Leptin & Insulin: the hormones of your weight
Your weight is not a pure arithmetic result of calories. It is a signal. Two hormones sit at the centre: leptin reports your reserves to the brain and dampens hunger. Insulin stores. When these signals are disturbed, the body stores fat and still reports hunger. That is biology, not weak willpower.
People who come to me wanting to lose weight often have a long history of setbacks behind them. Diets, going without, discipline, and in the end the yo-yo effect. The most common self-diagnosis is: I lack willpower. I see it differently. Weight is a hormonal signal, not a pure calculation. Hunger, satiety, storage and expenditure are steered by hormones, above all leptin and insulin. In overweight, the body is often not deaf to food, but deaf to its own satiety signal. That changes everything. It shifts the question from how do I force myself to eat less to how do I make the signals clear again. In this article I show you how leptin and insulin work, what leptin resistance means and which directions the evidence supports.
This article is the hormonal foundation of the weight cluster. We go through what leptin is and how satiety reaches the brain, why leptin resistance often develops in overweight, how insulin works as a storage hormone, how chronically high insulin levels can favour fat storage, how sleep, fructose and movement shape these signals, and which three levers you can set in motion yourself. How insulin resistance specifically slows weight loss is deepened in its own article.
Leptin: your reserve signal to the brain
Picture leptin as your body's fuel gauge. It is released from your fat cells, the more fat, the more leptin. Through the blood it reaches the hypothalamus, a small control centre in the brain. There it reports: the stores are full, you may eat less and burn more. When little leptin is present, the brain believes reserves are running low and turns up hunger and an energy-saving mode. Leptin is therefore not a slimming hormone but a survival signal against starvation.
This control is remarkably fine. The hypothalamus adds up leptin and insulin as so-called adiposity signals and adjusts eating behaviour accordingly. Schwartz and colleagues described this in 2000 in the journal Nature as a complex network of hormones and neurotransmitters. The core message: food intake is a hormonally regulated process, not a pure act of will. That is exactly why lasting hunger under a strict diet does not feel like a lack of discipline but like a biological alarm. Because that is what it is.
How the brain steers hunger and satiety
Mechanism review Michael Schwartz and colleagues summarised in 2000 in Nature how hypothalamic circuits regulate the energy balance. Leptin and insulin act as long-term signals about the fill level of the energy stores. When central signalling molecules of this system are missing, pronounced obesity develops in rodents and, in rare cases, in humans. This shows how strongly the body regulates weight hormonally. The authors describe a model in which individual hormone and neuropeptide pathways jointly steer food intake.
Schwartz MW, Woods SC, Porte D, Seeley RJ, Baskin DG. Nature. 2000;404(6778):661-671. doi:10.1038/35007534 · PMID: 10766253
Most weight-loss advice treats hunger as a matter of character. From a hormonal view, hunger is a message. If your brain believes the stores are empty, you will want to eat, no matter how disciplined you are. The lever is not to drown out the hunger, but to make the message true again.
Leptin resistance: the signal no longer arrives
Here it gets surprising. If more fat means more leptin, people with overweight should actually be especially satiated. The opposite is often the case. The reason is called leptin resistance. The signal is sent, but the brain no longer responds to it effectively. It is like a doorbell that rings, but behind which no one gets up any more. The brain believes, despite full stores, that the body is starving, and keeps hunger and appetite high.
The evidence for this is almost thirty years old and still foundational. Robert Considine and colleagues measured in 1996 in the New England Journal of Medicine the leptin in the blood of 275 people. People with overweight had not too little, but around four times as much leptin as normal-weight people. If a lot of leptin is present and still no satiety effect occurs, then the problem is not the amount but the sensitivity. That is exactly leptin resistance.
Overweight usually means too much, not too little leptin
Human study, n=275 Robert Considine and colleagues measured in 1996 in the New England Journal of Medicine the serum leptin in 136 normal-weight and 139 overweight people. The overweight group had on average 31.3 nanograms of leptin per millilitre, the normal-weight group only 7.5. The leptin level was strongly linked to the body fat percentage (correlation r equals 0.85). The authors concluded: most overweight people are insensitive to their own, body-produced leptin. This is precisely the basis of the term leptin resistance.
