Is leptin a serious player in the overall equation of type 1 diabetes?
- Julie Lane
- Jan 29, 2017
- 2 min read

January…thankfully nearly over! The long, dark nights and cold, dark mornings are almost unbearable. But there is a small way to capitalise on this cold, bitter weather to get fitter. As a health conscious t1d (Type 1 diabetic), I am always on the lookout for ways to stay healthy, eat well and keep my body moving.
Loads of new studies are telling us that being cold is actually good for us. Why? Because it enables our brown fat (yes, the other, good kind of fat in our bodies!) to help burn up our unwanted white fat. How do we do this? There are several ways. When we are cold, our brown fat kicks into action and heats up our white fat, essentially burning it off to keep our bodies warm. The colder it is outside, the more calories we will ultimately burn to stay warm. If we can stay outdoors a bit more in this bitterly cold time of year, even if only for a few extra minutes (try walking instead of taking the bus, plus it will warm you up even more), we can increase our fat-burning potential by essentially resetting our leptin resistance. Too good to be true? Maybe yes for the t1d.
Leptin is a blood-borne protein that is now seen as a revolutionary factor in a multitude of ways: most importantly for reducing food intake as it acts as an on/off switch for feeling satiated after eating. It is also critical for activating a second, back-up method to stop overeating. It sends a signal from the liver stimulated by insulin which is then sent to the brain to turn on the ‘off switch’.
However, it doesn’t work in t1ds because they don’t have the insulin to trigger the stimulus. For Type 2 diabetes, the overeating behaviour leading to diabetes can be modified through both motivational and behavioural change models, as it can be controlled by diet and lifestyle changes (however in extreme cases or frequently when people can’t commit to these, medication can be administered to control it). But as a Type 1 diabetic (not behaviourally related), I am curious to see where research might head on this ‘stimulated off switch’ issue as I am always hungry, but have been told for years it’s because I am on insulin (which makes a person hungrier). One might surmise that the insulin I am injecting should trigger the ‘off switch’, but in fact, the more insulin I take, the hungrier I feel. Or is this problem due to the fact when I take insulin, I regularly hypo and then feel the need to ‘panic eat’ to correct the hypo? I’m not sure I recognise the difference anymore.
Could unlocking the key to leptin be revolutionary for Type 1 diabetics in a multitude of ways? Maybe in time with more research leptin will prove to be the new ‘off switch’ allowing Type 1s the ability to finally feel satiated.
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