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Adipocyte

An adipocyte, commonly known as a , is a specialized that primarily functions as an energy reservoir by storing , mainly in the form of triglycerides, within a large central that occupies most of the volume, displacing the and to the periphery. These s are the predominant component of , a dynamic organ that not only buffers energy fluctuations but also acts as an by secreting adipokines such as and to regulate , insulin sensitivity, and systemic . Adipocytes originate from mesenchymal s in the stromal vascular fraction of and exhibit remarkable plasticity, expanding or contracting in response to nutritional cues to maintain and prevent ectopic deposition in organs like the liver and muscle. Mammals possess three main types of adipocytes, each with distinct morphological and functional properties: adipocytes, which dominate () and specialize in long-term through and release via ; adipocytes, found in () and characterized by multiple small droplets and iron-rich mitochondria expressing uncoupling protein 1 () for non-shivering to generate heat; and adipocytes, which arise within under stimuli like cold exposure or β-adrenergic signaling, acquiring thermogenic capabilities similar to adipocytes while retaining some adipocyte features. A fourth type, pink adipocytes, emerges transiently in subcutaneous during and in , facilitating secretion. These types differ in origin—white and from Myf5-negative progenitors, from Myf5-positive precursors—highlighting adipose tissue's developmental diversity and depot-specific roles, such as subcutaneous versus visceral in influencing metabolic health. Beyond and , adipocytes play pivotal roles in glucose homeostasis, modulation, and protection against metabolic disorders by secreting over 600 factors that communicate with distant organs, including the , liver, and . Dysfunctional adipocyte expansion, as seen in , leads to , , and impaired endocrine signaling, contributing to , , and through mechanisms like chronic low-grade and . Recent advances in have further refined our understanding of adipocyte heterogeneity, revealing transitional states and microenvironmental influences on their fate, including 2025 studies identifying depot-specific adipocyte subpopulations associated with metabolic outcomes in , underscoring their central position in metabolic adaptability and disease pathogenesis.

Overview and Classification

Definition and Role in the Body

Adipocytes, also known as fat cells, are specialized cells of that primarily function to store in the form of , particularly triglycerides, while also providing and mechanical cushioning to the body. These cells originate from mesenchymal precursor cells within the stromal vascular fraction of , undergoing a process known as to become mature lipid-laden cells. In humans, the total number of adipocytes is established during childhood and adolescence, with adults typically possessing 20–60 billion such cells on average, though this can vary based on factors like and status. Adipocytes are distributed across various depots in the body, including subcutaneous adipose tissue beneath the skin, visceral adipose tissue surrounding internal organs such as the liver and intestines, and intra-organ depots like epicardial fat around the heart. These locations allow adipocytes to serve as a dynamic energy reservoir, storing excess caloric intake during periods of abundance and mobilizing fatty acids through lipolysis when energy demands increase, such as during fasting or exercise. Beyond energy homeostasis, adipocytes contribute to thermal insulation by reducing heat loss from the body and offer mechanical protection by cushioning vital organs against physical trauma. From an evolutionary perspective, adipocytes play a crucial role in maintaining energy balance, enabling survival during periods of food scarcity or famine by providing a readily accessible reserve of calories that can sustain vital functions. This adaptation underscores the importance of adipose tissue as a metabolic buffer in fluctuating nutritional environments. Historically, adipocytes were first recognized as distinct cellular entities in the 19th century by anatomists studying connective tissues, marking the beginning of systematic investigations into their structure and function. While adipocytes are broadly classified into types such as white, brown, and beige based on their metabolic properties, their core role remains centered on lipid management across all variants.

