The secret life of… fat cells
Adipocytes commonly known as fat cells, play a pivotal role that goes beyond storing excess energy and maintaining body warmth. Far from passive, these cells discreetly govern energy balance, shape immune responses, manage inflammation, and produce hormones. Here we will delve into the nuanced intricacies of fat cells and their profound influence in keeping us alive!
Fat Cell Q&A
What is the medical term for fat cells?
Adipocytes. The word is derived from the Latin "adipo-" meaning fat and "-cyte" indicating a cell.
Any relationship between fat cells and adipose tissue?
Adipose tissue contains fat cells. Fat cells store and release energy in the form of lipids.
So, what’s inside fat cells?
Each fat cell contains a large single lipid or fat droplet housing chiefly triglycerides, also cholesterol esters, functioning as an energy reserve.
How are new fat cells formed?
Fat cells are formed through a biological process called adipogenesis, the development of mature fat cells from precursor cells.
How many fat cells are in a human adult?
A human adult can have 30-40 billion fat cells but can vary significantly between individuals. A single lipid has a caloric density of approximately 9 kcal per gram.
What is a core function of a fat cell?
Fat cells are both metabolic and endocrinal involved in the regulation of whole-body energy homeostasis.
What does metabolic mean?
Fat cells are actively involved in regulating how our body stores and breaks down energy from the food we eat.
What does endocrinal mean?
Fat cells produce hormones called adipocytokines that profoundly affect themselves and other hormones/cells in the body.
What is whole-body energy homeostasis?
Fat cells play an integral role in regulating our energy supply and demand.
What else can fat cells do?
Fat cells have a reservoir of stem cells to generate new fat cells and other cell types, including fat’s own immune cells.
So fat cells work with the immune system?
Yes, fat cells own immune cells are involved in aspects of regulating our immune system, including managing inflammation.
How do fat cells change and adapt?
Fat cells exhibit ‘plasticity’ properties, able to grow (hypertrophy), multiply (hyperplasia) and shrink (lipolysis).
Are there different types of fat cells?
Yes, white fat cells exhibit ‘phenotypic plasticity’, meaning they can transition between different functional states in response to environmental or physiological conditions.
Where are fat cells stored?
As subcutaneous fat under the skin and visceral fat in and around organs.
Are fat cells stored in other locations?
Yes, as essential fat in bone marrow, between muscles, breast tissue, and the liver and brain.
Is fat mass a simple equation of calories in/out?
No! Genes, hormones, pregnancy, puberty, menopause, gut microbiome, illness, fat cells themselves, and the environment all influence fat mass.
What is meant by environment?
It includes where we live, what, when and how often we eat, pollution, substance use, medications, sleep exercise, stress, pollution and light exposure levels, circadian physiology, and temperature extremes.
Starting As We Mean To Go On
Adipocytes or fat cells have long endured undue scrutiny, often wrapped up in the stigma surrounding obesity. Obesity is a complex medial condition that is frequently oversimplified in the popular press as a matter of “too many calories in vs. out” or reduced to the catch-all advice to “eat less, move more.”
Thanks to ongoing scientific research, we’re now better equipped than ever to challenge persistent myths. Our understanding of fat cells, and their dynamic interactions with other cells and systems in the brain and body, has deepened significantly over the years. We now know that fat cells play a systemic role in our nervous system and body, influencing mental, emotional, and physical health in both beneficial and challenging ways.
A blend of biopsychosocial factors, including genetics, physiology, emotions, cognition (intrinsic cues), and environment (extrinsic cues) shapes fat cell function, structure, and communication patterns. These patterns operate not only within the body and brain, but also between fat cells themselves. Why does this matter? Because fat cells are far more than passive storage units!
For example, Genes linked to fat, like the FTO gene, can influence how our fat cells work, from how many we have, to what type they become. They can also affect how our bodies regulate appetite, metabolism and even reproduction. These genetic differences do not determine outcomes on their own, but variations in these genes can lead to predispositions for weight loss or weight gain.
