How Your Body Fat Can Make You Hungrier

0:00Your body fat doesn't just store energy. It releases hormones, and one of those hormones can actually increase hunger. It's called Aspracin. Researchers discovered it in 2016, and animal studies show it does two important things. It tells the liver to release glucose into the blood, and it activates cells in the brain that drive hunger. During a fast, that makes some sense. Your body is helping maintain your blood sugar while encouraging you to find food. But what happens if that signal stays elevated when you're not fasting? Human studies often find higher Aspersin in people with obesity and insulin resistance.

0:39That's an interesting connection, but it doesn't prove that Aspersin is causing either necessarily. In mice, blocking Aspersin reduced hunger and blood glucose. Whether that approach works in people remains an open question. But the takeaway, body fat is an active organ sending signals that help influence both your blood sugar and your appetite. This is lecture 169 of the Metabolic Classroom.

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3:38Welcome back to the Metabolic Classroom. I'm Ben Bickman, metabolic scientist and professor of cell biology. When most people think about body fat, they think about stored energy. Fat is where the extra calories go, and fat is what we hope to lose. That's the traditional view, but that view leaves something out. Fat cells also release hormones into the blood. It is an active endocrine organ, in fact, a very active one. And some of those hormones reach other organs and change what those organs are going to do. Some of these fat-derived hormones are very, very well known. You, of course, have heard of leptin.

4:16It is the most famous one. But in 2016, 10 years ago now, researchers described a new hormone released from fat tissue that rises when we go without food. When it reaches the liver, the liver releases more glucose into the blood. When it reaches the brain, it activates the nerve cells that make us want to eat a little more. That combination is interesting because, of course, during a fast, you want to try to keep blood glucose up from the liver. And if you have increased hunger, well, that also makes sense because you're fasting. Your body is going to – the brain is going to want you to go eat a little more.

4:52Both of those things are going to help you get through a period of no food or to correct a period of no food. But if the same hormone stays high when a person is not fasting, then those same two effects are going to wreak some metabolic mayhem. Then you have blood sugar going up. You have appetite going up, even if you maybe have already eaten something and you have no reason for that hormone to be doing this. That hormone that I've been alluding to is called Aspirin. The main point is that fat tissue is an endocrine organ. And in animal studies, one of the effects of this hormone is what I said.

5:28In fact, the two effects, increasing or helping maintain blood glucose and driving hunger. To get started, let's define the hormone itself. Aspercin comes from a gene called FBN1. This gene makes a large protein called profibrillin. Most of profibrillin becomes fibrillin 1, which is a structural protein that just the body uses to help build connective tissue outside of cells. But mutations in FBF1 are actually the best known cause of Marfan syndrome, which is considered a connective tissue disorder. Those are people who will have hypermobile joints, the kind of person who can put their leg over their head or reach around with one arm and touch their ear coming under their, you know, pretty extreme examples of what they can do.

6:20Scratch the hard to reach part of your back. But that same big molecule, the profibrolin, has a small piece at the very end. That small piece was assumed to have no particular job. But as happens so often, it seems what we once considered junk in the body is not at all. And it just plays a role we haven't identified yet. That 2016 paper that I mentioned, that primary study that they named in that study, they named this unidentified – well, that segment, that cleaved segment, they named it Aspersin, and they showed that that piece is released and it acts like a hormone. Now, the word, the name Aspersin comes from the Greek word for white.

7:03The researchers chose it because the hormone appeared to come mainly from white adipose tissue, which is the, of course, the ordinary fat tissue under the skin, the fat that you can pinch or jiggle, but also the fat that you have viscerally tucked deeper in your body around your organs. and people who lack it have very little of that fat under their skin, especially that subcutaneous fat depot. In that first study, the researchers showed several basic features. Aspersin circulates in the blood at conventional concentrations with some hormones in a nanomolar concentration. That's pretty typical.

7:43In mice that are housed under very controlled conditions, blood Aspersin followed a daily rhythm and it dropped sharply when the animals began to eat. After an overnight fast, blood Aspersin has been shown to be higher in humans and in rodents compared with fed conditions. Each of those fasting comparisons in the animals and the rodents, well, in the human study rather, they used seven subjects. Now that's small and I'm going to come back to later in the lecture why some of that's a problem. because there's the lack of some human evidence just, of course, leads to some lack of clarity. But I'll get to that.