Types of Adipocytes

White adipocytes represent the predominant type of fat cells in adults, characterized by a unilocular morphology with a single large that occupies most of the cell volume, enabling efficient long-term primarily as triglycerides. These cells are distributed across subcutaneous depots beneath the skin and visceral depots surrounding internal organs, collectively accounting for the majority (~90%) of total body fat storage. In contrast, brown adipocytes are multilocular cells containing multiple small droplets and a dense concentration of mitochondria, adaptations that support their primary function of through uncoupled . These cells are concentrated in specific depots, such as the interscapular region in infants for non-shivering heat production, and persist into adulthood in areas like the and along the . Beige adipocytes constitute an inducible subtype of multilocular cells that arise within adipose depots in response to environmental or hormonal stimuli, including exposure and β-adrenergic signaling, thereby exhibiting thermogenic capabilities that bridge and adipocyte functions. This subtype was characterized in emerging in the early , highlighting their role as an adaptive thermogenic reserve. Specialized variants include marrow adipocytes, which populate and regulate hematopoiesis as a distinct adipocyte subtype, and pink adipocytes, which transiently form in mammary glands during to support and are also derived from adipocyte lineages. Adipocyte distribution evolves postnatally, with expanding to accommodate increasing energy storage demands, regressing after infancy while retaining adult depots for metabolic flexibility, and beige adipocytes emerging as an inducible response to physiological stressors.

Cellular Structure and Morphology

General Features

Adipocytes are defined by their unique cellular architecture, featuring a prominent central that occupies up to 90% of the volume and primarily stores triglycerides. This droplet is enveloped by a that interfaces with the surrounding , maintaining structural integrity while allowing metabolic interactions. The dominance of the lipid droplet compresses the and other organelles to the , creating a thin cytoplasmic rim that encases the storage core. Within this peripheral cytoplasm, essential organelles support cellular maintenance and lipid handling. The endoplasmic reticulum plays a key role in de novo lipid synthesis, facilitating the assembly of triglycerides from fatty acids and . The Golgi apparatus handles protein processing, , and packaging for or integration, while lysosomes contribute to the degradation of cellular waste and damaged components through hydrolytic enzymes. The of adipocytes is adapted for tissue integration and responsiveness, incorporating that anchor the cell to the via adhesion to and . Caveolae, flask-shaped invaginations rich in caveolin proteins, cluster signaling molecules and regulate mechanosensing and lipid transport at the membrane surface. Adipocyte size varies typically from 50 to 200 μm in , allowing flexibility in lipid storage capacity while the consistently dominates the intracellular volume. Electron provides high-resolution views of the 's and peripheral arrangement, revealing fine structural details not visible by light . In histological preparations, staining specifically targets neutral lipids, imparting a red coloration to the droplets for clear in frozen sections. While these general features are shared across adipocyte types, subtle variations exist in distribution and droplet characteristics.

Type-Specific Variations

adipocytes are characterized by a single large unilocular that occupies most of the volume, accompanied by few mitochondria and sparse , which optimizes the for efficient storage. This morphology results in a flattened pushed to the periphery and minimal intracellular space for other organelles. In contrast, brown adipocytes feature multiple small droplets distributed throughout the , creating a multilocular appearance, along with abundant mitochondria rich in uncoupling protein 1 () that supports uncoupled respiration. These cells also exhibit a dense network for enhanced nutrient and oxygen delivery, and their characteristic brown pigmentation arises from iron-containing in the mitochondria. The is typically centrally located amid the lipid droplets and organelles. Beige adipocytes display a transitional multilocular with inducible expression in their mitochondria, featuring an intermediate density of these organelles compared to and types. They exhibit heterogeneity across depots, with some cells showing clustered small droplets and others retaining larger ones, and their often shifts from a peripheral to a more central position upon activation. Vascularization in beige adipocytes is generally less dense than in brown but more prominent than in . Pink adipocytes, which appear transiently in the during late and in and other mammals, undergo from white adipocytes, resulting in smaller cells with reduced and fragmented droplets, enhanced secretory machinery, and an intermediate morphology between adipocytes and milk-producing alveoli to facilitate lipid transfer for production. Upon , they revert to white adipocyte morphology.
FeatureWhite AdipocytesBrown AdipocytesBeige AdipocytesPink Adipocytes
Lipid Droplet NumberSingle (unilocular)Multiple (multilocular)Multiple (transitional multilocular)Reduced/fragmented (transient)
Mitochondrial DensityLowHigh (-rich)Intermediate (inducible )Low (similar to white)
VascularizationSparseDense capillary networkModerate, variable by depotEnhanced in context
PigmentationNone (pale)Brown (iron in )Pale to light brownNone (pale)
Recent studies from the 2020s have demonstrated that adipocytes dynamically acquire brown-like organelles, such as increased mitochondria and multilocular droplets, while initially retaining a more white-like overall structure that adapts in response to stimuli. These structural variations underpin the specialized roles of each adipocyte type in .

