The Role Of Insulin Hypersecretion In Beta Cell Dysfunction In Type 2 Diabetes
Funder
National Health and Medical Research Council
Funding Amount
$318,622.00
Summary
The treatment of diabetes involves the use of drugs that stimulate the release of insulin from the pancreas to reduce the high blood sugar levels. However, we believe that while in the short term this is a good strategy, in the long-term it damages the cells that produce insulin leading to a worsening state of diabetes. It is the aim of this application to understand the mechanisms by which the insulin producing cells are damaged when forced to oversecrete insulin.
The Role Of Vitamin D In Beta Cell Function, Glucose Tolerance And Diabetes Mellitus.
Funder
National Health and Medical Research Council
Funding Amount
$102,820.00
Summary
A significant proportion of Australians are deficient in Vitamin D, a vitamin obtained from sunlight exposure and to a lesser extent from food. Vitamin D deficiency has been associated with increased risk of Type 2 diabetes. This study aims to demonstrate the mechanisms through which vitamin D affects the insulin-producing cells of the pancreas and to determine whether deficiency affects the body's handling of glucose and subsequent risk of Type 2 diabetes and diabetes in pregnancy.
I am a cellular physiologist investigating the role of ion channels, receptors and intracellular signalling systems in the control of hormone secretion from endocrine cells, contraction of cardiac myocytes and to a lesser extent, growth of endometrium can
The Role Of Endoplasmic Reticulum (ER) Stress In Pancreatic Beta-cell Dysfunction.
Funder
National Health and Medical Research Council
Funding Amount
$85,775.00
Summary
Diabetes results from pancreatic ß-cell failure which is characterised by insulin secretory defects and ß-cell destruction. This is mediated by inflammatory cytokines in type 1 diabetes and by high levels of fat in type 2 diabetes. The mechanisms by which ß-cells fail remain to be clarified but they are important considering the current epidemic of diabetes in Australia. This project will enhance our understanding of ß-cell failure and may provide therapeutic targets for diabetes treatment.
Investigations Of Beta Cell Dysfunction And Death In Type 2 Diabetes
Funder
National Health and Medical Research Council
Funding Amount
$314,433.00
Summary
Diabetes is a disease that affects 100 million people worldwide and this number is expected to double in the next twenty years. This disease is characterised by high blood sugar levels which over prolonged periods of time can affect the function of the kidneys and eyes as well as causing heart attacks and strokes. A main contributing factor to diabetes is the inability of the pancreas to secrete insulin, the hormone that is responsible for keeping blood sugar levels in the normal range. The reas ....Diabetes is a disease that affects 100 million people worldwide and this number is expected to double in the next twenty years. This disease is characterised by high blood sugar levels which over prolonged periods of time can affect the function of the kidneys and eyes as well as causing heart attacks and strokes. A main contributing factor to diabetes is the inability of the pancreas to secrete insulin, the hormone that is responsible for keeping blood sugar levels in the normal range. The reason for this inability of the pancreas to secrete enough insulin is not known. It is known however, that both genetic and environmetal factors are responsible. The aim of this investigation is to determine the biochemical and genetic reason for decreased insulin secretion from an animal model of diabetes called DBA-2J mouse. Specifically we will be studying the effects of long-term increased sugar and fat on the function of the insulin producing cells of the pancreas, in order to identify the biochemical pathway responsible for reduced insulin secretion. In parallel we will be investigating the gene or genes in DBA-2J mice that are responsible for decreased insulin secretion and pancreatic cell death. This will provide clues as to the genes that may be responsible for diabetes in humans. This project will provide crucial information on the cause of reduced insulin secretion both at the cellular and genetic level, and will lead to a better understanding of the cause of diabetes.Read moreRead less
Effect Of Oral Glutamine On GLP-1 And Insulin Secretion And Glycaemia In Humans.
Funder
National Health and Medical Research Council
Funding Amount
$397,444.00
Summary
Diabetes is an ever increasing problem with serious complications. We will investigate whether glutamine, one of the most common amino acids (protein building blocks) in the body, has a beneficial effect on blood glucose and insulin levels in the body in people who have type 2 (non-insulin dependent) diabetes. If so, glutamine supplementation may represent a novel, cheap and palatable way of improving outcomes and preventing the development of complications in people with type 2 diabetes.
Investigation Of The Genetic Basis Of Insulin Hypersecretion In A Mouse Model Of Pancreatic Islet Failure
Funder
National Health and Medical Research Council
Funding Amount
$406,980.00
Summary
Type 2 diabetes is a chronic disease that is associated with blindness, kidney failure, heart attacks and stroke and these are secondary to high blood sugar levels. Thus, determining the cause of high blood sugar levels in type 2 diabetes will lead to better management of the disease and ease the financial burden on the public health system. High blood sugar in type 2 diabetes results from the inability of the body to secrete enough insulin. Insulin is the main hormone that lowers blood sugar le ....Type 2 diabetes is a chronic disease that is associated with blindness, kidney failure, heart attacks and stroke and these are secondary to high blood sugar levels. Thus, determining the cause of high blood sugar levels in type 2 diabetes will lead to better management of the disease and ease the financial burden on the public health system. High blood sugar in type 2 diabetes results from the inability of the body to secrete enough insulin. Insulin is the main hormone that lowers blood sugar levels and is produced by the pancreas. The reason for reduced insulin secretion in type 2 diabetes is not known. Paradoxically, it has been shown that some people who are at an increased risk of developing diabetes (eg people with obesity or a family history of diabetes) secrete more insulin than normal. It is not clear why this is, but a few studies have suggested that reducing insulin secretion in these circumstances can protect the pancreas and preserve its ability to secrete the appropriate amount of insulin. The DBA-2 is a mouse strain that like humans with type 2 diabetes, its pancreas can also fail to secrete the appropriate amount of insulin and under these circumstances becomes diabetic. Furthermore our laboratory has generated evidence that shows that like people who are at risk of diabetes, DBA-2 mice in fact secrete more insulin prior to becoming diabetic. Whether the cause of this increased insulin secretion is linked to the eventual reduction of secretion is not known. The aim of this study is to identify the gene that causes increased insulin secretion in the DBA-2 mouse. Furthermore, genetically manipulated animals will be produced that contain only this gene to determine its effect on insulin secretion. Should the identification of this gene be related to the eventual failure of the pancreas to secrete enough insulin, then it would provide a target for drug therapy to correct insulin levels and therefore reduce blood sugar levels.Read moreRead less
Inhibition Of Glucose-stimulated Insulin Secretion By Protein Kinase C Epsilon
Funder
National Health and Medical Research Council
Funding Amount
$555,693.00
Summary
Type 2 diabetes is a chronic disease which occurs when the pancreas is unable to produce enough insulin for the body to cope with rising blood glucose levels after a meal, and is strongly linked to obesity. We have discovered that fat oversupply activates an enzyme in the pancreas causing defects in insulin release due to glucose. Inhibiting this enzyme helps overcome diabetes, through poorly defined mechanisms that we aim to clarify here. Our work could lead to new therapies for diabetes.