The Secret Life of Fat Cells explores fat cells vital contributions to our immune (defence), endocrine (hormonal), and metabolic (energy) systems, and our nervous system. The unassuming fat cell helps regulate whole-body energy homeostasis or balance, modulate immune responses, manage inflammation, and produce key hormones and glucose ‘on demand’. Much of this is happening outside of conscious awareness, subtly shaping motivation, behaviours, emotional states and our overall health.
Fat Cell ‘Plasticity’
Adipocytes exhibit plasticity properties, meaning they can alter their size (hypertrophy and atrophy), shape (remodelling), and number/volume (hyperplasia). In some cases, fat cells can adopt the characteristics of other cell types, or transition between different states in response to changing environmental or extrinsic cues, such as diet or temperature, and physiological or intrinsic cues, such as metabolic (energy) or hormonal fluctuations.
For example, during pregnancy and lactation, white fat cells undergo structural and functional changes in response to hormonal changes; a process known as pinking. The term “pinking” comes from the visible change in colour of the fat tissue, as it changes due to the appearance of milk-producing epithelial-like cells in the mammary gland, making the fat appear pink rather than white. After lactation, these cells usually revert to their original white fat state. This remarkable plasticity allows the body to adapt rapidly to the demands of supporting pregnancy and feeding a newborn.
Another example is brown fat, named for its colour and known for its inherently thermogenic or fat burning ability that comes from each brown fat cell having a high number of mitochondria. Mitochondria are often called the “powerhouses of a cell”, which are rich in iron, giving brown fat its darker hue.
In response to external cues like cold exposure or exercise or pollution, some white fat cells can take on characteristics of brown fat, a process known as beiging. Beige fat shares brown fat’s energy-burning properties, and this adaptive shift is a striking example of the plasticity of fat cells. There is much interest in this adaptation for novel treatments regulating body weight and metabolic health.
Adipose tissue is remarkably adaptable. Chronic overfeeding can suppress the activity of beige fat, prompting a shift back toward energy-storing white fat. This reversible transition is yet another example of fat cell plasticity - the ability of fat cells to adapt their function and even colour in response to energy balance and environmental or external cues.
During weight loss, the body breaks down stored triglycerides within fat cells through a process called lipolysis, releasing free fatty acids (FFAs) and glycerol to be used as energy. Contrary to popular belief, most of the “weight” lost during this process leaves the body as carbon dioxide (CO₂) through respiration, while a smaller amount is excreted as water via sweat, urine, and other fluids.
As fat stores are used, the fat cells shrink, but in most cases, they do not disappear. Lipolysis for fat cells releasing energy also occurs during periods of rest, such as sleep, to fuel essential functions like breathing, circulation, and body temperature regulation. This ongoing adaptability underscores the vital role fat cells play in maintaining metabolic balance, even when the body is at rest.
Fat Cells and Insulin
Insulin is a hormone produced in the pancreas that helps regulate blood sugar by promoting glucose uptake into fat, muscle, and liver cells. It binds to insulin receptors on these cells, activating a complex intracellular signalling or communication cascade that regulates how glucose is transported, stored, or used for energy. While the brain uses glucose as its main fuel, its uptake is largely insulin-independent.
Insulin signals fat cells to store fat rather than burn it, promoting fat storage, by encouraging the conversion of glucose into triglycerides. This is part of insulin’s broader role in maintaining energy balance, body weight, and blood sugar stability - a key metabolic function, that ensures energy is saved for later use. By contrast, and demonstrating the earlier point, extreme thinness, can be seen in undiagnosed or poorly managed type 1 diabetes, where the pancreas produces little to no insulin.
When insulin signalling is disrupted due to factors like type 2 diabetes, chronic over-nutrition, inflammation, or inactivity, fat cells and other tissues become less responsive to insulin. This condition, known as insulin resistance, causes the pancreas to produce even more insulin in an attempt to compensate. The result is chronically elevated insulin levels, or hyperinsulinemia.
Hyperinsulinemia is problematic for several reasons:
Increased Fat Storage: High insulin promotes fat storage, particularly in the abdominal area, and inhibits fat breakdown.