Development and Differentiation

Embryonic and Postnatal Origins

Adipocytes arise during embryonic development from the , primarily through the of mesenchymal stem cells (MSCs). These MSCs, derived from mesodermal progenitors, give rise to various lineages, including adipocytes, under the influence of spatiotemporal cues in the developing . Lineage tracing studies have established that white adipocytes predominantly originate from the for visceral depots and from somitic mesoderm (dermatomes) for subcutaneous depots, highlighting a depot-specific embryonic patterning that contributes to the heterogeneous distribution of . In contrast, brown adipocytes primarily derive from the paraxial , specifically somite-derived myogenic precursors expressing markers such as Myf5 and Pax7, which commit to the adipogenic lineage during early embryogenesis. Certain brown adipose depots, particularly in the head and neck regions, receive contributions from cells in addition to mesodermal origins, as demonstrated in and murine models, though this influence varies across species. These embryonic origins underscore the distinct developmental trajectories for white and brown adipocytes, with white fat forming later and in more varied locations compared to the earlier appearance of brown fat depots essential for in neonates. Postnatally, adipose tissue expands through a combination of hyperplasia and hypertrophy, with hyperplasia—recruitment and differentiation of preadipocytes—predominating during childhood to increase the total number of adipocytes. This proliferative phase peaks around adolescence, stabilizing the adipocyte count at approximately 25–30 billion cells in humans, after which expansion in adulthood primarily occurs via hypertrophy (enlargement of existing cells) rather than new cell formation. Historical lineage mapping using Cre-lox recombination systems in the 2000s confirmed the persistence of these MSC-derived precursors into postnatal life, enabling depot-specific growth in response to nutritional and environmental demands. Species differences further illustrate these origins: exhibit well-defined brown adipose depots arising from , supporting robust , whereas in humans, and adipocytes are more dispersed within subcutaneous and visceral , reflecting an evolutionary with less segregated classical in adulthood.

Molecular Regulation of Adipogenesis

, the process by which mesenchymal cells (MSCs) differentiate into adipocytes, proceeds in two main stages: commitment and terminal . During commitment, multipotent MSCs adopt a preadipocyte fate, becoming irreversibly restricted to the adipocyte while losing potential for other types such as osteoblasts or myocytes. This stage involves the downregulation of multipotency markers and upregulation of lineage-specific genes. Terminal follows, where growth-arrested preadipocytes undergo mitotic clonal expansion—a brief proliferative —before expressing mature adipocyte characteristics, including accumulation and insulin responsiveness. Central to these stages are master regulatory transcription factors that orchestrate cascades. Peroxisome proliferator-activated receptor gamma (PPARγ) serves as the principal master regulator, driving terminal by forming heterodimers with (RXR) to activate genes involved in and insulin sensitivity. PPARγ expression is induced early in preadipocytes and peaks during maturation, with its activation threshold determining the efficiency of in a dose-dependent manner. The CCAAT/enhancer-binding protein (C/EBP) family complements PPARγ through a sequential cascade: C/EBPβ and C/EBPδ initiate early by promoting PPARγ and C/EBPα expression, while C/EBPα sustains PPARγ activity in mature adipocytes, ensuring maintenance of the differentiated state. Cross-regulation between PPARγ and C/EBPα forms a positive feedback loop essential for full adipogenic commitment. Several signaling pathways modulate these regulators to fine-tune adipogenesis. Insulin and insulin-like growth factor-1 (IGF-1) promote growth and differentiation by activating the PI3K/Akt pathway, enhancing glucose uptake and stimulating PPARγ and C/EBP expression during the post-confluent phase. In contrast, Wnt/β-catenin signaling inhibits commitment by stabilizing β-catenin, which represses PPARγ and C/EBPα transcription, thereby favoring alternative lineages like . Bone morphogenetic proteins (BMPs), particularly , BMP4, and BMP7, support preadipocyte commitment via Smad signaling, inducing C/EBPβ and PPARγ; BMPs also bias toward brown adipocyte fate at higher concentrations. Type-specific regulation distinguishes , , and adipogenesis. PRDM16 acts as a key determinant, promoting and fates over by interacting with PPARγ to activate thermogenic genes like while repressing white-specific markers such as . Loss of PRDM16 shifts preadipocytes toward muscle, underscoring its role in lineage switching. MicroRNAs provide fine-tuning; for instance, miR-133 targets the 3' of PRDM16 mRNA, suppressing its expression and thereby inhibiting / , with its levels decreasing during cold-induced to allow PRDM16 upregulation. In vitro models have been instrumental in elucidating these mechanisms. The 3T3-L1 preadipocyte cell line, established in the 1970s, mimics adipogenesis when induced with insulin, dexamethasone, and , enabling studies of the full cascade from to lipid accumulation. Recent advances using CRISPR/Cas9 editing in 3T3-L1 cells have revealed epigenetic contributions, such as histone acetylation at PPARγ promoters, which facilitates accessibility and enhances transcriptional activation during early . These edits confirm that disrupting acetyltransferases like p300 reduces adipogenic efficiency by maintaining repressive states. Obesity alters adipogenesis rates, often impairing the process to favor adipocyte over , which contributes to metabolic dysfunction. In obese states, chronic and elevated free fatty acids elevate Wnt/β-catenin signaling, raising the PPARγ activation threshold and reducing efficiency in a context-dependent manner—higher doses are needed to overcome repression, leading to fewer but larger adipocytes. This conceptual dose-response shift highlights how environmental factors modulate the molecular , promoting unhealthy adipose expansion.

