This is how Merlin Thomas, a physician-scientist from Monash University, begins his talk when asked to explain how type 2 diabetes works.
"Each week, you bring home your shopping and put it in the pantry. This way you've got food ready for when you need it during the week.
"Now, imagine a week that you get invited out a lot — so you eat out most nights. By the end of
the week, there's a little more food in your pantry than normal because you haven't used it up. So, it just sits there."
Over time, he explains, the food in your pantry starts to pile up; the shopping continues to arrive, but you've stopped using the supplies that you've already bought.
"When the next batch of shopping arrives, you have nowhere left to put it … so you look around and think, 'I'll just stick it in the hallway or in the bathroom, and I'll get rid of it later'.
"The problem with that is that it starts to interfere with the functions of the hallway and the bathroom — causing all sorts of problems.
"That's essentially what type 2 diabetes is. It's fat stuck in the wrong place.
"That fat that interferes with normal functioning, which, in the case of diabetes, is healthy blood glucose control."
The challenge of diabetes
Putting aside the pantry metaphor for a moment (and how type 2 diabetes comes to be), it's important first to understand what diabetes is: a chronic condition that stops the body from producing and/or using insulin.
Insulin is an essential hormone produced by the pancreas. It regulates blood sugar levels by telling the cells of the liver, muscles, and fat to move glucose out of blood and into cells, where it is broken down and used for energy (or stored for later use).
When a person has diabetes, their body is unable to pull glucose out of their blood and break it down. This results in high blood glucose levels, which can lead to serious complications such as heart attack, stroke, amputation, blindness, kidney failure, depression and nerve disease.
"Someone with diabetes at the age of 60 will lose roughly six years of their life compared to someone without diabetes," Professor Thomas says.
"Most of that shortening of their lifespan is due to heart attacks and strokes."
There are a number of reasons why a person does not produce enough insulin, or the cells in their body stop responding to insulin properly (what's known as insulin resistance).
Type 1 diabetes is an autoimmune condition where a person's immune system destroys their insulin-producing cells, meaning they require daily insulin injections to survive. Type 1 diabetes usually appears in childhood or early adulthood, and accounts for around 10 per cent of all cases of diabetes.
In gestational diabetes, pregnant women are unable to overcome the insulin-resistance that naturally occurs during pregnancy, meaning blood sugar levels rise dangerously in both the mother and baby. Usually, gestational diabetes disappears following the birth of the baby, but it puts women at a higher risk of subsequently developing type 2 diabetes.
This brings us to the most common form of the condition — type 2 diabetes — which accounts for 85 per cent of all cases, and is largely preventable.
Type 2 diabetes is a combination of insulin resistance and impaired insulin production, and is strongly associated with high blood pressure, abnormal cholesterol levels, and excess weight (particularly around the waist).
The role of fat
Most people with type 2 diabetes are overweight or obese.
Normally, calories you consume over your daily requirements are stored as fat. These fat cells tend to be located under your skin, in your buttocks, thighs and breasts.
Just as your pantry fills up with food you're not using, so too do your fat cells with energy you're not burning.
Eventually, your body reaches a tipping point: faced with nowhere left to put excess energy, it starts to dump fat outside of where it's normally stored. This is known as ectopic fat.
"This really is the problem for most people with type 2 diabetes," Professor Thomas says.
"The liver, pancreas and other organs become fat-dumping sites, so they can't do their job as well as they need to."
Not only does excess fat damage your body's ability to make insulin, it also stops other cells in your body responding to what insulin you do produce (insulin resistance).
"On the one hand, you're not making enough insulin because the insulin-producing cells of the pancreas are fat-comatose," Professor Thomas says.
"On the other hand, any insulin that is made isn't working as well as it should because the cells that would normally respond to the insulin — in the liver, muscles and other places — are also fat-inundated."
When that happens, the pancreas works doubly hard to produce more insulin to keep your blood glucose levels within normal range.
"Eventually, as a result of the extra work demanded of it and the less ability to do that work, the pancreas burns out," Professor Thomas says.
"Over time, your sugar levels rise and rise, and when they rise above a certain level … you're said to have diabetes."
Understanding the risk factors
Understanding ectopic fat can help explain why some people who are overweight or obese do not develop type 2 diabetes: they are better at safely storing fat, and remain capable of producing enough insulin.
It also explains why some people develop type 2 diabetes without being overweight: they have less capacity to store fat in the right places (their buttocks, thighs and breasts), and a higher propensity to accumulate fat in all the wrong places (in and around their organs).
"The point of fat spill-over — when 'your pantry' is full and is spilling over into other areas — is different for different people, and depends on their ethnic background and gender, among other things," Professor Thomas says.
Research shows people from South-East Asia, North Africa, the Middle East, and Oceania have higher rates of diabetes than other Australians.
Indigenous Australians are also around four times as likely to have type 2 diabetes as non-Indigenous Australians.
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