Satiation is a feeling that is actually triggered in the brain by specific neurons in the hypothalamus. These neurons respond to a number of factors, including circulating levels of blood glucose, free fatty acids (ie energy availability) and hormones such as leptin.
In this paper, the authors show that ROS is necessary for satiation. The authors infused rats with fat into their blood stream, incresing available energy levels. In response to this fat, the rats started burning fat in their hypothalamus’ neurons, which created ROS. The rats spontaneously reduced their food intake over the next several hours. The authors then gave the rats a pharmaceutical grade antioxidant, and the rats went go back to normal levels of food consumption despite the high levels of circulating fat/energy availability. Because ROS is the signal and if you mop them all up with antioxidants you eliminate the satiation signal. Pretty neat.
If we think about this in the context of the previous post, we see another problem for the obese subjects. When they re burning their own body fat they will not achieve satiation quickly or strongly because their body fat is highly unsaturated and will therefore not produce significant superoxide in the hypothalamus to trigger satiation! This is yet another disadvantage for long term weight loss in the obese subjects.
Hi Brad.
I have a doubt about your superhero Superoxide.
What about people like me who have defective variants of SOD2 gene?
That should mean less endogenous antioxidant capacity.
Following a high saturated diet, don’t we risk ending up with too much of a good thing (ROS)?
Thanks.
Hi Marco!
Obviously having a defective SOD2 gene makes you a unique case. And yes, I would suppose in your case you might want to avoid saturated fat for this reason, but with the understanding that starch will also be converted into saturated fat by de novo lipogenesis. Perhaps salads with olive oil are your best bet, I’m not sure. Good luck!
Brad