Physiological Functions

Energy Storage and Mobilization

Adipocytes serve as the primary site for in mammals, storing excess as triglycerides in lipid droplets during periods of nutrient abundance and mobilizing these reserves as free fatty acids and during energy demand. This bidirectional process, known as for storage and for mobilization, is tightly regulated to maintain systemic metabolic balance. White adipocytes, in particular, excel in this role due to their large unilocular lipid droplets, which allow for efficient expansion and contraction in response to nutritional cues. Lipid storage in adipocytes begins with the uptake of glucose, facilitated by the insulin-responsive GLUT4, which translocates to the plasma membrane upon insulin stimulation to enhance glucose influx. Inside the cell, glucose is converted to , serving as the substrate for lipogenesis, where (ACC) catalyzes the carboxylation of to malonyl-CoA, and (FAS) assembles fatty acids from malonyl-CoA units. These fatty acids are then esterified with glycerol-3-phosphate to form triglycerides, which accumulate in the central . This process is upregulated in to buffer postprandial nutrient surges, preventing ectopic lipid deposition in other organs. Mobilization of stored energy occurs through , a sequential enzymatic of triggered by catabolic hormones such as and catecholamines, which bind to G-protein-coupled receptors on the adipocyte surface. These signals activate (PKA), which phosphorylates and activates hormone-sensitive (HSL), alongside adipose triglyceride (ATGL) as the rate-limiting initiator and monoacylglycerol (MGL) for the final step. The overall reaction can be represented as: \text{Triglyceride (TAG)} \xrightarrow{\text{ATGL}} \text{Diacylglycerol (DG) + FFA} \xrightarrow{\text{HSL}} \text{Monoacylglycerol (MG) + FFA} \xrightarrow{\text{MGL}} \text{[Glycerol](/page/Glycerol) + FFA} The released free fatty acids (FFAs) are transported via in circulation for oxidation in peripheral tissues, while is directed to the liver for . This pathway is essential during or exercise to provide substrates for energy production. Regulation of these processes ensures precise energy balance: insulin promotes lipogenesis by activating and while inhibiting lipolysis through phosphodiesterase 3B (PDE3B)-mediated reduction of cAMP levels, thereby suppressing and HSL activity. Conversely, (AMPK), activated by low cellular energy (high AMP/ATP ratio), inhibits to curb and enhances under nutrient scarcity, integrating signals from whole-body energy status. Dysregulation, such as , can lead to unchecked and elevated circulating FFAs, contributing to metabolic disorders. White adipocytes possess a remarkable storage capacity, containing approximately 80-90% lipid by tissue weight, equivalent to 800-900 g of fat per kg of , enabling them to sequester vast amounts of reserves. In humans, handles a substantial daily flux, buffering postprandial influx and efflux on the order of 100-200 g of triglycerides to maintain steady-state supply to other organs. Recent studies have revealed that exhibits circadian rhythms, with regulatory T cells in visceral upregulating clock genes like BMAL1 to enforce diurnal suppression, preventing excessive FFA release during active periods; disruption of this rhythm, as in BMAL1 deficiency, abolishes these oscillations and results in enhanced suppression of throughout the day. While white adipocytes prioritize net storage for long-term , brown adipocytes couple mobilization more directly to , differing in efficiency for heat versus fuel production.

