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Gestational Diabetes: Treatment With Metformin Compared To Insulin
Funder
National Health and Medical Research Council
Funding Amount
$257,400.00
Summary
Gestational diabetes (GDM) is diagnosed when women have elevated blood sugar levels detected in pregnancy. Treatment aims to keep the mother's blood sugar normal and to prevent extra sugar transferring to the baby, as this can lead to elevated insulin levels, and subsequent complications, in the baby. Initial treatment is by diet, but more than 30% of women need further treatment with insulin injections. Metformin, which can be taken by as a tablet, is an alternative to insulin that is used wide ....Gestational diabetes (GDM) is diagnosed when women have elevated blood sugar levels detected in pregnancy. Treatment aims to keep the mother's blood sugar normal and to prevent extra sugar transferring to the baby, as this can lead to elevated insulin levels, and subsequent complications, in the baby. Initial treatment is by diet, but more than 30% of women need further treatment with insulin injections. Metformin, which can be taken by as a tablet, is an alternative to insulin that is used widely outside pregnancy for people with diabetes. There are good data to support the safety of metformin in pregnancy. We plan to test that metformin is not only safe but also an effective alternative to insulin for women with GDM. Metformin works by reducing resistance to insulin, which is a key factor for the development of GDM and also for high blood pressure complications. We hope to demonstrate a reduction in these complications with metformin treatment. Metformin is associated with less weight gain than insulin and we hope to demonstrate an associated reduction in the risk of diabetes following pregnancy in women with GDM treated with metformin. It is likely that metformin crosses the placenta, and if so, it may reduce elevated insulin levels in the baby. The study will measure insulin levels in the cord blood, hoping to demonstrate that more babies have normal insulin levels in pregnancies treated with metformin.Read moreRead less
Metformin In Gestational Diabetes: Follow-up Of Mothers And Offspring: Body Composition, Insulin Resistance, Development
Funder
National Health and Medical Research Council
Funding Amount
$630,142.00
Summary
Children born to women with gestational diabetes are at increased risk of later obesity and diabetes. This study will help to assess if giving such women during their pregnancy the cheap oral diabetes drug metformin rather than insulin injections can safely reduce this risk, measuring growth, fatness and blood glucose-insulin in the children at 2 and 5 years of age, as well as assessing the mothers. If so, such treatment might help to reduce the worldwide burden of disease related to obesity.
Biochemical Basis Of Islet Beta-cell Compensation And Failure In Normal Pregnancy And Gestational Diabetes Mellitus
Funder
National Health and Medical Research Council
Funding Amount
$480,828.00
Summary
The factors causing the current world-wide crisis of rapidly rising diabetes prevalence remain poorly understood. Of potential major importance, however, is the hypothesis that abnormalities in the maternal metabolic environment, as occur in gestational diabetes (GDM) (diabetes that develops in pregnancy), result in abnormal development of metabolic systems in the baby resulting in higher risk of adult onset diabetes in the babies. Therefore, it is of importance to understand the mechanisms caus ....The factors causing the current world-wide crisis of rapidly rising diabetes prevalence remain poorly understood. Of potential major importance, however, is the hypothesis that abnormalities in the maternal metabolic environment, as occur in gestational diabetes (GDM) (diabetes that develops in pregnancy), result in abnormal development of metabolic systems in the baby resulting in higher risk of adult onset diabetes in the babies. Therefore, it is of importance to understand the mechanisms causing GDM, such that effective measures can be developed to counter this passing on of diabetes risk from mother to baby. It is known that a key factor causing GDM is failure of maternal pancreatic islet beta-cells to compensate for increased demands for insulin production in pregnancy. Poorly understood, however, are the cellular mechanisms of islet beta-cell compensation in normal pregnancy and failure of this compensation in GDM pregnancy. We have recently shown that there is a pathway of fat metabolism (triglyceride- free fatty acid cycle) within the