Blood Sugar Dysregulation: Over time, the pancreas may struggle to keep up with demand, leading to elevated blood glucose and the onset of type 2 diabetes.
Cardiovascular Risk: Insulin resistance is linked to high blood pressure, abnormal cholesterol and triglyceride levels, and increased risk of heart disease and stroke.
Wider Health Impacts: Insulin resistance is associated with obesity, non-alcoholic fatty liver disease (NAFLD), polycystic ovary syndrome (PCOS), certain cancers, and cognitive decline.
Crucially, insulin resistance is not just a consequence of obesity - it can precede and even promote it. Fat cells themselves can contribute to this cycle: when overloaded through chronic overnutrition, they release inflammatory signals and lose their sensitivity to insulin, driving further metabolic dysregulation.
This highlights the importance of maintaining insulin sensitivity, where smaller amounts of insulin are needed to regulate blood sugar effectively. We can tell if this is the case by how fast blood sugar levels recover to a healthy range following a meal. A healthy blood sugar range means your levels rise after eating but return to normal within an hour or two, without big spikes or crashes. Managing insulin sensitivity helps preserve energy balance, prevent excessive fat storage, and reduce chronic disease risk.
The brain plays a vital role in this system by constantly monitoring hormones like insulin and also leptin (produced in fat cells). Leptin tells your brain when you have enough energy stored, signalling fullness, reducing appetite and increasing energy expenditure. Both insulin and leptin assess the body’s energy status. In response, the brain regulates appetite, metabolism, and energy expenditure, in order to maintain homeostasis or balance.
Fat Cells and Energy Homeostasis
Fat cells are central to regulating the dynamic balance between energy storage and energy expenditure, referred to as whole-body energy homeostasis. The hypothalamus, deep within the brain, orchestrates this complex balancing act in collaboration with other brain regions, as well as fat cells, the gut microbiota, pituitary gland, liver, and other peripheral systems to respond to metabolic fluctuations.
The Basal Metabolic Rate (BMR) is a key determinant of energy balance. A low BMR reflects a slower metabolism and may predict future weight gain, while a high BMR corresponds to a faster metabolism, requiring more calories to sustain basic physiological functions. BMR is influenced by factors such as age, sex, body composition, and genetic predisposition.
Mitochondria within fat cells convert nutrients into a usable energy form called adenosine triphosphate (ATP). In energy metabolism, ATP functions as the body's "energy currency," fuelling various cellular processes by releasing stored chemical energy, much like a rechargeable battery powering cellular stability and body-wide function.
When glucose availability is low, insulin levels decrease, and mitochondria may shift toward thermogenesis (heat production) rather than ATP synthesis. This triggers lipolysis (the breakdown of stored fat), increasing the release of fatty acids into the bloodstream and promoting energy expenditure. In this state, the body switches from burning glucose to burning fat.
As fat is metabolised, the liver produces ketones (ketone bodies), which can serve as an alternative energy source, especially for the brain. This metabolic shift, known as ketosis, can increase the activity of white adipose tissue, making it behave more like energy-burning beige or brown fat. While ketosis has gained popularity as a weight management strategy in diets like Keto, medical supervision is recommended, as its safety and effects can vary by individual health status.
In contrast, chronic over-nutrition and hyperinsulinemia (high insulin levels) may cause brown fat to behave more like white fat, promoting energy storage over expenditure. This highlights that obesity is not merely a passive accumulation of fat, but rather a dysfunction of the energy homeostasis system.
When this system becomes dysregulated, it impairs fat cell plasticity and disrupts communication between the brain and peripheral tissues. This miscommunication interferes with normal hunger and satiety signals, creating a vicious cycle of abnormal appetite and abnormal fat storage, altered signalling, and further metabolic imbalance and possibly low-grade systemic inflammation. Potentially contributing to overeating, as blood sugar yo-yo’s, weight gain, and persistent difficulty in regulating body weight.
