CD36 (Cluster of Differentiation 36) is a multifunctional transmembrane protein and scavenger receptor primarily known as a fatty acid transporter and signaling molecule.
CD36 (fatty acid translocase or FAT) is a membrane glycoprotein and scavenger receptor best known for its role in fat taste perception in addition to its functions in fatty acid uptake, inflammation, and other tissues.
CD36 (also known as platelet glycoprotein IV / GPIV or SR-B2) is a multifunctional scavenger receptor and pattern recognition molecule expressed on a wide variety of cell types.
It is widely expressed across many cell types in the body, including fat cells, heart muscle, macrophages, and platelets.
CD36 (also called fatty acid translocase) is a scavenger receptor and fatty acid transporter found on the surface of many cell types, including adipocytes, macrophages, muscle cells, and intestinal epithelial cells.
CD36 facilitates the transport of long-chain fatty acids into cells, acting as a primary energy source for tissues like the heart and skeletal muscle.
Receptor Activity: It acts as a receptor for a wide variety of ligands, including oxidized low-density lipoprotein (LDL) and thrombospondin.
Cd36 helps macrophages identify and clear apoptotic (dead) cells, and facilitates the recognition of certain pathogens.
It has an active involvement in metabolism and inflammation, CD36 is closely linked to several metabolic and cardiovascular conditions.
Metabolic Disorders: It plays a role in the development of atherosclerosis, diabetes, and fatty liver disease.
In the heart, excessive CD36 activity can lead to lipid accumulation and dysfunction.
In obese and insulin-resistant individuals, CD36 is overexpressed in skeletal muscle, promoting excessive fatty acid uptake and leading to intramyocellular lipid accumulation — a key driver of insulin resistance.
Cancer: CD36 is heavily involved in tumor metabolism, particularly in mediating metastasis, tumor growth, and drug resistance in various cancers such as breast, brain, and ovarian cancers, and is increasingly being explored as a potential therapeutic.
Gene: CD36 is located on chromosome 7q11.2
A 88 kDa glycoprotein with a hairpin topology-two transmembrane domains, short cytoplasmic tails, large extracellular loop.
Expression:
Platelets, monocytes/macrophages, dendritic cells Microvascular endothelial cells Adipocytes, skeletal and cardiac muscle Retinal pigment epithelium
Function |
Lipid uptake-Binds and internalizes oxidized LDL and long-chain fatty acids — major role in foam cell formation
Fatty acid transport- Facilitates FA uptake in heart, muscle, and adipose tissue |
Innate immunity-Pattern recognition of bacterial diacylglycerides, amyloid-β, and other DAMPs/PAMPs | Angiogenesis-Mediates thrombospondin-1 (TSP-1) anti-angiogenic signaling. |
Phagocytosis-Aids clearance of apoptotic cells and photoreceptor outer segments in the retina |
Disease Relevance
Atherosclerosis — oxidized LDL uptake via CD36 drives macrophage foam cell formation in plaques
Metabolic syndrome / obesity — dysregulated FA uptake; CD36 upregulated in insulin resistance
Malaria — P. falciparum-infected erythrocytes cytoadhere to CD36 on endothelium; relevant to cerebral malaria pathogenesis
Alzheimer’s disease — CD36 involved in microglial recognition of amyloid-β
Macular degeneration — role in RPE phagocytosis of photoreceptor outer segments
CD36 Deficiency
A naturally occurring polymorphism; more common in individuals of African and East Asian descent (~3–4%).
Associated with:
Altered platelet function Changed susceptibility to malaria Possible metabolic phenotypes
Role in Taste Humans can detect fatty acids (particularly long-chain fatty acids, as a distinct “fat taste” or orosensory cue, separate from the classic five tastes (sweet, sour, salty, bitter, umami).
CD36 acts as a key candidate receptor for this.
Location: Expressed on taste bud cells (especially in papillae on the tongue).
Mechanism: CD36 binds long chain fatty acids (e.g., linoleic acid, oleic acid).
This triggers intracellular signaling, including rises in calcium (Ca²⁺), leading to neurotransmitter release and signals to the brain via gustatory nerves.
Genetic variants in the CD36 gene influence fat taste sensitivity thresholds, creaminess perception, and preferences for high-fat foods.
Lingual lipase helps release free fatty acids from dietary fats, which then activate CD36.
This “fat taste” contributes to the appeal of fatty foods, influencing food choice, intake, and potentially overeating.
Polymorphisms in CD36 are linked to:
Differences in oral fat sensitivity as some people are “hypersensitive” or “hyposensitive” to fat taste.
Associations with obesity, BMI, and metabolic traits in some populations with higher thresholds for detecting fat in certain genotypes may lead to higher fat consumption.
Interactions with diet and conditions like type 2 diabetes.
Obesity can alter CD36 expression or signaling in taste buds, potentially changing fat perception.
CD36 is involved in: Fatty acid transport in muscle, adipose tissue, and other cells.
Aptherosclerosis, inflammation, and immune responses as a receptor for oxidized LDL.
Pathogen recognition and platelet function.
Enhanced fat taste sensitivity via CD36 may promote preference for energy-dense foods.
Research explores its role in obesity, eating behaviors, and potential therapeutic targeting by modulating fat perception for weight management.
Obesity is strongly associated with elevated CD36 expression.
CD36 in the small intestine plays a role in dietary fat absorption and chylomicron secretion.
Obese states are linked to increased intestinal CD36, potentially promoting greater fat uptake from meals.
In obesity-associated inflammation, macrophage CD36 is upregulated and facilitates oxidized LDL uptake, contributing to foam cell formation and atherosclerotic risk — which is already elevated in obese patients.
Hepatic CD36 is markedly elevated in obesity and non-alcoholic fatty liver disease (NAFLD), where it drives excessive hepatic fatty acid uptake and contributes to steatosis.
Drivers:
Elevated free fatty acids and insulin in obesity transcriptionally upregulate CD36 (via PPARγ and other pathways)
Chronic low-grade inflammation further induces CD36 expression
CD36 upregulation then creates a feed-forward loop, worsening lipid dysregulation
Elevated CD36 in obesity is linked to insulin resistance, dyslipidemia, NAFLD, and cardiovascular risk. It has emerged as a potential therapeutic target.
Obesity and elevated CD36 are bidirectionally linked — obesity drives CD36 upregulation, and elevated CD36 exacerbates metabolic dysfunction.