Considine RV, Sinha MK, Heiman ML, et al. N Engl J Med. 1996;334(5):292-295. doi:10.1056/NEJM199602013340503 · PMID: 8532024
Why does the brain go deaf to leptin? This is being researched, and there are mechanistically plausible explanations. Myers and colleagues described in 2008 cellular brakes in the leptin signalling pathway, among them a molecule called SOCS3 that dampens signal transmission in the hypothalamus. Münzberg and Myers showed in 2005 that this dampening occurs especially in the arcuate nucleus, a core region of appetite control. Important for context: these are mechanistic works, much of it from animal models. They explain the how, without a finished therapy following from it.
What brakes leptin action in the brain
Mechanism review Martin Myers, Michael Cowley and Heike Münzberg summarised in 2008 in Annual Review of Physiology how leptin acts through its receptor and how this action can be braked. Elevated leptin levels no longer reliably suppress eating behaviour in obesity. As mechanisms the authors name the phosphorylation of certain receptor sites and the molecule SOCS3, which together promote cellular leptin resistance. A large part of these findings comes from animal models, and transfer to humans is not documented in every detail.
Myers MG, Cowley MA, Münzberg H. Annu Rev Physiol. 2008;70:537-556. doi:10.1146/annurev.physiol.70.113006.100707 · PMID: 17937601
An elegant counter-test confirms that leptin really steers causally and is not just a marker. In people with congenital leptin deficiency or with lipodystrophy, leptin is almost entirely missing. If they are given leptin as a medication (metreleptin), satiety, insulin sensitivity and a healthier lipid profile largely return (Paz-Filho 2014). In common obesity with already high leptin, additional leptin barely does anything. The lesson is clear: it is not about more leptin, but about the existing signal arriving again.
Insulin: the storage hormone
The second hormone at the centre is insulin. It has a bad reputation, often undeserved. Insulin is vital and primarily a storage and building hormone. After eating, blood sugar rises, the pancreas releases insulin, and insulin ensures that the sugar moves from the blood into the cells. In the fat cells it additionally promotes the storage of fat and at the same time slows fat breakdown. Insulin is the acute conductor that decides where the nutrients go (Baumgard 2015).
Insulin conducts fat storage
Mechanism review Lance Baumgard and colleagues described in 2015 in Domestic Animal Endocrinology how insulin is released and how it steers the fat cells. Their core statement: insulin is the primary acute anabolic coordinator of nutrient partitioning. In the fat cell it promotes fat storage in a dose-dependent way. When blood sugar rises, that is the strongest trigger for insulin release. Insulin thus links the composition of the meal directly to the body's decision to store or release fat.
Baumgard LH, Hausman GJ, Sanz Fernandez MV. Domest Anim Endocrinol. 2015;54:76-84. doi:10.1016/j.domaniend.2015.07.001 · PMID: 26521203
As long as insulin only rises briefly after meals and then falls again, all is well. It can become a problem when insulin levels stay chronically high. This is called hyperinsulinemia. It often arises when the cells respond less well to insulin and the pancreas counters with more insulin. If the level stays permanently high, metabolism shifts towards storage. Bódis and Roden showed in 2018 how fat handling in the tissue derails in insulin resistance, with increased fat breakdown in the wrong place and the release of inflammatory and lipid substances.
Insulin is not the enemy. A short insulin rise after eating is healthy and necessary. The unfavourable state is the permanently high level. The goal is not to abolish insulin, but to smooth the peaks and make the cells sensitive again. That is an important distinction that gets lost in many diet debates.
The carbohydrate-insulin model: one view among several
Why do some people seemingly eat normally and still gain weight? One explanation is offered by the carbohydrate-insulin model from David Ludwig and Cara Ebbeling. Their idea: highly processed, quickly digested carbohydrates drive blood sugar and with it insulin upwards. The high insulin channels energy preferentially into the fat depots, then intensifies hunger and can lower energy expenditure. It is not the calorie amount alone that counts in this model, but the hormonal effect of the food.
More than calories in, calories out
Review David Ludwig and Cara Ebbeling presented in 2018 in JAMA Internal Medicine the carbohydrate-insulin model of obesity. Their thesis: high-glycaemic carbohydrates trigger hormonal changes that channel energy into fat cells, intensify hunger and lower expenditure. Animal studies and some shorter human studies support individual predictions. The authors themselves stress that decisive, long-term feeding studies are still missing. The model is scientifically debated and stands opposite the classic energy-balance model. I present it here as one plausible view among several, not as proven truth.