8:24Before that, let's move on to the first target organ, which is the liver. During a fast, the liver still needs some or the body still needs some glucose. And remember something I've discussed previously, red blood cells are a primary example of a cell type, maybe, in fact, the only actual cell type that we know can only use glucose. It's tempting for me to say, and you may be inclined for me to say it, that the brain requires or must have glucose. That's the kind of textbook organ that is always mentioned. And yet my lab just published a paper a couple of weeks ago finding that in other mammal models and rodents specifically, the brain appears to function well without any glucose whatsoever.

9:09So maybe we're trying to rewrite the textbook. But anyway, the body needs glucose. Some cells must have it, at least the red blood cells. And so it's thankful, we're thankful that the liver can supply it. Part of that comes from breaking down stored glycogen, that storage form of glucose. And part of it is through building new glucose, that process of gluconeogenesis. Now, several hormones control that overall output, the breakdown of glycogen, which is called glycogenolysis, and the synthesis of new glucose from scratch, gluconeogenesis. Glucagon is the best known influence there, and there are others, but Aspergsin appears to be another.

9:51In the original study, Aspergsin given to mice raised blood glucose within just minutes. And when researchers exposed liver cells to Aspergsin, the cells released more glucose. Inside the liver, Aspergsin worked through a signaling pathway that is the same general pathway that glucagon actually uses. So there's some redundancy. Activation of that path, whether it's glucagon or aspercin, tells the liver to release glucose. The scientists in that study also tested what happens when aspercin is removed. They used two approaches. One was genetic, using mice with reduced aspercin levels. The other was immunologic, meaning they gave an antibody that binds aspercin in the blood and stops it from acting.

10:38In both cases, blood glucose and blood insulin went down, and the cause was reduced glucose output from the liver. There's another finding from that study that matters for anyone interested in insulin, which, of course, you all are, I hope. When liver cells were treated with insulin, insulin suppressed Aspersin's activation and suppressed glucose release that Aspersin normally would be causing. In other words, insulin opposed Aspersin at the liver cell, much as insulin opposes a glucagon. At that point, the receptor, meaning the protein on the cell surface that the hormone binds, it was not known.

11:17So we didn't know how Aspersen actually did what it does to the liver. It's not binding the glucagon receptor. I hope what I just said wasn't confusing. It starts to overlap with the same pathway, but it is a distinct receptor, which allows us to skip a few years to 2019, which were in a different group identified that this specific receptor is an olfactory receptor. Olfactory receptors, if that name sounds familiar, they're actually best known for detecting odors in the nose. But some are made and present in other tissues. And you wouldn't think of the liver as smelling anything, but in a way you could say it's smelling Aspersin.

12:00The researchers found that mice lacking the receptor, this Aspersin or the specific olfactory receptor had a blunted response to Aspersin. Their livers released less glucose and their insulin sensitivity got better. Loss of the receptor also reduced the rise in liver glucose output caused by fasting. Okay, now let's move from the liver to the second target organ, which is the brain. and the effects on appetite. So I had fast forwarded us to 2019. Now we go back to 2017. The same group that discovered Aspersin reported that it also affects hunger. They found that Aspersin in the blood crosses the blood-brain barrier, which is that tightly regulated border between blood and brain.

12:49Once in the brain, it reaches the hypothalamus. That's the small region near the base of the brain that helps control appetite. The hypothalamus contains two well-studied groups of nerve cells, and they work in opposite directions. When the first group of these nerve cells is active, the animals will eat more. When the second group is active, animals will eat less. Well, Aspersin turns on the first group, and those cells in turn quieted or inhibited the second group. The net effect of this maybe complicated signaling as I described it, and believe me, I'm actually making it simpler, but the net effect was more eating.

13:30And over time, more body fat and higher body weight levels in the animals. The receptor in the brain is not the same receptor as in the liver. In 2022, the same initial Aspersin discovering group identified that brain receptor. Aspersin attached to it very tightly, even at very low concentrations. And mice that lacked this receptor ate a lot less. they were lean and did not eat more when they were even given injections of Aspergillin. When the receptor was removed only from the hunger-promoting nerve cells, the mice were resistant to weight gain, even on a diet that would have normally made them fat, a high-sugar, high-fat diet.