Fat Metabolism & Survival Physiology
Prolonged stress on the metabolic system, such as intense physical exertion, extended fasting, or low evening food intake before sleep, can act as intrinsic cues, triggering the hormone glucagon from the pancreas. Glucagon signals the liver to release a fast-acting energy source: glucose stored as glycogen. This maintains blood sugar when dietary glucose isn’t available.
But liver glycogen reserves are limited, typically around 100–120 grams in adults, and can become depleted within 12–24 hours, depending on metabolic demands. During the fragile window when glycogen is low, glucose is scarce, and the brain hasn’t yet adapted to using ketones (a secondary source of fuel for the brain if glucose is depleted), this is where fat cells step in.
Fat cells begin breaking down stored triglycerides, releasing:
Fatty acids, which most body tissues can use for energy
Glycerol, which is sent to the liver for gluconeogenesis, a slower process of making new glucose
This shift is life-sustaining, but not immediate. The conversion of glycerol into glucose is slower and more metabolically demanding than the liver's direct release of glycogen. If blood sugar drops too low during this transition, especially during sleep, the brain perceives it as a threat.
In response, the body launches a full stress response to rapidly restore glucose levels. This involves a surge of counter-regulatory hormones, including:
Adrenaline, to trigger emergency energy release
Cortisol, to break down protein for glucose and raise the alert
Glucagon, to signal the need for further glucose production in the liver
Growth hormone, to protect tissues and support longer-term balance post stress event
While these hormones are helpful for survival, they also stimulate the nervous system, which can wake you up. You might feel jittery, anxious, sweaty, restless, or simply wake abruptly without knowing why. It's your body doing what it must to fuel your brain.
When this pattern repeats, sleep can become fragmented, and your recovery systems can suffer. Over time, this can lead to:
Cognitive and emotional effects: brain fog, poor concentration, mood instability, and increased anxiety
Nervous system dysregulation: feeling wired but exhausted, emotionally reactive, and less able to shift into rest-and-repair
Metabolic impacts: blood sugar instability during the day, sugar cravings, appetite hormone disruption and fatigue cycles
Fat Cells and Metabolism
Here we briefly explore two dietary conditions that influence fat cell metabolism in different ways:
Condition 1: Meals that help maintain blood sugar levels and insulin sensitivity
Diets low in simple carbohydrates, high in complex carbohydrates, rich in healthy fats, and containing adequate protein can enhance insulin sensitivity and promote fat cells' metabolic activity. These dietary patterns have been shown to help stabilise blood glucose, reduce fat storage signals, and support energy expenditure, particularly by encouraging fat oxidation and thermogenesis.
Condition 2: Meals that stimulate high blood sugar and insulin spikes
Diets high in simple carbohydrates (e.g. sugar and refined grains), low in complex carbohydrates and healthy fats, even with normal protein levels, can produce sharp fluctuations in blood glucose. This can lead to persistently high insulin levels in the bloodstream, with downstream effects on fat cell metabolism and poor hunger regulation. This is influenced by individual differences in insulin sensitivity and metabolic flexibility.
Condition 2: High Glycaemic Meals and Their Metabolic Impact
Meals rich in high-glycaemic foods (like sugar and refined carbs) can trigger rapid spikes in blood glucose, prompting the pancreas to release insulin to shuttle glucose into our cells. While this response is natural, frequent insulin surges can disrupt metabolic balance by:
Inhibiting fat breakdown (lipolysis)
Enhancing glucose conversion into fat
Suppressing glucose availability in the bloodstream
Hypothalamic Perception of Energy Deficit
In this scenario, even when there is adequate stored energy in the form of glycogen, glucose, and fatty acids in the system, the brain, particularly the hypothalamus part of the brain (which monitors real-time levels of glucose in the bloodstream), may misinterpret the signals.
After a spike, the rapid drop in blood glucose can be misinterpreted by the hypothalamus as a sign of energy scarcity. This misinterpretation triggers hunger signals, even shortly after a meal. The brain’s primary concern is ensuring a stable fuel supply, especially to itself, and it responds protectively with food seeking habits, regardless of whether actual energy reserves are sufficient.