Ludwig DS, Ebbeling CB. JAMA Intern Med. 2018;178(8):1098-1103. doi:10.1001/jamainternmed.2018.2933 · PMID: 29971406
„A calorie is a calorie, that is all you need to know." Physically, energy conservation holds. But the claim ignores what actually steers hunger, satiety, storage and expenditure. 200 calories from a soft drink and 200 calories from eggs and vegetables act completely differently on insulin, satiety and the next bout of hunger. The calorie is a unit of accounting, not a control lever.
How lifestyle shifts the signals: sleep, fructose, movement
The good thing about the hormonal view is that it reveals levers that have nothing to do with counting calories. The first is sleep. Too little sleep shifts the hunger hormones directly. In a clean randomised study, just two short nights lowered the satiety hormone leptin and raised the hunger hormone ghrelin. The result was more hunger, especially for carbohydrate-rich foods. That is not a head problem, that is measurable endocrinology.
Two short nights shift the hunger hormones
RCT, n=12 Karine Spiegel and colleagues studied in 2004 in Annals of Internal Medicine 12 healthy young men in a randomised cross-over study. After two nights of sleep restriction, leptin fell by about 18 percent, ghrelin rose by about 28 percent, and hunger and appetite increased by around a quarter, especially for calorie- and carbohydrate-rich foods. Calorie intake and physical activity were controlled. Sleep deprivation can therefore shift the hunger signals measurably towards eating more.
Spiegel K, Tasali E, Penev P, Van Cauter E. Ann Intern Med. 2004;141(11):846-850. doi:10.7326/0003-4819-141-11-200412070-00008 · PMID: 15583226
Short sleep, low leptin, higher BMI
Cohort study, n=1024 Shahrad Taheri and colleagues analysed in 2004 in PLoS Medicine the Wisconsin Sleep Cohort with 1024 people. People with short sleep had lower leptin and higher ghrelin, independent of the body mass index. For 5 instead of 8 hours of sleep, the model predicted around 15 percent less leptin. Between sleep duration and body mass index a U-shaped relationship appeared. What Spiegel found in the lab is confirmed here in a large population sample.
Taheri S, Lin L, Austin D, Young T, Mignot E. PLoS Med. 2004;1(3):e62. doi:10.1371/journal.pmed.0010062 · PMID: 15602591
The second lever is the type of carbohydrate, keyword fructose. Here I must phrase carefully, because the strongest data come from animal models. Vasselli and colleagues summarised in 2013 that a high-fructose diet can trigger leptin resistance in normal-weight rats, even without overweight. What is meant is mainly added fructose from soft drinks and highly processed products, not fruit with its fibre. In humans this effect is not yet documented with the same certainty. But it fits the picture that not only the amount, but also the quality of the carbohydrates can influence the satiety signal.
Can the diet itself create leptin resistance?
Review, mostly animal data Joseph Vasselli and colleagues summarised in 2013 in Advances in Nutrition how certain dietary components can promote leptin resistance. A central finding from rodent studies: a high-fructose diet can trigger leptin resistance in normal-weight rats, independent of body fat. Discussed mechanisms are a disturbed leptin transport into the brain, an altered glucose metabolism and a dampened receptor signalling. In humans this is not yet conclusively documented, I describe here mainly animal-model findings.
Vasselli JR, Scarpace PJ, Harris RBS, Banks WA. Adv Nutr. 2013;4(2):164-175. doi:10.3945/an.112.003152 · PMID: 23493533
The third lever is movement, and here it is mainly about the insulin side. The skeletal muscle is the largest organ by mass and the most important taker of sugar from the blood. It takes up around 80 percent of the glucose after a meal (Merz and Thurmond 2020). Active muscle can partly take up sugar even without much insulin and becomes more insulin-sensitive over time. Anyone who moves lowers the insulin demand and works directly at the root of hyperinsulinemia. Muscle is literally a metabolic organ.
Muscle is the biggest sugar taker
Mechanism review Karla Merz and Debbie Thurmond described in 2020 in Comprehensive Physiology the role of the skeletal muscle in glucose uptake. The muscle is responsible for around 80 percent of the sugar uptake from the blood after a meal and is thus central to the insulin sensitivity of the whole body. When sugar uptake in the muscle works poorly, this contributes substantially to peripheral insulin resistance. Conversely, muscle work can improve the uptake. That is why movement is a direct lever on the insulin side of weight regulation.
Merz KE, Thurmond DC. Compr Physiol. 2020;10(3):785-809. doi:10.1002/cphy.c190029 · PMID: 32940941
The KPNI lenses: why leptin and insulin rarely come alone
From the view of clinical psychoneuroimmunology, weight is an interplay of several systems. Four lenses help complete the picture. They do not replace the hormonal view, they complement it.