Thermogenesis and Heat Production

Brown and beige adipocytes are specialized for non-shivering thermogenesis, a process that generates heat by uncoupling mitochondrial respiration from ATP production, primarily through uncoupling protein 1 (UCP1). Located in the , UCP1 facilitates the re-entry of protons into the matrix, bypassing and dissipating the proton gradient as heat rather than storing it as . This mechanism is essential for adaptive thermogenesis in response to cold exposure, where adipocytes in interscapular and perirenal depots, as well as beige adipocytes recruited in , elevate heat output to maintain core body temperature. Thermogenesis is activated by the , which releases norepinephrine upon , binding to β3-adrenergic receptors on adipocyte surfaces. This binding elevates intracellular cyclic AMP () levels, activating (), which in turn phosphorylates key regulators to enhance and UCP1 activity. The proton leak induced by UCP1 reduces the mitochondrial \Delta \Psi_m, such that the heat produced Q can be conceptualized as the energy derived from oxidation minus the energy allocated to ATP : Q \approx E_{\text{oxidation}} - E_{\text{ATP}} where E_{\text{oxidation}} represents the total free energy from β-oxidation and the electron transport chain, and E_{\text{ATP}} is the portion coupled to ATP production. Fatty acids released from intracellular lipid droplets via lipolysis serve as primary substrates, undergoing β-oxidation in mitochondria to fuel the electron transport chain and sustain proton pumping, thereby supporting sustained heat generation. In physiological contexts, non-shivering thermogenesis is critical for neonatal warmth, where provides rapid heat to prevent in newborns transitioning from the womb. In adults, it enables cold adaptation by increasing metabolic rate, with beige adipocytes emerging in subcutaneous depots to augment capacity; factors like irisin, released from during exercise, and (FGF21), secreted by the liver, promote beige activation and expression. Recent advances have identified -independent thermogenic pathways, including futile calcium cycling mediated by sarco/endoplasmic reticulum Ca²⁺-ATPase (), where drives calcium reuptake into the , dissipating energy as heat without proton uncoupling; this mechanism contributes to thermogenesis in UCP1-deficient models and may enhance overall adipose heat production under specific stimuli.

Endocrine and Paracrine Signaling

Adipocytes function as active endocrine organs by secreting that exert systemic effects on , , and . These hormones are primarily produced by white adipocytes, with circulating levels influenced by mass and nutritional status. A key is , a 16-kDa discovered in 1994 through positional cloning of the in mice. is secreted by adipocytes in proportion to fat stores and acts on hypothalamic neurons to suppress and promote energy expenditure. Plasma concentrations strongly correlate with body fat mass, typically ranging from 1.2 to 97.9 ng/mL in humans and exhibiting a of r = 0.71 with percent body fat. Adiponectin, another major adipokine identified in 1995, is abundantly secreted by adipocytes and circulates at high micromolar concentrations. It enhances insulin sensitivity in peripheral tissues, such as liver and skeletal muscle, and exerts anti-inflammatory effects by inhibiting pro-inflammatory cytokine production. Additional adipocyte secretions include resistin, a pro-inflammatory cytokine primarily expressed by macrophages (in humans) or adipocytes (in rodents) in white adipose tissue, that promotes insulin resistance. Visfatin, also known as nicotinamide phosphoribosyltransferase, contributes to NAD+ synthesis and mimics insulin's effects on glucose uptake. Cytokines such as tumor necrosis factor-alpha (TNF-α) are upregulated in adipocytes during obesity, driving local inflammation and impairing insulin signaling. Paracrine signaling within stroma involves factors like (VEGF), which adipocytes secrete to stimulate and support tissue expansion. Adipocytes also release that recruit immune cells, such as macrophages, influencing local inflammatory responses and remodeling. secretion is regulated by environmental cues, including and nutrient excess, which upregulate pro-inflammatory factors like TNF-α and via hypoxia-inducible factor pathways. In contrast, brown adipocytes preferentially secrete (FGF21), which promotes thermogenic and browning. In obesity, dysregulated adipokine secretion contributes to leptin resistance, where elevated leptin levels fail to suppress appetite effectively due to impaired hypothalamic signaling.