Condition 1 and The Role of Metabolic Hormones
Weight management is not only about choosing meals that stabilise blood sugar and improve insulin sensitivity — it's also about making nutritional choices that support hormonal balance and overall metabolic health.
Research shows that the effects of diet on blood sugar, insulin, and fat storage can vary significantly between individuals. Studies such as the Zoe Predict Studies have demonstrated that these differences are partly shaped by the gut microbiome — the unique ecosystem of bacteria in our digestive tract.
The emerging proposal is that diets tailored to individual responses can support a healthier gut microbiome, promote more stable energy levels, reduce cravings, and improve communication with brain regions like the hypothalamus that regulate hunger and satiety.
The Role of Stress and Hormonal Regulation
Chronic stress can elevate cortisol levels, which may worsen insulin resistance and disrupt appetite regulation. Stress management techniques, such as good sleep hygiene, exposure to natural light, mindfulness, meditation, and breathwork, have been shown to support hormonal balance, promote healthier eating behaviours, and reduce emotional eating triggers, among other benefits.
However, these strategies may not be accessible to everyone, especially those juggling shift work, caregiving responsibilities, or the demands of a busy household. That’s where personalised, flexible approaches to stress and nutrition management are a possible avenue for sustainable long-term metabolic health. What do. we mean by this?
Personalised, flexible approaches are not just idealistic, they’re backed by neuroscience and can be made practical for real life:
You don’t need perfect routines — you need awareness of how your body responds
Apps like ZOE and data from continuous glucose monitors are making this insight actionable
Even small changes (timing of eating, gut-friendly foods, meal composition - e.g., eat protein first) matter, especially under stress or time pressure
Intermittent Fasting and Metabolic Flexibility
Intermittent fasting can enhance metabolic flexibility, the body’s ability to efficiently switch between glucose and fat as fuel, improving insulin sensitivity and reducing fat storage over time. When combined with regular physical activity, which boosts muscle glucose uptake and overall insulin responsiveness, fasting may support more stable energy levels and better metabolic regulation.
However, individual differences, including hormonal factors and gender, mean that intermittent fasting may not be suitable or beneficial for everyone. Personalised strategies that consider lifestyle, health status, and biological variation, are important considerations to sustainable outcomes.
Personalised Strategies
Sustainable weight and metabolic health require a multifaceted approach that focuses on a more personalised way to address nutrition. Understanding and predicting individual post-meal glucose (blood sugar) and lipid (blood fat) responses is a critical aspect of such personalised nutrition recommendations.
It’s now possible to track how your body responds to food in real time using wearable sensors to monitor glucose, while new technologies are emerging that will make it easier to assess fat metabolism and heart health from home. These tools offer valuable insights that can help individuals make informed food choices, support energy balance, and reduce long-term health risks, tailored to individuals unique biology and lifestyle.
Fat Cells and Gut Microbiome
A growing body of evidence indicates a dynamic interplay between fat cells and the gut microbiome. Gut microbiota can influence the body’s metabolic functions, including those of adipose tissue, through mechanisms such as immune modulation, inflammatory signalling, and hormone regulation.
Diets low in carbohydrates have been shown to shift gut microbiota composition, including increased representation of bacterial groups such as Bacteroides species, which are associated with energy balance and body weight regulation. Similarly, ketogenic diets may promote the growth of beneficial bacteria such as Akkermansia muciniphila and certain Lactobacillus strains, which contribute to lipid metabolism, gut barrier integrity, and overall metabolic health. While findings vary by study design and individual variability, these patterns have been observed in both clinical and preclinical research.
The relationship between gut microbiota and fat cells extends beyond diet, with evidence showing responsiveness to factors such as temperature exposure, intermittent fasting, and caloric restriction. Fat-derived hormones, including leptin and adiponectin, can influence microbial composition and function, which in turn affects host metabolism by modulating inflammation, immune activity, and intercellular signalling pathways.
