Type 2 Diabetes
Type 2 diabetes is commonly referred to as ‘mature onset’, as it is usually diagnosed in people over 45 years of age, but is now sometimes diagnosed in children in Australia. As the obesity epidemic hits the Western world, the cases of teenagers and children developing Type 2 diabetes are becoming alarmingly frequent.
At least three quarters of the estimated 366 million people with diabetes world-wide are Type 2 and the World Health Organisation expects numbers to double to over 500 million by 2030. In 2003, the countries with most people living with diabetes are: India (35.5 million), China (23.8 million), United States (16 million), Russia (9.7 million) and Japan (6.8 million).
There are more than 1.5 million people with diabetes in Australia, with probably half undiagnosed. In the last 20 years, the number of Australians diagnosed with diabetes has trebled and 275 people develop diabetes every day. Diabetes costs Australia up to $10 billion per year.
The causes of Type 2 diabetes
Insulin is an important hormone made in the human pancreas – a small organ that sits close to the intestine. Insulin regulates the body’s use of glucose (sugar), which is one of our major energy sources. Insulin is particularly important after we eat a meal when glucose enters the blood stream from the intestine. The elevation in blood glucose at this time triggers the release of insulin from the pancreas. Insulin then travels through the blood and assists the transfer of glucose from blood into cells so it can be used for energy.
Type 2 diabetes occurs because some people cannot respond normally to the insulin they make and sufferers are not able to make enough insulin to compensate for the insulin "resistance". This results in high concentrations of glucose in the blood, which can damage many of the body’s systems, especially blood vessels and nerves. Evidence of an underlying genetic predisposition now exists, with some genes associated with an increased risk for Type 2 diabetes. The inability of the body to utilise glucose (insulin resistance) is strongly correlated with waist measurements and abdominal fat levels. Garvan’s research shows that fat directly around organs in the stomach, rather than fat under the skin, is a major risk factor.
If left untreated, diabetes can cause serious long-term complications including kidney disease, retina damage, cardiovascular disease, and nerve damage, often resulting in amputation.
The risk factors of Type 2 diabetes
You may be at increased risk of developing Type 2 diabetes if you fit any of the following criteria:
- Over 45 years of age, overweight and/or have a high blood pressure
- Over 45 years of age and have a family member with diabetes
- Have heart disease or have suffered a heart attack
- Have/had high blood glucose levels or have impaired glucose tolerance
- Have/had gestational diabetes
- Are overweight (i.e. have a Body Mass Index higher than 25)
The symptoms of Type 2 diabetes
Type 2 diabetes develops gradually, so symptoms often go unnoticed. These may include frequent urination, thirst, blurred vision, skin infections, slow healing, tingling and numbness in the feet. Sometimes no symptoms are noticed at all or the individual assumes that they are part of the normal ageing process. Diagnosis is made by either a Fasting Blood Glucose (FBG) or Oral Glucose Tolerance Test (OGTT), which are ordered by a doctor.
People with diabetes are significantly more likely to develop serious health problems like heart disease, stroke, high blood pressure, circulation problems, nerve damage, and damage to the kidneys and eyes. The appearance and severity of these complications is dependent on the duration of Type 2 diabetes and can be delayed or even prevented by early detection and treatment.
Garvan's research into Type 2 diabetes
Diabetes represents a defect in metabolism or an inability to use and store energy correctly. Energy, being the fundamental unit of life, is required for every single process in the human body ranging from each heartbeat to every thought. Throughout the millions of years of evolution that have brought us to where we are today, a major biological pressure that has more or less molded our very existence is the pressure to survive periods of starvation. The massive technological developments that have occurred over the past century have almost instantaneously exposed the human population to an environment never before seen, and so providing a major challenge to our genetic ability to cope. This essentially represents the challenge that we, as metabolic researchers, face. In a sense, we are trying to unravel millions of years of evolution to determine how we can resolve this potentially catastrophic situation.
We know that in many cases diabetes can either be avoided or sent into remission with diet and exercise. However, the desire to eat is hard wired in each of us and as long as food is available, we are, in a sense, programmed to eat it. In other words, the default state is to eat, not the converse.
At Garvan we believe that the solution to this problem will not be simple because metabolism has had millions of years of trial and error to get to where it is today. We are now undertaking the challenge to embrace this complexity and we are ideally placed to do this.
Garvan’s Diabetes and Metabolism Division comprises nearly 100 research scientists and clinicians working together to untangle the complexity of metabolic disease. Our team comprises expertise in a host of areas. This includes functional analysis of individual molecules, either on their own or in the context of the living cell, as they work together to coordinate complex actions like burning energy to coordinate muscle contraction. We have people who specialise in the function of different metabolic organs including the liver, pancreas, muscle and adipose tissue. In particular, we are interested in understanding how these organs work together to control the fate of food and how it is either stored or utilised.
We have considerable expertise in working with whole animals and how they respond to genetic manipulations or environmental perturbations. Finally, we have a very advanced clinical group who study humans with diabetes or those who are at risk of acquiring diabetes.
More and more of our studies involve the acquisition of huge amounts of data that describe the behavior of the organism. To analyse this we rely on people with very sophisticated expertise in branches of mathematics or physics to help us. It is our philosophy that through the coordinated efforts of all these individuals and their expertise, we will be able to establish how people in our community are likely to respond to certain environmental cues at the individual level. We believe that, in the end, there will not be just one solution to this problem, so we need to devise ways of predicting at an individualistic level how best to treat metabolic disease.
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