Dynamics and Adaptation

Cell Turnover and Lifespan

Adult adipocytes in humans display remarkably low turnover rates, with approximately 10% of the total fat cell population renewed each year across all adult ages and body mass index levels. This renewal occurs primarily through the differentiation of resident preadipocytes into mature adipocytes, maintaining tissue homeostasis despite the stability of overall adipocyte numbers. The estimated half-life of these cells is 8-10 years, underscoring their longevity compared to more rapidly renewing tissues. These findings were established using carbon-14 (¹⁴C) bomb pulse dating, a method that leverages the elevated atmospheric ¹⁴C levels from nuclear tests between 1955 and 1963 to retrospectively date the birth of long-lived cells by analyzing ¹⁴C incorporation into genomic DNA. This technique demonstrated minimal adipocyte replacement in adults, with no significant variation based on age or obesity status, challenging earlier assumptions of negligible turnover. Studies have primarily focused on subcutaneous adipose tissue due to accessibility. Over time, accumulated cellular damage from , , and metabolic overload contributes to adipocyte senescence, resulting in dysfunctional cells that secrete pro-inflammatory factors and impair tissue function, particularly in aging and . Senescent adipocytes accumulate in expanded adipose depots, exacerbating local and contributing to metabolic dysfunction. Recent lineage tracing studies in models, extended to contexts, confirm ongoing but limited adult adipogenesis, with cells contributing to modest renewal without substantial increases in cell numbers under steady-state conditions.

Plasticity and Response to Environmental Cues

Adipocytes exhibit remarkable , enabling them to undergo reversible structural and functional changes in response to environmental stimuli such as dietary alterations, fluctuations, and . This adaptability primarily occurs through modifications in cell size, profiles, and interactions with the surrounding , allowing to balance with metabolic demands. In , for instance, adipose expansion favors —increases in adipocyte volume—over , the generation of new adipocytes, with the former enabling cells to significantly enlarge before reaching a limit that triggers pathological responses. , while prominent during early development or extreme caloric surplus, remains rare in adults, contributing minimally to tissue growth beyond . A key example of functional plasticity is the beiging process, where white adipocytes transdifferentiate into beige adipocytes capable of thermogenesis, induced by chronic cold exposure at 5–10°C or sustained exercise. Cold activates sympathetic nervous system signaling, leading to norepinephrine release that stimulates β-adrenergic receptors on adipocytes, while exercise promotes secretion of myokines like irisin, both converging on AMP-activated protein kinase (AMPK) activation to upregulate uncoupling protein 1 (UCP1) and mitochondrial biogenesis. This shift enhances energy expenditure but is reversible; high-fat diets suppress UCP1 expression and promote lipid accumulation, causing beige adipocytes to revert to a white phenotype and reducing thermogenic capacity. Beyond thermogenic adaptations, adipocytes respond to local microenvironmental cues, such as in expanding obese tissue, which stabilizes hypoxia-inducible factor 1α (HIF-1α) and drives deposition, resulting in that impairs tissue expandability. Conversely, exercise stimulates and vascularization in adipose depots, increasing density to improve oxygen delivery and support metabolic remodeling. These changes occur across distinct timescales: acute responses like , triggered by or catecholamines, manifest within hours to mobilize stored , whereas chronic adaptations, such as depot remodeling or beiging, require days to weeks of sustained stimuli. Recent research highlights the role of epigenetic mechanisms in modulating adipocyte plasticity, with (HDAC) inhibitors emerging as potential enhancers of adaptive responses. Studies from 2023 and 2024 demonstrate that HDAC inhibition promotes to boost thermogenic , increasing beiging efficiency and energy expenditure in high-fat diet models, offering therapeutic promise for management.

