabolism is critical during development, the mechanisms
and timing affected by impaired glucose homeostasis remain poorly
understood.
We have developed a zebrafish model in which the expression of the
facilitative glucose transporter, Glut1, is abrogated. Decreasing
the expression of this nutrient transporter results in a striking
phenotype of impaired neurogenesis, abnormal apoptosis and
ultimately embryo demise. To further elucidate how impaired Glut1
expression is linked to the activation of mitochondrial death
pathways, ongoing projects aim to systematically define mechanisms
linking glucose metabolism and programmed cell death.
Contact Information
Mary O. Carayannopoulos, Ph.D. Washington University School of Medicine Department of Pediatrics Developmental Biology & Genetics Unit 660 S. Euclid Ave, CB 8208 St. Louis, MO 63110 Ph: (314) 286-2844 Fx: (314) 286-2784 E-mail:
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