Emerging research also suggests that gut microbiota play a key role in fat cell inflammation associated with obesity and related metabolic disorders. Alterations in microbial diversity and abundance, particularly reductions in beneficial species, are correlated with heightened inflammation in adipose tissue. Some probiotic bacteria, such as species from the Bifidobacterium genus, have demonstrated potential in modulating microbiota composition and improving fat metabolism when included in functional foods or supplements.
Other probiotic strains, including Lactobacillus paracasei, Akkermansia muciniphila, Faecalibacterium prausnitzii, Parabacteroides distasonis, and Clostridium leptum, have been associated with improved insulin sensitivity and reduced adipose inflammation in early studies. These microbes are under investigation for their potential therapeutic roles in managing obesity and metabolic disease.
Despite these associations, the precise mechanisms underlying the interaction between gut microbiota and adipose tissue remain incompletely understood. Ongoing research continues to explore how these microbial communities influence, and are influenced by host metabolism at a detailed cellular and molecular level.
Fat Cells and Hormones
Fat cells function as an endocrine organ, producing hormone-like signalling molecules called adipokines (or adipocytokines). These molecules have wide-ranging effects, including both pro-inflammatory and anti-inflammatory actions, and play a critical role in whole-body energy homeostasis. Imbalances in adipokine signalling can disrupt energy storage and expenditure, contributing to insulin resistance, chronic inflammation, obesity, type 2 diabetes, and cardiovascular disease.
White Adipose Tissue (WAT)–Derived Adipokines:
Leptin – Primarily pro-inflammatory in excess.
Best known for regulating appetite and energy expenditure by signalling the brain when fat stores are sufficient. Leptin deficiency is associated with severe obesity, while leptin resistance (high leptin but low brain responsiveness) is linked with chronic inflammation, metabolic syndrome, and persistent hunger.Adiponectin – Anti-inflammatory and insulin-sensitising.
Increases fatty acid oxidation and improves glucose uptake, protecting against type 2 diabetes and cardiovascular disease. Higher levels are typically beneficial, though paradoxical elevations may occur in chronic inflammatory diseases (e.g. rheumatoid arthritis, IBD), possibly as a compensatory response.Adipsin – Emerging evidence suggests mixed roles.
Involved in complement system activation and glucose homeostasis. High levels are associated with increased fat mass and may contribute to insulin resistance. It also has a novel role in bone marrow adiposity, influencing bone health.Resistin – Predominantly pro-inflammatory.
Linked with insulin resistance, inflammation, and obesity. Elevated levels may contribute to systemic inflammation and are being studied in relation to type 2 diabetes and cardiovascular pathology.
Brown and Beige Adipose Tissue (BAT)-Associated Adipokines:
Fibroblast Growth Factor 21 (FGF21) – Anti-inflammatory and metabolic regulator.
Plays a key role in increasing insulin sensitivity, fat oxidation, and energy expenditure. It stimulates adiponectin release and is being explored as a therapeutic candidate for obesity and diabetes.Interleukin-6 (IL-6) – Context-dependent: both pro- and anti-inflammatory.
While chronically elevated IL-6 contributes to inflammation in obesity and metabolic syndrome, transient elevations during exercise or cold exposure may have beneficial metabolic effects, such as improving glucose uptake and fat breakdown.Irisin – Generally anti-inflammatory and pro-metabolic.
A myokine/adipokine released during physical activity and cold exposure, promoting the browning of white fat and enhancing energy metabolism. Its role in improving insulin sensitivity and reducing fat accumulation is under active investigation.Tumor Necrosis Factor-alpha (TNF-α) – Strongly pro-inflammatory.
Elevated in obesity and directly impairs insulin signalling, contributing to insulin resistance and metabolic dysfunction. Also implicated in a range of inflammatory conditions such as rheumatoid arthritis and IBD.
These examples represent only a subset of the adipokines secreted by fat cells, whose roles in whole-body energy homeostasis, metabolic and inflammation regulation, remain active areas of ongoing research. What we know is fat-derived adipokines are central to energy homeostasis, inflammation, and metabolic health.
A healthy balance between pro-inflammatory and anti-inflammatory adipokines supports insulin sensitivity, glucose regulation, and lipid metabolism. In contrast, chronic elevation of pro-inflammatory adipokines can contribute to metabolic disease, fat tissue dysfunction, and low-grade systemic inflammation.
