Jeffrey Bland, PhD explains emerging research linking appetite/satiety regulation to a glycosylation enzyme expressed in specific hypothalamic neurons that acts as a nutrient sensor sensitive to blood glucose. He describes how postprandial rises in blood sugar can increase protein glycosylation, potentially weakening satiation signaling and promoting overeating, and suggests low-glycemic, minimally processed foods to moderate this effect. The talk frames this glycosylation pathway as an important new chapter in understanding the psychobiology of eating, not a definitive sole explanation.
Chapters
So why are we hungry and why do we overeat? And are they related to at all the epidemic of obesity? These are interesting questions, by the way, which have been on the minds of many investigators, researchers and clinicians for decades. I wish I could give you a specific, unequivocal answer to all those questions. I can't. But I can give you a little bit of insight as to how we're learning something about this concept of the satiation signal, meaning how we stop eating because we feel like we're full. As you know, the lateral nucleus of the hypothalamus, that gland that sits in the center of our brain, has a very important role to play in the regulating of appetite. And there are many signals, some of which come from the gut. These are hormonal signals. They're called the enteroendocrine hormones that are secreted by our gut mucosal cells that go to the brain, and then there are brain signals that go to the gut that all work together as a system and to regulate appetite in the feel of hunger. Well, it turns out that there is now new evidence of another part of this satiation signal, and it is called a glycosylation enzyme that is found in specific brain neurons. That's a nutrient sensor that controls body weight. This is another part, another chapter in this evolving story. So I don't want to say this is the answer all, but it's certainly part of the story. Now, the thing that I want to bring to your attention in this particular component of discovery is that this glycosylation enzyme is in fact sensitive, in fact to blood sugar levels, because glycosylation is a process that occurs as a consequence of the non enzymatic connection of sugar in the blood to various proteins that then regulate and alter function. So there is a connection then between postprandial sugar levels, meaning blood sugar, when it goes up, like when you eat a lot of sugar, and how that influences this glycosylation pathway that's associated with satiety or satiation. So you probably had people say, you know, if I eat a candy bar to get energy, then I feel more hungry later. Is there really some, you know, physiological mechanism for that or is it just psychological? Well, there appears there could be a mechanism by which that occurs by altering then the satiation signal through elevated blood sugar. Postprandial, after consuming a candy bar, then you start to drive different kinds of cell signaling mechanisms that then creates this synthetic sense that, gee, you're hungry, you should be eating more. So I think that regulating the release of sugar into the blood, which is more your complex carbohydrates, your unrefined starches, whole grains and vegetables and fruits that are still fibrous, is a very desirable thing, because this time release uptake into the blood of sugar, then greatly lowers the ability of that sugar to exceed certain values, which then causes protein glycosylation and can alter the whole signaling mechanism of appetite and appetite regulation. So this is just another part of the psychobiology of eating and how it interrelates with satiety and ultimately the low glycemic load, diet and unrefined, minimally processed foods, and trying to in fact regulate sugar postprandially in your blood so that it will signal appropriately to those eating and satiety centers that manage your hunger.