14:15The researchers also made a free-floating copy of a part of the receptor that would bind to Aspergillin and put it into the blood. So they injected this. And this piece would then bind to Aspersin before it could reach the target receptor in the brain. And as expected, as the Aspersin now can't signal at the brain, appetite and blood glucose both went down. So the animal data described two receptors for one hormone. In the liver, the effect is glucose release. In the brain, the effect is hunger. These receptor findings come largely from just exclusively from lab work. And most of the brain work only comes from one single group of researchers.

14:59That's not a problem necessarily, but it does limit just how much we know. What we hope for in the near future at some point is that we can start to kind of stack on and get more findings from other groups. Now, let's go back and look at how Aspersen was found because the human genetics are actually part of the story, and there's some of the strongest evidence in it. The discovery started with a rare condition called neonatal progeroid syndrome. Babies with this condition are born with very little fat under the skin, especially in their face and limbs. And that word progeroid is a little misleading.

15:36It means resembling premature aging. I would say that in quotes if you couldn't tell from the way I read or stated and italicized phrase resembling premature aging because the facial features of the baby look a little older, but that does not in any way mean they age any faster. So the name is misleading. Again, it's just to suggest that the babies look a little older because they don't have that kind of chubby, typical cherubic face of a newborn. The researchers studied two unrelated patients with this syndrome. Both had normal glucose, but their blood insulin was about half that of unaffected people.

16:16Genetic testing found that both had a new mutation in one copy of FBN1 near the very end of the gene. Remember, that little end where Aspersen is clipped off. The researchers then searched the medical literature and found five more reports of single patients with the same syndrome and the same kind of mutation. In all seven people, the mutations fell within a very short stretch at the end of the gene, right where the Aspersin piece is normally cut free and then free to act in the body. So these mutations cut the protein short at the spot where Aspersin would normally be. The cell is able to still make the fibrillin protein, but the Aspersin piece is lost from that mutated copy of the protein from the mutated gene.

17:07And patients with this syndrome, no surprise, had lower blood Aspersin levels than control patients. People who lack a lot of that Aspersin will have very little fat, very low insulin, but they'll have a normal blood glucose. And that's just because of all the myriad inputs and outputs that come from glucose regulation. Back to that 2017 study, it added that these patients also have very low appetite and they're very lean. Mice engineered to carry similar mutations as the humans in these studies actually had the same kind of mouse version of appearance. Very, very lean, very low appetite, and giving the mice Aspersin restored the appetite and the body weight.

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19:17The human evidence here is legitimate and very real, but it does come from, of course, a very small number of patients. This is a very rare condition. And so there's not a lot we can necessarily know. But what we know is what I just articulated. Okay, next, let's look at what happens in people with obesity and insulin resistance and how strong that evidence is. In the original study, the researchers measured blood aspirin in a very small group. It was eight subjects with obesity and insulin resistance, and then eight subjects matched for age and sex, but not with – they were metabolically controls, if you will.

20:02Aspersin was higher in the men with insulin resistance. It was also higher in two mouse models of obesity and insulin resistance. That 2017 study that I've now mentioned multiple times reported higher Aspersin in people and mice with obesity as well, just in general. So this is general animals overfed to become obese and humans that had obesity. Since then, many groups have measured Aspersin in human populations. In fact, very recently, a 2024 meta-analysis, so a study that will pool the results of a lot of other studies, it in fact included 26 studies and it had almost 4 ,000 total study subjects included across those studies.

20:47On average, people with type 2 diabetes or metabolic syndrome or obesity had higher Aspersin than people without those conditions. Just last year in 2025, a meta-analysis, a smaller one of 14 studies, also found higher Aspersin in people with diabetes than in healthy controls. Those pooled results do support a link. However, the individual studies, when you looked at each one individually, they don't have a lot of consensus. and that's because of just how there's a lot of inconsistency across the actual levels of Aspersand that within the pooled averages, which is what the meta-analyses are doing, you end up, it ends up kind of covering a lot of noise.

21:36And a part of this is just because it's so difficult to measure it. There's no, measurement is the biggest problem. Almost all of the human studies are using commercial test kits that will detect the protein using antibodies. That's not uncommon. But it just indicates that with the lack of a consistent test, what we find in the human studies is that it can range from nanograms per milliliter up to like one nanogram or even lower levels up to the hundreds of nanograms per milliliter across people who should be the same. In children, some of the studies that have been done find a 10 ,000-fold difference in the levels of Aspersin.

