Diet and nutritionAdipose tissue — a lazy storage depot or an organ that controls your hunger?
Sources: 11 · Article: 13 632 characters
Henryk Różański describes it as an energy reservoir in which fat is both stored and broken down.
- Prof. David Ludwig writes that the brain regulates hunger and that signals from adipose tissue can reach it.
- Prof. David Ludwig also presents a model in which fat cells store too much energy, causing a person to feel hungry and their metabolism to slow down.
What the authors write
prof. David Ludwig
Adipose tissue is a specialized organ and, among other functions, serves as an energy reserve.
„But body fat is a highly specialized organ, critically important for health and longevity. Among its many functions, fat surrounds and cushions vital organs like the kidneys and insulates us against the cold. Body fat also signifies health, conferring beauty when distributed in the right amounts and locations. But critically, fat is our fuel tank — a strategic calorie reserve to protect against starvation.”But body fat is a highly specialized organ, critically important for health and longevity. Among its many functions, fat surrounds and cushions vital organs like the kidneys and insulates us against the cold. Body fat also signifies health, conferring beauty when distributed in the right amounts and locations. But critically, fat is our fuel tank — a strategic calorie reserve to protect against starvation.
prof. David Ludwig
The brain regulates food intake, energy expenditure, and adipose tissue metabolism; the brain also mediates the feeling of hunger.
„5. Body fatness is regulated by the brain, not by fat tissue or the pancreas. There is a vast research literature showing that the brain regulates food intake, energy expenditure, and fat tissue metabolism to regulate the size of body fat stores (10). There is no known mechanism intrinsic to fat tissue or the insulin-secreting pancreas that does this. Genetic differences that impact body fatness tend to be located in genes that affect brain function, not fat tissue or insulin signaling (11, 12).
The brain of course mediates hunger and metabolic rate, but that fact tells us nothing about peripheral and external influences.”5. Body fatness is regulated by the brain, not by fat tissue or the pancreas. There is a vast research literature showing that the brain regulates food intake, energy expenditure, and fat tissue metabolism to regulate the size of body fat stores (10). There is no known mechanism intrinsic to fat tissue or the insulin-secreting pancreas that does this. Genetic differences that impact body fatness tend to be located in genes that affect brain function, not fat tissue or insulin signaling (11, 12).
The brain of course mediates hunger and metabolic rate, but that fact tells us nothing about peripheral and external influences.
prof. David Ludwig
In the model described, excess insulin causes fat cells to store calories, leaving too few for the rest of the body. As a result, a person feels hungry and their metabolism slows down.
„High insulin levels — caused by our modern processed diet and other influences — have programmed fat cells to take in and store too many calories, leaving too few for the rest of the body. So we get hungry, and metabolism slows down. Eventually, fat tissue develops chronic inflammation, setting the stage for diabetes and heart disease.”High insulin levels — caused by our modern processed diet and other influences — have programmed fat cells to take in and store too many calories, leaving too few for the rest of the body. So we get hungry, and metabolism slows down. Eventually, fat tissue develops chronic inflammation, setting the stage for diabetes and heart disease.
prof. David Ludwig
In the fat-cell model, insulin and other signals stimulate fat cells to store too many calories, and the brain responds by increasing hunger and lowering the metabolic rate.
„According to this unconventional way of thinking, weight gain occurs because fat cells are stimulated by insulin and other anabolic signals to take in and store excessive calories. When this happens, the concentration of calories in the blood becomes depleted, leaving too few for the rest of the body. Perceiving this problem, the brain responds by increasing hunger and lowering metabolic rate — akin to a state of starvation — antagonizing long-term weight loss.”According to this unconventional way of thinking, weight gain occurs because fat cells are stimulated by insulin and other anabolic signals to take in and store excessive calories. When this happens, the concentration of calories in the blood becomes depleted, leaving too few for the rest of the body. Perceiving this problem, the brain responds by increasing hunger and lowering metabolic rate — akin to a state of starvation — antagonizing long-term weight loss.
Henryk Różański
Adipose tissue provides an energy reserve sufficient for about 40 days.
„Fat is an energy-bearing nutrient, so adipose tissue is a reservoir of energy material sufficient for about 40 days. Adipose tissue has a lobular structure, because fat cells are arranged in groups separated by connective tissue proper.”Tłuszcz jest składnikiem energetycznym, zatem tkanka tłuszczowa stanowi rezerwuar materiału energetycznego, wystarczający na około 40 dni. Tkanka tłuszczowa ma budowę płacikową, czyli zrazikową, bowiem komórki tłuszczowe są zorganizowane w pewne grupy pooddzielane tkanka łączną właściwą.
Henryk Różański
Both lipid synthesis and fat breakdown take place in fat cells.
