Dietary vitamin and lipid therapy rescues aberrant signaling and apoptosis and prevents hyperglycemia-induced diabetic embryopathy in rats.

Abstract

OBJECTIVE:

Maternal diabetes causes developmental malformations in the embryo. Dietary supplementation with antioxidants can reduce the malformation rates in animal models. To investigate the molecular mechanisms underlying diabetes-induced embryonic abnormalities and dietary interventions, activity of mitogen-activated protein kinases and factors associated with apoptotic pathways were examined in the maternal diabetic rat model.

STUDY DESIGN:

Diabetes was induced in pregnant rats using streptozotocin. In the yolk sacs of the embryos, activity of the extracellular signal-regulated kinases, Raf-1, and Akt was dramatically reduced in diabetic rats, whereas that of c-jun N-terminal kinases/stress-activated protein kinases was increased.

RESULTS:

When the diabetic dams were fed with arachidonic acid, vitamin E, or a combination of arachidonic acid, vitamin E, and myoinositol, the changes in the expression of these kinases were reversed and correlated with the decreases in the rates of apoptosis and embryonic malformations.

CONCLUSION:

These results suggest that mitogen-activated protein kinases are involved in diabetic embryopathy, and dietary supplementations can rescue the aberrant signaling pathways and reduce embryonic malformation rate.

• Authors: E Albert Reece, Ying-King Wu, Zhiyong Zhao, Danny Dhanasekaran
• Journal: American journal of obstetrics and gynecology (Am J Obstet Gynecol) Vol. 194 Issue 2 Pg. 580-5 (Feb 2006) ISSN: 1097-6868 [Electronic] United States
• PMID: 16458664 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antioxidants
• Vitamin E
• Arachidonic Acid
• Mitogen-Activated Protein Kinases

Topics

• Animals
• Antioxidants (administration & dosage, pharmacology)
• Apoptosis (physiology)
• Arachidonic Acid (administration & dosage, pharmacology)
• Blotting, Western
• DNA Fragmentation
• Diabetes Mellitus, Experimental (physiopathology)
• Dietary Supplements
• Disease Models, Animal
• Female
• Hyperglycemia (physiopathology)
• Mitogen-Activated Protein Kinases (physiology)
• Pregnancy
• Rats
• Rats, Sprague-Dawley
• Signal Transduction (physiology)
• Vitamin E (administration & dosage, pharmacology)