Metabolism and storage
Insulin and leptin are the core axis. Chronically high insulin levels favour fat storage, leptin resistance keeps hunger high. A steadier blood sugar through fewer highly processed carbohydrates can relieve both signals. The article on blood sugar spikes shows more.
Immune system and silent inflammation
Overweight fat tissue releases inflammatory substances, among them TNF-alpha and IL-6 (Engin 2024). This silent inflammation can additionally disturb the insulin signals and maintain the resistance. The article on inflammation deepens this.
Nervous system and sleep
The hypothalamus adds up the satiety signals. Sleep deprivation shifts leptin and ghrelin measurably (Spiegel 2004). Too little or poor sleep is thus a direct hormonal disruptor, not a side stage.
The hormone system in concert
Leptin and insulin work together with ghrelin, cortisol, thyroid and GLP-1. Stress and a cortisol out of rhythm can promote belly fat. Weight is a network, not a single dial.
What does not work (and is everywhere anyway)
An honest look at the advice that promises much and delivers little belongs here.
- Just eating less with the same food quality. Chronic calorie restriction can lower resting metabolism and drive cravings. If the hormonal situation stays the same, this often ends in the yo-yo. The quality and hormonal effect of food is the better lever than sheer quantity.
- Buying leptin as a supplement. Leptin as a capsule does nothing, it would be broken down in the digestive tract. And even injected it barely does anything in common obesity with high leptin, because the problem is the resistance, not the deficiency (Paz-Filho 2014).
- Willpower as the sole solution. If your brain reports hunger despite full stores, more discipline is rarely the answer. It is more sensible to clarify the signals, through sleep, blood sugar, movement and inflammation.
- Demonising fat across the board. The focus on dietary fat and calories alone falls short when highly processed carbohydrates drive insulin. It is worth looking at both sides.
Not your will is the problem, but the signal
When your body stores fat and still reports hunger, that is not a failure. It is a disturbance of the signals that steer hunger, satiety and storage. And signals can be clarified. That is the difference between fighting your own body and working with it.
Three levers you can start this week
Take sleep seriously as a hormone lever
Aim for regular, sufficient nights. Just a few short nights can lower leptin and raise ghrelin (Spiegel 2004). A fixed wake-up time and less screen time in the evening are a good start. This is not a side topic for weight, but a direct lever on the hunger hormones.
Smooth the blood sugar spikes
Fewer highly processed, quickly digested carbohydrates, instead more protein and fibre. This can dampen the insulin peaks and keep you satiated longer. It is not about going without, but about order and quality. The article on blood sugar spikes shows concrete directions.
Move your muscles, especially after eating
Active muscle takes up sugar from the blood and becomes more insulin-sensitive (Merz and Thurmond 2020). Even a short walk after the meal can dampen the blood sugar and insulin response. Muscle is a metabolic organ, not just aesthetics.
If you are not losing weight despite sensible eating and movement, if you notice strong cravings, marked fatigue, increased thirst or belly fat, have your blood sugar, insulin and further values checked medically. This applies especially with a family history of diabetes. On weight-loss injections: they are prescription-only and belong in medical supervision, this text does not replace consultation and gives no tip on how to obtain them.
Frequently asked questions about leptin, insulin and weight
What is leptin resistance?
Leptin is a hormone from your fat cells. It tells the brain how full the energy stores are and, when reserves are sufficient, dampens hunger. In leptin resistance the body still sends the signal, but the brain no longer responds to it effectively. Considine showed in 1996 in the New England Journal of Medicine, in 275 people, that people with obesity do not have too little but clearly more leptin in the blood (on average 31.3 versus 7.5 nanograms per millilitre), strongly linked to the body fat percentage. Most people with obesity are insensitive to their own leptin. The brain believes, despite full stores, that the body is starving. Leptin resistance is a biological state, not weak willpower.
Does insulin make you fat?
That blanket claim is not accurate, but there is a kernel of truth. Insulin is the anabolic storage hormone. After eating it ensures that sugar reaches the cells, and in the fat cells it promotes storage and slows fat breakdown. That is a healthy, necessary function. It can become a problem when insulin levels stay chronically high, for example from frequent, highly processed carbohydrates. Then metabolism shifts towards storage. The carbohydrate-insulin model (Ludwig and Ebbeling 2018) describes this as a hypothesis that is scientifically debated. Insulin itself is not the enemy, chronically high levels are the unfavourable state.