„Fat is stored in adipocytes in the form of fatty acid esters. Lipid synthesis (lipogenesis) and fat breakdown (lipolysis) also take place in them. Fat reaches adipocytes through the lymph and blood. Fat is transported to adipocytes in the form of tiny droplets — chylomicrons (droplets 100 to 500 micrometers /um/ in diameter) and lipoproteins 20–500 nanometers /nm/ in diameter.”W adipocytach gromadzony jest tłuszcz w postaci estrów kwasów tłuszczowych. Zachodzi w nich także synteza lipidów (lipogeneza) oraz rozkład tłuszczów (lipoliza). Tłuszcz do adipocytów dociera za pomocą limfy i krwi. Tłuszcz transportowany jest do adipocytów w formie maleńkich kropelek – chylomikronów (kropelki o średnicy 100 do 500 mikrometrów /um/) i lipoprotein o średnicy 20-500 nanometrów /nm/.
Henryk Różański
Brown adipose tissue produces heat.
„Brown adipose tissue is not responsible for obesity; its main role is to produce heat. It is also well developed in animals that undergo hibernation (it prevents excessive cooling of the body). Brown adipose tissue cells (lipocytes) have numerous fat droplets in their cytoplasm and are richly supplied with blood.”Tkanka tłuszczowa brunatna nie jest odpowiedzialna za otyłość, a jej główna rola polega na produkowaniu ciepła. Jest też dobrze rozwinięta u zwierząt przechodzących hibernację (zapobiega nadmiernemu wyziębieniu ciała). Komórki tkanki tłuszczowej brunatnej (lipocyty) mają w cytoplazmie liczne krople tłuszczu i są silnie ukrwione.
Paul Clayton
Fat pads in joints do not store calories and provide, among other things, adipokines and growth factors.
„The fat pads do not take part in calorie storage, but they play a role in joint health and maintenance by providing adipokines, local growth factors (7, 8), and progenitor stem cells (8, 9), all of which perform key functions in the replacement of worn or damaged cartilage.”Poduszki nie biorą udziału w magazynowaniu kalorii, ale odgrywają rolę w zdrowiu i utrzymaniu stawów poprzez dostarczanie: adipokin, lokalnych czynników wzrostu (7, 8) i progenitorowych komórek macierzystych (8, 9), z których wszystkie pełnią kluczowe funkcje w wymianie zużytych/uszkodzonych chrząstek.
Research from PubMed · Europe PMC
We selected 4 studies with the best, positive results. This is a selection, not a full review of all research.
Total number of studies on this topic in PubMed: 894.
The review indicates that white adipose tissue is an endocrine organ that communicates with the brain, among other ways, through leptin.
Aim of the study: There has been a rapid rise in the incidence of obesity, primarily as a result of changes in lifestyle (diet and activity levels). Obesity has provided considerable impetus for the investigation of the fundamental mechanisms involved in the regulation of energy balance.
Results: There is a rapidly expanding list of protein factors released by white adipose tissue, including the key hormone, adiponectin. Of particular note is the range of cytokines, chemokines, and other inflammation-related proteins secreted by white fat as tissue mass rises; indeed, obesity is characterized by chronic mild inflammation. The adipokines provide an extensive network of communication both within adipose tissue and with other organs, and some are implicated directly in the pathologies associated with obesity, particularly the metabolic syndrome. Although the focus remains very much on obesity in humans, the disorder and its sequelae are also a growing concern in companion animals.
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies
“Not stated” does not mean nobody paid — the database does not always record it.
Leptin from adipose tissue has been described as conveying long-term information about fat stores to the brain and helping to regulate food intake.
Aim of the study: Food intake and energy expenditure are closely regulated by several mechanisms which involve peripheral organs and nervous system, in order to maintain energy homeostasis.Short-term and long-term signals express the size and composition of ingested nutrients and the amount of body fat, respectively.
Results: Food intake and energy expenditure are closely regulated by several mechanisms which involve peripheral organs and nervous system, in order to maintain energy homeostasis.Short-term and long-term signals express the size and composition of ingested nutrients and the amount of body fat, respectively. Ingested nutrients trigger mechanical forces and gastrointestinal peptide secretion which provide signals to the brain through neuronal and endocrine pathways. Pancreatic hormones also play a role in energy balance exerting a short-acting control regulating the start, end, and composition of a meal.
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies
“Not stated” does not mean nobody paid — the database does not always record it.
The review describes the gut–brain–adipose axis as a neuroendocrine network that regulates appetite and adipose tissue function.
Aim of the study: Polyendocrine Metabolic Ovarian Syndrome (PMOS), formerly polycystic ovary syndrome (PCOS), is a common, complex, and heterogeneous endocrine disorder characterized by reproductive and metabolic dysregulation that significantly increases long-term cardiometabolic risk.
Results: The gut-brain-adipose axis represents a neuroendocrine network regulating appetite, energy homeostasis, and adipose tissue function. Within this framework, oxytocin and glucagon-like peptide-1 (GLP-1), alongside gut- and adipose-derived mediators including glucose-dependent insulinotropic polypeptide (GIP), leptin, and other adipokines, may also contribute to these processes. Evidence demonstrating altered fasting and postprandial oxytocin and GLP-1 responses in women with PMOS suggests that impaired neuroendocrine signaling may be associated with dysregulated adipose partitioning and could contribute to visceral and ectopic fat accumulation and increasing metabolic risk. This review discusses the gut-brain-adipose axis as a conceptual framework for understanding how neuroendocrine signaling influences adipose tissue distribution and insulin resistance in PMOS.