Fat Cells as Immune Tissue
Fat cells are an active immunological organ. Fat cells coexist with various immune cells within the adipose tissue micro-environment. These include macrophages, dendritic cells, and lymphocytes (T and B cells), all of which contribute to immune surveillance, tissue homeostasis, and inflammatory regulation.
Adipocytes secrete hormone-like signalling molecules known as adipokines (also called adipocytokines), which influence both local and systemic immune responses. For example, the hormone leptin plays a role in regulating appetite and energy balance, but it also acts as a pro-inflammatory adipocytokine by modulating T-cell activity. Conversely, adiponectin generally has anti-inflammatory properties and helps improve insulin sensitivity.
In obesity, adipose tissue undergoes significant functional and structural changes, including hypoxia, oxidative stress, and altered cellular signalling. These conditions promote a shift toward a pro-inflammatory state, characterised by increased infiltration of immune cells, especially M1-type macrophages, and elevated production of pro-inflammatory cytokines such as TNF-α and IL-6.
This state of chronic low-grade inflammation, often referred to as meta-inflammation, is strongly associated with the pathogenesis of insulin resistance, type 2 diabetes, cardiovascular disease, and other obesity-related metabolic disorders. Maintaining a healthy balance between pro-inflammatory and anti-inflammatory signalling within fat cells adipose tissue is essential for immune resilience, and overall metabolic and systemic health.
Fat Cells Revisited
By now we know that fat cells are a crucial component of whole-body homeostasis or balance. Once considered passive storage units, they are now recognised as dynamic, adaptive cells involved in energy regulation, immune responses, hormonal signalling, and brain–body communication:
Plasticity: fat cells exhibit plasticity, adapting in colour, size, function and structure in response to intrinsic (internal) and extrinsic (environmental) cues.
Insulin: insulin is a peptide hormone that supports glucose uptake into fat and other cells. Chronic elevation of blood sugar can lead to insulin resistance, affecting how, and how much fat is stored and used.
Energy Homeostasis: fat cells act as energy reservoirs, playing a central role in maintaining whole-body energy homeostasis or balance. Acting as an ‘energy bank’, through storage, release, and signalling functions; just one role of the secret life of fat cells.
Hormones: fat cells are metabolically active, producing various hormones and signalling molecules and release adipocytokines, such as leptin and adiponectin, that regulate hunger, satiety, inflammation, and energy metabolism.
Metabolism: fat cells respond to dietary composition; individual responses vary depending on genetic and metabolic factors, influencing fat storage and breakdown.
Immune System: fat tissue contains immune cells and interacts with inflammatory pathways, linking adipose dysfunction with systemic inflammation and chronic disease.
Gut Microbiome: bidirectional communication between fat cells and gut microbes influences appetite, fat storage, inflammation, and even mood regulation.
Fat–Brain Axis: fat cells and the brain communicate via hormonal and neural pathways, affecting appetite, satiety, mood, and metabolic regulation.
Fat Metabolism & Survival Physiology: fat cells fuel the body during glucose scarcity by releasing fatty acids and glycerol. This system supports survival but may trigger stress responses if energy balance is disrupted.
As research advances, fat cells secret life as central players in personalised nutrition, metabolic flexibility, and systemic health, is emerging, offering new opportunities to support individual health and wellbeing through targeted, evidence-based novel strategies. Their dynamic role in hormone regulation, immune function, and energy balance is reshaping how we understand, and intervene in, metabolic conditions, including obesity, opening the door to more precise and preventative approaches for overall longevity.
The content presented in this blog incorporates evidence-based information along with perspectives and opinions. It is designed to stimulate discussions and explorations of emerging research. However, it does not represent official advice or exhaustive factual claims. The goal is to offer readers valuable insights on particular topics of interest while respecting the boundaries of objectivity and subjectivity. Alternative viewpoints are highly encouraged and welcomed at Blindspot. Readers of course consider multiple sources when forming their opinions.