Can leptin resistance be reversed?
There is no pill that simply switches off leptin resistance, and I deliberately promise no cure. What is mechanistically plausible and what I find sensible clinically as a direction: address the factors that disturb the leptin and insulin signals. These include enough sleep (sleep deprivation lowers leptin, Spiegel 2004), a steadier blood sugar through fewer highly processed carbohydrates, more movement for insulin sensitivity (Merz and Thurmond 2020) and lowering silent inflammation (Engin 2024). These are directions, not recipes. In congenital leptin deficiency, leptin replacement can help, in common obesity with high leptin it barely does (Paz-Filho 2014).
Which hormones control hunger and satiety?
Several hormones work together. Leptin from the fat cells is the long-term reserve signal, it dampens hunger when the stores are full. Ghrelin from the stomach is the counterpart, it reports hunger before meals. Insulin steers blood sugar in the short term and also serves as a satiety signal in the brain over time (Schwartz 2000). GLP-1 from gut and brain is another satiety signal and the basis of modern weight-loss medications (McLean and Drucker 2021). The hypothalamus adds up these signals. That is why hunger is not a pure act of will, but the result of a hormonal calculation.
Does sleep affect body weight through hormones?
Yes, and the link is well documented. Spiegel and colleagues showed in 2004 in a randomised cross-over study of 12 healthy young men: just two nights of sleep restriction lowered the satiety hormone leptin by about 18 percent, raised the hunger hormone ghrelin by about 28 percent and increased hunger and appetite, especially for carbohydrate-rich foods. Taheri and colleagues found the same association in 2004 in the Wisconsin Sleep Cohort of 1024 people epidemiologically: short sleep went with low leptin, high ghrelin and a higher body mass index. Too little sleep can therefore shift the hunger hormones towards eating more.
Is losing weight really only a matter of calories?
The calorie balance holds physically, energy is not lost. But the phrase eat less, move more falls short, because it ignores what actually steers hunger, satiety, storage and expenditure. That is exactly what hormones such as insulin, leptin, ghrelin and GLP-1 regulate, together with sleep, inflammation and the gut. Two people can eat the same number of calories and react differently. Chronic calorie restriction can also lower resting metabolism and drive cravings. That is why I put the quality and hormonal effect of food ahead of sheer quantity. The calorie is a unit of accounting, not a control lever.
What does hyperinsulinemia mean?
Hyperinsulinemia means chronically elevated insulin levels in the blood. It often arises as a response to early insulin resistance: the cells respond less well to insulin, so the pancreas releases more of it. Insulin is the acute anabolic coordinator of nutrient partitioning (Baumgard 2015) and promotes fat storage in fat cells in a dose-dependent way. If the level stays chronically high, this can favour storage and make fat breakdown harder. Bódis and Roden showed in 2018 how fat handling derails in insulin resistance. A steadier blood sugar through fewer highly processed carbohydrates can help keep insulin levels lower.
Can fructose trigger leptin resistance?
There are hints, but the strongest data come from animal models. Vasselli and colleagues summarised in 2013 in Advances in Nutrition that a high-fructose diet can trigger leptin resistance in normal-weight rats, even without increased body fat. As mechanisms a disturbed leptin transport into the brain, an altered glucose metabolism and a dampened receptor signalling are discussed. In humans this is not yet documented with the same certainty. What is meant is mainly added fructose from soft drinks and highly processed products, not fruit with its fibre. I phrase this carefully on purpose, because the human evidence here is thin.
How are leptin and insulin connected?
Both are signals that report the energy state to the brain, and they interlock. Insulin promotes fat storage, more fat mass means more leptin. Leptin in turn steers hunger and energy expenditure in the hypothalamus (Schwartz 2000). In overweight, leptin resistance and insulin resistance often occur together, and silent inflammation in fat tissue can maintain both (Engin 2024). This explains the vicious circle: the body preferentially stores fat and still reports hunger. Making the signals clearer, through sleep, blood sugar, movement and inflammation, works at the cause rather than the symptom.
Are weight-loss injections the same as leptin?
No. Modern weight-loss medications act on GLP-1, a satiety signal from gut and brain (McLean and Drucker 2021), not on leptin. GLP-1 dampens appetite, slows gastric emptying and acts on satiety centres in the brain. They use a body-own mechanism. Their effect on weight and metabolism is clear in studies. At the same time they are prescription medications with possible side effects, a risk of muscle loss and the question of what happens after stopping. They do not replace the foundations. For leptin this path does not exist: additional leptin barely does anything in common obesity with high leptin (Paz-Filho 2014).