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies
“Not stated” does not mean nobody paid — the database does not always record it.
The authors indicate that adipose tissue dysfunction and altered appetite signaling may sustain biological mechanisms that promote weight regain.
Aim of the study: Although incretin receptor agonists deliver profound weight loss, clinical data reveal a consistent challenge: treatment discontinuation routinely triggers rapid weight regain. We define this phenomenon as the "Incretin Mirage"-a state where pharmacologically induced weight reduction temporarily conceals the persistent metabolic and neuroendocrine adaptations established during chronic obesity.
Results: To explain why the body aggressively resists sustained weight loss after treatment cessation, we introduce the "Epigenetic Detent." This novel conceptual mechanism links adipocyte epigenetic memory with neuroendocrine plasticity to preserve a high-adiposity set-point. Consequently, the moment pharmacological suppression is lifted, this persistently defended set-point serves as a potential driver of weight regain. Achieving a durable therapeutic response therefore requires moving beyond transient appetite suppression. We advocate for a coordinated, multitiered strategy that couples lifestyle and environmental restructuring with emerging epigenetic therapies aimed at erasing these cellular marks and achieving a complete cellular metabolic reset.
Money for the studygovernment, public institutions · Canadian Institutes of Health Research (CIHR) Institute of Nutrition, Metabolism and Diabetes
Do the authors have ties to companies?no — the authors say so
Did a manufacturer help with the study?NO
Type of studyother
“Not stated” does not mean nobody paid — the database does not always record it.
Perspectives and opinion materials
The content below presents the authors’ opinions, interpretations and hypotheses. It is not treated as equal to scientific studies and systematic reviews.
Orthomolecular Medicine News Service Opinion material
„Synergistic effect of metformin and vitamin D3 on osteogenic differentiation of human adipose tissue-derived mesenchymal stem cells under high d-glucose conditions. Regen Ther. 2024 Mar;25:147-56. 119. Leão IS, Dantas JR, Araújo DB, Ramos MEN, Silva KR, Batista LS, et al. Evaluation of type 1 diabetes' partial clinical remission after three years of heterologous adipose tissue derived stromal/stem cells transplantation associated with vitamin D supplementation. Diabetol Metab Syndr. 2024 May 24;16(1):114. 120. Araujo DB, Dantas JR, Silva KR, Souto DL, Pereira M de FC, Moreira JP, et al.”Synergistic effect of metformin and vitamin D3 on osteogenic differentiation of human adipose tissue-derived mesenchymal stem cells under high d-glucose conditions. Regen Ther. 2024 Mar;25:147-56. 119. Leão IS, Dantas JR, Araújo DB, Ramos MEN, Silva KR, Batista LS, et al. Evaluation of type 1 diabetes' partial clinical remission after three years of heterologous adipose tissue derived stromal/stem cells transplantation associated with vitamin D supplementation. Diabetol Metab Syndr. 2024 May 24;16(1):114. 120. Araujo DB, Dantas JR, Silva KR, Souto DL, Pereira M de FC, Moreira JP, et al.
Orthomolecular Medicine News Service Opinion material
„These GLP-1 receptor site locations include the following: Central nervous system, including the hypothalamus, brainstem, and other sites that are involved in appetite regulation and energy homeostasis. [46] Also receptor sites working to promote olfactory function and to prevent neurological complications, cognitive impairment, and peripheral neuropathy. [47,48] Also promotion of stem cells and progenitor cells in the brain.”These GLP-1 receptor site locations include the following: Central nervous system, including the hypothalamus, brainstem, and other sites that are involved in appetite regulation and energy homeostasis. [46] Also receptor sites working to promote olfactory function and to prevent neurological complications, cognitive impairment, and peripheral neuropathy. [47,48] Also promotion of stem cells and progenitor cells in the brain.
Orthomolecular Medicine News Service Opinion material
„Endothelial dysfunction - characterized by impaired nitric oxide signaling, increased permeability, oxidative stress, and inflammatory activation - precedes and drives sustained vascular stiffness and pressure dysregulation. High blood pressure, in this context, reflects loss of endothelial boundary regulation and structural vascular resilience. Neuroinflammatory Disorders Blood-brain barrier compromise permits peripheral inflammatory mediators and immune cells to enter neural tissue, amplifying oxidative stress and microglial activation.”Endothelial dysfunction - characterized by impaired nitric oxide signaling, increased permeability, oxidative stress, and inflammatory activation - precedes and drives sustained vascular stiffness and pressure dysregulation. High blood pressure, in this context, reflects loss of endothelial boundary regulation and structural vascular resilience. Neuroinflammatory Disorders Blood-brain barrier compromise permits peripheral inflammatory mediators and immune cells to enter neural tissue, amplifying oxidative stress and microglial activation.
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