22:22So it's not to say that you don't have differences in people. You do. Some people will and likely should. We could reasonably assume have higher levels than others, but not 10 ,000 times higher. So the authors of some of these meta-analyses just start to suggest that a lot of the problem here that's preventing Aspersin from being measured correctly is just wildly different ways of measuring it. In one of the studies that developed their own test kits and then validated it and repeated it, they consistently find – so this is, I think, where we can come to a general range – that Aspersin levels are around 10 nanograms per mil.

23:02So that kind of low nanogram per milliliter level. But in that same study that identified a consistent level of the hormone, they didn't know directly. It was hard for them to find the direct effects that their data suggested that cartilage may also contribute to blood aspirin in addition to fat tissue. So to say that again another way, as much as the hormone was originally identified as coming from fat tissue, they find that it also can come from cartilage. That's not been settled yet, but that's novel in a lot of ways, not only because of just a new location for Aspersin, but novel in that it identifies cartilage as an endocrine organ as well, producing its own set of hormones.

23:52In the midst of all of this confusion, I think there is a solid finding, and that's that in mice, Aspersin rises with fasting and obesity. It raises liver glucose output. It increases appetite. And if you remove it, you are lowering glucose, insulin, and food intake and body weight. The early findings is on that human side where the general consensus shows that there are higher levels of Aspersin and obesity and insulin resistance and type 2 diabetes. But those studies have wildly different ways of measuring Aspersin and wildly different levels. Although, again, the trend is there. And at the moment, it's no surprise, Aspersin is not a validated clinical test.

24:38So you can't go into your clinician and say, I want you to measure my Aspersin levels. there's just no way for them to do it. It's something that's strictly within the realm of academia for now. Hey, Pablo Torre here. And if you listen to my show, Pablo Torre finds out, I think you have a sense of what it's all about. I, you know, dig past the surface level of stuff. And right now, as the NBA season tips off, I do need a reliable and smart way to actually watch these games. And that is why we're talking about Sling TV. Sling gives you not just basketball, but sports at a great price, starting at just$19.99 a month.

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26:44Okay, let's put Aspergsin next to some other hormones that affect hunger, because these hormones are often blended together under a single label of hunger hormone. But that label can cause some confusion. It's misleading. Ghrelin is a pretty big one when it comes to hunger. It's made from the stomach. In humans, ghrelin rises before a person eats and it falls right after they eat. And that timing, it suggests a role in wanting someone to eat, initiating the meal. Like Aspersin, ghrelin acts on the hunger-promoting nerve cells in the hypothalamus. But it comes from a very different organ. It's coming from the stomach.

27:26It uses a very different receptor, and its main job appears to be signaling short-term hunger and kind of meal cues. Leptin, of course, is an obvious one. It's made by the fat tissue just like Aspersin is, but it acts in the opposite direction. Leptin levels generally track the amount of body fat, and leptin reduces appetite through the hypothalamus. During fasting, leptin will fall, and that fall is a major signal that energy starts to get a little scarce, even if it's not actually. But in mice, the drop in leptin during fasting will drive other hormones in response to hunger. And so that's kind of a typical role as we understand leptin.

28:10So during a fast, fat tissue sends at least two signals that both favor eating, less leptin, and according to the animal data, more Aspergson. Now, of course, you're wondering about GLP-1. GLP-1 is made mostly by cells in the gut, the L cells, in response to a meal. GLP-1 has been implicated in having an effect on insulin, but that's something I've talked about before, that it's actually insulin sparing in the context of a real meal because it reduces the digestion and the glucose input into the blood so much that the actual amount of insulin released is less. But it will, yeah, and that's the main effect.

28:53It slows the rate at which food is moving through, which definitely has that insulin sparing effect, and it will reduce appetite. Of course, you know GLP-1 because that's the hormone that is being activated with these famous weight loss drugs. When it comes to timing and effect, GLP-1 you could consider to be the closest opposite of Aspergine. GLP-1 rises with food and it lowers glucose and appetite. Aspergine rises without food and it raises glucose and appetite. Each of these hormones, of course, has its own source. It has its own timing and circulation. It has its own receptor, its own effects.