Connections to other topics
How ghrelin, leptin and GLP-1 together steer appetite and why some people never feel really full. The continuation of this hormonal picture.
Why the body preferentially stores fat in insulin resistance and how insulin sensitivity can be improved again. The practical deep-dive article.
How silent inflammation from fat tissue and gut maintains the insulin and leptin signals and makes losing weight harder.
Which hormonal and blood-sugar-related patterns lie behind cravings and which directions can take the edge off them.
How you smooth the insulin peaks with order, protein and fibre and stay satiated longer. The concrete nutrition page.
Sources and further reading
- Considine RV, Sinha MK, Heiman ML, et al. Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med. 1996;334(5):292-295. doi:10.1056/NEJM199602013340503 · PMID: 8532024 [Human study, n=275]
- Schwartz MW, Woods SC, Porte D, Seeley RJ, Baskin DG. Central nervous system control of food intake. Nature. 2000;404(6778):661-671. doi:10.1038/35007534 · PMID: 10766253 [Mechanism Review]
- Myers MG, Cowley MA, Münzberg H. Mechanisms of leptin action and leptin resistance. Annu Rev Physiol. 2008;70:537-556. doi:10.1146/annurev.physiol.70.113006.100707 · PMID: 17937601 [Mechanism Review]
- Münzberg H, Myers MG. Molecular and anatomical determinants of central leptin resistance. Nat Neurosci. 2005;8(5):566-570. doi:10.1038/nn1454 · PMID: 15856064 [Mechanism Review]
- Baumgard LH, Hausman GJ, Sanz Fernandez MV. Insulin: pancreatic secretion and adipocyte regulation. Domest Anim Endocrinol. 2015;54:76-84. doi:10.1016/j.domaniend.2015.07.001 · PMID: 26521203 [Mechanism Review]
- Bódis K, Roden M. Energy metabolism of white adipose tissue and insulin resistance in humans. Eur J Clin Invest. 2018;48(11):e13017. doi:10.1111/eci.13017 · PMID: 30107041 [Review]
- Ludwig DS, Ebbeling CB. The Carbohydrate-Insulin Model of Obesity: Beyond "Calories In, Calories Out". JAMA Intern Med. 2018;178(8):1098-1103. doi:10.1001/jamainternmed.2018.2933 · PMID: 29971406 [Review]
- Vasselli JR, Scarpace PJ, Harris RBS, Banks WA. Dietary components in the development of leptin resistance. Adv Nutr. 2013;4(2):164-175. doi:10.3945/an.112.003152 · PMID: 23493533 [Review, mostly animal data]
- Spiegel K, Tasali E, Penev P, Van Cauter E. Brief communication: Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med. 2004;141(11):846-850. doi:10.7326/0003-4819-141-11-200412070-00008 · PMID: 15583226 [RCT, n=12]
- Taheri S, Lin L, Austin D, Young T, Mignot E. Short sleep duration is associated with reduced leptin, elevated ghrelin, and increased body mass index. PLoS Med. 2004;1(3):e62. doi:10.1371/journal.pmed.0010062 · PMID: 15602591 [Cohort study, n=1024]
- Merz KE, Thurmond DC. Role of Skeletal Muscle in Insulin Resistance and Glucose Uptake. Compr Physiol. 2020;10(3):785-809. doi:10.1002/cphy.c190029 · PMID: 32940941 [Mechanism Review]
- Paz-Filho G, Mastronardi CA, Licinio J. Leptin treatment: facts and expectations. Metabolism. 2015;64(1):146-156. doi:10.1016/j.metabol.2014.07.014 · PMID: 25156686 [Review]
- McLean BA, Wong CK, Campbell JE, Hodson DJ, Trapp S, Drucker DJ. Revisiting the Complexity of GLP-1 Action from Sites of Synthesis to Receptor Activation. Endocr Rev. 2021;42(2):101-132. doi:10.1210/endrev/bnaa032 · PMID: 33320179 [Mechanism Review]
- Engin A. Reappraisal of Adipose Tissue Inflammation in Obesity. Adv Exp Med Biol. 2024;1460:297-327. doi:10.1007/978-3-031-63657-8_10 · PMID: 39287856 [Review]