Over the past few weeks we’ve gone over hormones related to our metabolism and diet. Examples of such hormones are leptin, ghrelin, insulin and glucagon. In particular, last week’s post had us briefly cover the lipostatic hypothesis, which we’ll cover in greater detail in this post alongside the glucostatic hypothesis and others.
The glucosctatic hypothesis
All information for this section comes from: Chaput, J. P., & Tremblay, A. (2009). The glucostatic theory of appetite control and the risk of obesity and diabetes. International journal of obesity, 33(1), 46.
The glucostatic hypothesis posits that changes in blood glucose concentrations are sensed by the appropriate receptors in our body, and those receptors also affect energy intake. In this way, when blood glucose levels rise satiety kicks in, and when blood glucose levels fall we feel hungry.
The mechanism by which this happens is that there are certain regions in the brain which rely on glucose. Once glucose utilization is reduced in these regions, perception and expression of hunger happens. On the other hand, if there is an increased glucose utilization in those regions then we no longer feel hungry and stop eating.
As far as studies and experiments have shown, things are more complicated and the glucostatic hypothesis isn’t quite right. Although the hypothesis had been abandoned during the 1970s, it’s experienced somewhat of a resurgence, especially because we can make better and more frequent measurements of blood glucose. Due to this resurgence, the current view of the hypothesis is that there is indeed some connection between blood glucose levels and satiety or hunger, but that those perceptions are not tied to a specific level but rather to a pattern of changes in the level of blood glucose.
The lipostatic hypothesis
The lipostatic hypothesis is similar to the glucostatic one, the key difference being that it’s lipid levels rather than glucose which trigger the sensations of hunger or satiety. As we covered in our post on leptin, leptin is mainly produced by adipocytes (fat cells) and acts as a sort of signal of energy reserves in the body. Production of leptin is proportional to the amount of adipocytes in our body so the more fat that is carried then also the greater amount of leptin in the blood.
According to the lipostatic hypothesis, once fat reserves get below a certain threshold leptin levels do so too, and the sensation of hunger is triggered. Unsurprisingly, once fat levels increase, leptin levels rise and satiation happens.
Just like with the glucostatic hypothesis, reality is a little bit more complicated. In the overweight and obese, due to constant higher levels of leptin, a form resistance to it is developed and increased levels of leptin are needed in order to be feel sated. At the same time, leptin is not the only hormone involved in feeling hunger or satiation, so the lipostatic hypothesis is somewhat incomplete.
Some proposals have been made regarding the marriage of the glucostatic and lipostatic hypotheses. These propose that the glucostatic hypothesis works well when it comes to short term hunger and satiation, while the lipostatic one helps explain long-term trends regarding weight loss or gain. Still, more work needs to be done in this area.
Since neither the glucostatic nor the lipostatic hypotheses seem able to fully model how our feeding comes about, other mechanisms have been proposed like:
- The aminostatic hypothesis – So if glucose and (indirectly) fat levels are good candidates for hunger or satiety, why not aminoacids as well? The idea behind the aminostatic hypothesis comes from the idea that amino acids in the blood mainly come from the breakdown of muscle, and act on the brain as trackers of body mass changes experienced over days or weeks. At the same time, a diet composed of high protein intake also has the effect of ceasing hunger as long as blood levels of amino accids remain high.
- The thermostatic hypothesis – This time it’s about changes in temperature, experienced over several days or weeks, in the different tissues that make up our body. Given those changes, behaviours like feeding or increased activity seek to balance energy intake and expenditure. Decreases in body temperature lead to increased feeding while higher body temperatures lead to satiety.
Just as with the glucostatic and lipostatic hypotheses, the aminostatic and thermostatic ones have some merits and some mishaps, so there remains work to be done.
In this post we’ve covered several of the hypotheses of feeding. Although they all propose interesting ideas, they are all somewhat correct and somewhat incorrect. It’s clear that further work is required in order to understand what the mechanisms behind the sensations of hunger and satiety are.
In next week’s post we’ll cover the satiety cascade, if you’ve enjoyed this week’s post and would like to see more content like it, check out our page on Rebuttals to Fatlogic.
See you next week!