Clinical and Pathophysiological Significance

Role in Metabolic Disorders

Adipocytes play a central role in the of , where excessive energy storage leads to adipocyte , characterized by enlarged cells that exceed their capacity for handling. This triggers local through the recruitment and infiltration of macrophages into , shifting the immune profile toward a pro-inflammatory state that exacerbates systemic . Visceral adipocytes, located around abdominal organs, are particularly pathogenic compared to subcutaneous ones, as they release higher levels of free fatty acids and pro-inflammatory cytokines directly into the portal circulation, promoting hepatic and metabolic dysregulation more aggressively than subcutaneous fat depots. Global prevalence reached approximately 13% in 2022, affecting over 1 billion adults and underscoring the scale driven by adipocyte dysfunction. In , dysfunctional adipocytes contribute to disease progression by reducing secretion of the insulin-sensitizing hormone , which normally enhances in and liver. Concurrently, elevated circulating free fatty acids (FFAs) from in insulin-resistant adipocytes impair insulin-mediated glucose transport in peripheral tissues, fostering and further beta-cell exhaustion. Adipocyte dysfunction is also central to , a cluster of conditions including , , and , where inflammation and altered profiles amplify systemic metabolic imbalance. Lipodystrophy syndromes, often genetic, result in profound loss of adipocytes, leading to an inability to store in subcutaneous depots and consequent ectopic deposition in organs like the liver and muscle, which precipitates severe and features such as and . In cancer, particularly , adipocytes promote tumor growth by secreting adipokines like and hepatocyte growth factor (HGF), which enhance cancer cell , , and through . Emerging research highlights the role of marrow adipocytes in , where these cells secrete receptor activator of nuclear factor kappa-B ligand (), stimulating activity and independent of traditional regulation.

Implications for Therapy and Research

Therapeutic strategies targeting adipocytes have emerged as promising interventions for metabolic diseases such as and , focusing on modulating function to enhance and energy expenditure. Pharmacological approaches include thiazolidinediones (TZDs), which act as agonists of (PPARγ) to promote adipocyte and improve by reducing and enhancing in . Similarly, β3-adrenergic receptor agonists like stimulate the "beiging" of adipocytes, converting them into thermogenically active cells that increase energy expenditure and ameliorate glucose in preclinical and early clinical studies. Surgical interventions also play a key role in adipose remodeling. effectively removes subcutaneous , reducing fat mass in targeted depots, but it does not prevent compensatory adipocyte or shifts toward visceral fat accumulation, which can limit long-term metabolic benefits. In contrast, bariatric procedures such as Roux-en-Y gastric bypass induce profound remodeling of adipose depots, leading to substantial fat mass loss, reduced inflammation, and improved adipose function, which contributes to sustained remission of in many patients. Emerging therapies aim to harness genetic and microbial influences on adipocyte . CRISPR-based has been used to overexpress uncoupling protein 1 () in human adipocytes, enhancing their thermogenic capacity and preventing diet-induced in models, paving the way for cell-based therapies to combat metabolic dysfunction. Additionally, modulation of the gut through or prebiotics can influence by altering microbial metabolites that regulate adipose precursor and reduce -associated . Ongoing clinical research highlights the potential of (FGF21) analogs, with Phase 2 trials reporting results in 2024 and 2025 demonstrating their ability to reduce liver fat and in patients with metabolic dysfunction-associated (MASH), while preclinical data support enhancement of fat activity to improve systemic . However, key research gaps persist, including significant differences between and adipose browning responses, where humans exhibit limited inducible fat compared to , complicating translational efficacy. The role of senolytics, such as plus , in clearing senescent and dysfunctional adipocytes also shows promise for alleviating obesity-induced metabolic dysfunction by promoting healthy adipose turnover. Despite these advances, challenges remain in therapeutic development, particularly off-target effects of thermogenic agents like β3-agonists, which can elevate heart rate and pose cardiovascular risks, necessitating refined targeting to adipose-specific pathways for safer clinical application.

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