29:38So none of them should be called the hunger hormone. They're all part of a suite, a small choir of signals, kind of singing to the body when it's time to eat or not eat. Okay, now let's look at what lowers Aspersin and what we still don't know. The clearest suppressor in the original work is simply eating. In mice, blood Aspersin dropped when the animals started eating. The researchers then asked whether glucose itself could be the signal. When they exposed fat cells in a dish to high glucose, the fat cells released much less Aspersin than fat cells kept without glucose. That supports a feedback loop in which Aspersin raises glucose and glucose lowers Aspersin.

30:27This was shown in cultured cells. So that's just a nice feedback. It's not been confirmed in humans yet. Now, insulin's role has two parts. As I described earlier, insulin opposed Aspersin's effect inside liver cells. That is an effect on what Aspersin does, which is not the same as an effect on how much Aspersin is released. Whether insulin directly lowers Aspersin release from fat tissue in humans is not known yet. Human meal studies are limited, unfortunately, and there's not a clear consensus. In one study of children and teenagers with obesity, average Aspergson did not change between the fasting sample and the sample taken two hours into a glucose tolerance test.

31:13About 56 % of the children actually had an increase. That goes back to some of the problem with measuring it. Those with an increase had more insulin resistance and higher fasting glucose. This raises the possibility that the normal fall in Aspersin after eating is impaired in insulin resistance. But this was a single study that measured each child at one point in time. And it used, again, one of those commercial test kits that have just been shown to not be overly reliable. Now, several questions remain when it comes to our understanding of Aspersin. We do not know precisely how fat cells control the cutting and release of Aspergsin in response to fasting.

31:59We do not know how much of human blood Aspergsin comes from fat tissue compared to other tissues like cartilage. We also don't know whether the two receptors that were identified and described in the mouse studies account for all of Aspergsin's effects in humans. and we do not yet have human studies that show what happens to glucose or appetite when Aspersin is raised or lowered on purpose. Okay, let's move on and look at the research on blocking Aspersin. In the original study, a single injection of an antibody against Aspersin lowered blood insulin in obese mice. In that 2017 study, an antibody that neutralized Aspersin in the blood reduced appetite and body weight in obese mice and improved their blood glucose.

32:47A 2021 study tested it a little more broadly. The researchers made three separate antibodies, each recognizing a different part of Aspersin. All three lowered appetite, body weight, and blood glucose in three different mouse models of metabolic syndrome. So they made them overweight and insulin resistant through different means. The effects increased as the dose did. The antibodies lasted more than three days in the blood of the mice. And the free floating receptor approach that I described earlier also lowered appetite and glucose in mice. These results are consistent, but they're animal studies from a very small group of researchers.

33:31So if they have problems in their methods and the problems are just kind of being propagated into the studies. So it's difficult to fully know all the consequences. So in the midst of all my teaching, I worry that I'm introducing a lot of confusion, but that's unfortunately par for this course when it comes to Aspersen. Blocking Aspersen is a very early research stage idea in humans. There is no anti-Aspersen treatment approved for use in people, and I'm not even aware of published human trial results or even proposal for human trials. Finally, let's bring this together. An endocrine organ releases hormones into the blood to act on distant tissues.

34:16That is the definition of an endocrine organ. One organ releases something, it goes to another tissue and tells that tissue to do something. Fat tissue is one of those, as I said, very busy endocrine organs. It releases leptin, it releases adiponectin, and so many more. One of them, according to this work that I mentioned, is Aspersin. What makes Aspersin useful to understand is that it links two responses to an energy deficit in a single molecule. In mice, when food is absent, fat tissue releases more Aspersin. Aspersin reaches the liver and it increases glucose output. Aspersin also, as I noted, crosses the blood-brain barrier and it activates those nerve cells that drive hunger, which is going to increase the drive to eat.

35:04Feeding or higher glucose will bring aspersin back down and insulin opposes the effects of aspersin at the liver. the problem arises when levels stay high outside of a fast as they appear to do in obese in obesity and insulin resistance and the human studies on average point that same direction but as i've said multiple times they're inconsistent and they're pretty limited by some uncertain measurement techniques the practical lesson here i think is just at this level until there are more definitive treatments and evidence in humans is just more insight into the very active role of our fat tissue.

35:47Fat is an active organ that sends signals throughout the body that can affect blood sugar and appetite. So when we talk about insulin resistance and hunger, we should include fat tissue as a source of those signals, right alongside when we talk about the pancreas, the gut, and the brain. Class dismissed. Until next time, more knowledge, better health.

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