We used to believe that type 2 diabetes was a problem of obesity: eat too much sugar and junk food and you’ll gain weight and get diabetes. Simple. But through using sophisticated scanning technology, my team has been able to show that diabetes can strike whatever your girth. Interestingly, this is never a random attack problem that only occurs if you accumulate more fat than your body can safely store.
Anyone can get type 2 diabetes, regardless of your body size, but only if you gain sufficient weight to push you through what we call your ‘personal fat threshold’. This is the metabolic tipping point based on your genetic make-up and is individual to you.
Key to this is the discovery, by my team in Newcastle, of the precise mechanisms that prompt type 2 diabetes to take hold. When you eat a meal, the levels of glucose (sugar) in your blood will rise and insulin (produced in the pancreas) is released to make sure that glucose is taken out of the blood and stored as glycogen in temporary storage depots in the liver and in muscles around your body.
When those glycogen stores are full, excess blood sugar is instead transformed into fat to be stored elsewhere. Then, when you’re not eating (such as at night when you’re asleep) your body will tap into these glycogen stores to keep blood glucose levels topped up.
However, if, as many people do these days, you get into the habit of grazing constantly throughout the day, your blood sugar levels never drop low enough to require topping up from your glycogen stores. It becomes a perpetual one-way process: excess blood glucose converted to fat.
If this continues, at some point you will reach your own ‘personal fat threshold’ and the safe stores of fat under the skin become overfilled and start to spill over to build up in the liver and pancreas where — crucially — fat impedes the ability of these vital organs to function effectively.
When your liver is clogged with fat, it seeks to redress the balance by pumping out extra glucose into the bloodstream and passing excess fat to the pancreas. Ultimately, this fat will consume the pancreas’s insulin-producing cells, causing them to malfunction. When my team discovered this connection, it was pretty revolutionary.
