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Maternal Diabetes Causes Damage To Offspring's Beta Cell Functions
The
link between a woman's maternal diabetes and her child's increased risk
for diabetic complications is one step closer to being understood.
According to recent research performed at the University if Louisville,
there are many functional and metabolic changes that occur in such a
child's pancreatic β cells, which could help explain this increased
risk.
Maternal, or gestational, diabetes is a condition in which women
previously undiagnosed with diabetes show high levels of blood glucose
during pregnancy. It has been indicated previously that the occurrence
of gestational
diabetes increases the risk for many ailments in the woman's adult
offspring, including obesity, glucose intolerance, and type 2 diabetes
mellitus.
In
contrast, type II diabetes is linked to a failure of the β cells of the
pancreas to produce sufficient insulin. This affects many parts of the
glucose metabolic pathway. The biochemical mechanisms behind these
effects on the offspring of a woman who suffers from gestational
diabetes are
not well understood. In particular, this research set out to learn how
diabetes during the period of gestation could influence the β cell
function in the offspring, and thus potentially influence diabetes
incidence.
To
this end, Dr. Jianxiang Xu and Dr. Junying Han, of the Kosair
Children's Hospital Research Institute, used a rat diabetes
model to detail the mechanism. Diabetes was induced in female rats by
the administration of streptozotocin (STZ) at the age of eight
weeks, and once diagnosed, these females were mated with normal males.
After delivery, the offspring were immediately transferred to
normal foster mothers who had delivered other litters at the same time.
This was done in order to prevent any potential effects caused by
breast-feeding from a diabetic lactating mother. Additionally, a
control group was established by administering a buffer solution
without STZ.
When examined at birth, the
birthweights of the pups was significantly decreased in the population
from diabetic mothers, and the litter size was half of that of the
control group. The premature death rate for the pups with diabetic
mothers was 16%, while none of the control group showed mortality or
health problems.
The β cell function of the offspring was analyzed at 15 weeks of age
using various methods, both in vivo and in
vitro, including blood titers and radioactive tracing. The
resulting analysis showed:
Insulin secretion ability, the primary function of
the pancreatic β cells,
was significantly impaired in both male and female pups. This includes
a decrease of 40-50% when stimulated by glucose.
Both glucose utilization and oxidation,
two commonly used indexes for the metabolic function of
pancreatic β cells, were reduced by 55% and 41% respectively. These
results indicate that metabolic function of the cells was
impaired.
Phosphofructokinase
(PFK), pyruvate carboxylase (PC) and pyruvate dehydrogenase (PDH)
levels decreased by 44-51%. All of these chemicals have important roles
in the glucose metabolic pathway and indicate a disturbance in glucose
levels as well as have an influence on insulin secretion.
The
authors postulate that the damage done to the β cells in the offspring
of the diabetic group could have two potential causes. The first could
be an increased level of free radical oxygen species during the
diabetic pregnancy, as pancreatic β cells are especially sensitive to
ROS. The second could be the abnormally high glucose levels the β cells
experience during gestation -- this could prevent the upregulation of
certain enzymes during pregnancy, making the β cells more susceptible
to damage during the period of maternal diabetes.
They
conclude that maternal diabetes can cause many disturbances in the
metabolic and other functions of the pancreatic β cells of the
offspring. These disturbances could contribute to later development of
type 2 diabetes, and could hold many clues to the link between
gestational diabetes and type II diabetes in humans.
Written by Anna Sophia McKenney
Copyright: Start Sanatate
Not to be reproduced without permission of Start Sanatate
Maternã a diabetului zaharat de a produce daune de urmaºi, a celulelor beta funcþii - Maternal Diabetes Causes Damage To Offspring's Beta Cell Functions - articole medicale engleza - startsanatate