islet beta-cell that has an important role in amplyfing insulin secretion necessary to maintain normal blood glucose and protecting the islets from failure in obese rats. The major focus of this project is to test the hypothesis that this pathway has a key role in the adaptation of pancreatic islets to normal pregnancy and its dysfunction contributes to the causation of GDM. Of great interest from preliminary findings is that a master regulator of glucose and fat metabolism, PGC1alpha, is markedly reduced in islets during normal pregnancy. Studies will also be directed to PGC1alpha's role in islet adaptation to pregnancy and failure in GDM. We expect that successful completion of this project will lead to the development of highly targeted counter measures to prevent GDM and to slow and reverse the current epidemic of diabetes.Read moreRead less
A Longitudinal Study Of Nerve Morphology In Diabetic Neuropathy Using Novel Non-invasive Ophthalmic Surrogate Markers
Funder
National Health and Medical Research Council
Funding Amount
$540,372.00
Summary
This research project will use two new ophthalmic instruments - the corneal confocal microscope and non-contact corneal aesthesiometer - to directly monitor changes in corneal nerves and corneal sensitivity, over a 5 year period, in diabetic patients suffering from a painful condition of the arms and legs known as diabetic neuropathy. This study will generate important new information that could allow diabetic doctors to more accurately monitor the progression of the disease.
The Role Of Hypoxia Inducible Factor 1a In Beta-Cell Function And Diabetes
Funder
National Health and Medical Research Council
Funding Amount
$362,303.00
Summary
HIF1a is a gene which our preliminary data shows is needed for normal beta-cell function and insulin secretion. When beta-cells cannot release enough insulin, blood sugar levels rise, and diabetes develops. This research plan will look at the effects of deletion of HIF1a and of increasing HIF1a to see how this affects function of beta-cells and - or diabetes development. This work may show that HIF1a is a potential therapeutic target for the treatment of diabetes in humans.
Aldosterone Inhibition And Diabetic Retinopathy: Treatments And Mechanisms Of Action
Funder
National Health and Medical Research Council
Funding Amount
$511,294.00
Summary
The World Health Organization predicts that by 2030, more than 360 million people will have diabetes. Despite almost all patients developing retinopathy, current treatments do not prevent disease progression. One strategy being evaluated is blockade of a hormone called angiotensin II. We have new evidence that a related system called aldosterone exists in retina and contributes to damage. This project will determine if aldosterone blockade is a potential treatment for diabetic retinopathy.
Mediation Pathways For The Receptor For Advanced Glycation End Products In Diabetic Nephropathy
Funder
National Health and Medical Research Council
Funding Amount
$333,812.00
Summary
Excess sugar in the blood from diabetes is detrimental and can accelerate a process where sugar attaches itself to proteins, fats and DNA. Although facilitated by high sugar, the reaction occurs happily in the presence of low sugar with high levels of free oxygen radicals. These complexes are called advanced glycation end products or AGEs. In addition, we ingest vast volumes of AGES from our diet which are taken into the blood. These AGEs are known to be involved in the development of kidney dis ....Excess sugar in the blood from diabetes is detrimental and can accelerate a process where sugar attaches itself to proteins, fats and DNA. Although facilitated by high sugar, the reaction occurs happily in the presence of low sugar with high levels of free oxygen radicals. These complexes are called advanced glycation end products or AGEs. In addition, we ingest vast volumes of AGES from our diet which are taken into the blood. These AGEs are known to be involved in the development of kidney disease in diabetic subjects. AGEs exert most of their effects on the body by binding to specific proteins, the most common and nasty of which is the receptor for advanced glycation end products, RAGE. RAGE is a known participant in other serious diseases such as Alzheimer's disease and evidence is mounting for its central role in the development of kidney disease in diabetic subjects. There is not much known about the processes which mediate RAGE which is why this is the aim of this proposal. This will enable us to stop the relentless progression of kidney disease in diabetes.Read moreRead less