Exp Mol Med.
1999 Dec;31(4):179-184.
Increased expression of Galphaq protein in the heart of streptozotocin-induced diabetic rats
- Affiliations
-
- 1Department of Biochemistry and Molecular Biology, Seoul National University College of Medicine, Korea.
Abstract
- Heart disease is one of the major cause of death in diabetic patients, but the
thogenesis of diabetic cardio-myopathy remains unclear. In this experiment, to
sess the significance of G protein signaling pathways in the pathogenesis of
abetic cardiomyopathy, we analyzed the expression of G proteins and the
tivities of second messenger dependent protein kinases: cAMP-dependent protein
nase (PKA), DAG-mediated protein kinase C (PKC), and calmodulin dependent
otein kinase II (CaM kinase II) in the streptozotocin induced diabetic rat
art. The expression of Galphaq was increased by slightly over 10% (P<0.05) in
abetic rat heart, while Galphas, Galphai, and Gbeta remained unchanged. The
A activity in the heart did not change significantly but increased by 27%<0.01) in the liver. Insulin treatment did not restore the increased activity
the liver. Total PKC activity in the heart was increased by 56% (P<0.01), and
sulin treatment did not restore such increase. The CaM kinase II activity in
e heart remained at the same level but was slightly increased in the liver
4% increase, P<0.05). These findings of increased expression of Galphaq in the
reptozotocin-diabetic rat heart that are reflected by the increased level of
C activity and insensitivity to insulin demonstrate that alteration of Galphaq
y underlie, at least partly, the cardiac dysfunction that is associated with
abetes. Copyright 2000 Academic Press.