| Adipocyte | |
|---|---|
 Illustration depicting white fat cells. | |
 Morphology of three different classes of adipocytes | |
| Details | |
| Identifiers | |
| Latin | adipocytus |
| MeSH | D017667 |
| TH | H2.00.03.0.01005 |
| FMA | 63880 |
| Anatomical terms of microanatomy | |
Adipocytes, also known aslipocytes andfat cells, are thecells that primarily composeadipose tissue, specialized in storing energy asfat.[1] Adipocytes are derived frommesenchymal stem cells which give rise to adipocytes throughadipogenesis. Incell culture, adipocyte progenitors can also formosteoblasts,myocytes and other cell types.
There are two types of adipose tissue,white adipose tissue (WAT) andbrown adipose tissue (BAT), which are also known as white and brown fat, respectively, and comprise two types of fat cells.
White fat cells contain a single largelipid droplet surrounded by a layer ofcytoplasm, and are known as unilocular. Thenucleus is flattened and pushed to the periphery. A typical fat cell is 0.1 mm in diameter[2] with some being twice that size, and others half that size. However, these numerical estimates of fat cell size depend largely on the measurement method and the location of the adipose tissue.[2] The fat stored is in a semi-liquid state, and is composed primarily oftriglycerides, andcholesteryl ester. White fat cells secrete many proteins acting asadipokines such asresistin,adiponectin,leptin andapelin. An average human adult has 30 billion fat cells with a weight of 30 lbs or 13.5 kg. If a child or adolescent gains sufficient excess weight, fat cells may increase in absolute number until age twenty-four.[3] If an adult (who never was obese as a child or adolescent) gains excess weight, fat cells generally increase in size, not number, though there is some inconclusive evidence suggesting that the number of fat cells might also increase if the existing fat cells become large enough (as in particularly severe levels of obesity).[3] The number of fat cells is difficult to decrease through dietary intervention, though some evidence suggests that the number of fat cells can decrease if weight loss is maintained for a sufficiently long period of time (>1 year; though it is extremely difficult for people with larger and more numerous fat cells to maintain weight loss for that long a time).[3]
A large meta-analysis has shown that white adipose tissue cell size is dependent on measurement methods, adipose tissue depots, age, and body mass index; for the same degree of obesity, increases in fat cell size were also associated with the dysregulations in glucose and lipid metabolism.[2]
Brown fat cells arepolyhedral in shape. Brown fat is derived from dermatomyocyte cells. Unlikewhite fat cells, these cells have considerable cytoplasm, with severallipid droplets scattered throughout, and are known as multilocular cells. The nucleus is round and, although eccentrically located, it is not in the periphery of the cell. The brown color comes from the large quantity ofmitochondria. Brown fat, also known as "baby fat," is used to generate heat.
Marrow adipocytes are unilocular like white fat cells. Themarrow adipose tissue depot is poorly understood in terms of its physiologic function and relevance to bone health. Marrow adipose tissue expands in states of low bone density but additionally expands in the setting of obesity.[4] Marrow adipose tissue response to exercise approximates that ofwhite adipose tissue.[4][5][6][7] Exercise reduces both adipocyte size as well as marrow adipose tissue volume, as quantified byMRI orμCT imaging of bone stained with the lipid binderosmium.
Pre-adipocytes are undifferentiatedfibroblasts that can be stimulated to form adipocytes. Studies have shed light into potential molecular mechanisms in the fate determination of pre-adipocytes although the exact lineage of adipocyte is still unclear.[8][9] The variation of body fat distribution resulting from normal growth is influenced by nutritional and hormonal status dependent on intrinsic differences in cells found in each adipose depot.[10]
Mesenchymal stem cells can differentiate into adipocytes,connective tissue, muscle orbone.[1]
The precursor of the adult cell is termed alipoblast, and a tumor of this cell type is known as alipoblastoma.[11]
Fat cells in some mice have been shown to drop in count due to fasting and other properties were observed when exposed to cold.[12]
If the adipocytes in the body reach their maximum capacity of fat, they may replicate to allow additional fat storage.
Adult rats of various strains became obese when they were fed a highly palatable diet for several months. Analysis of their adipose tissue morphology revealed increases in both adipocyte size and number in most depots. Reintroduction of an ordinarychow diet[13] to such animals precipitated a period of weight loss during which only mean adipocyte size returned to normal. Adipocyte number remained at the elevated level achieved during the period of weight gain.[14]
According to some reports and textbooks, the number of adipocytes can increase in childhood and adolescence, though the amount is usually constant in adults. Individuals who become obese as adults, rather than as adolescents, have no more adipocytes than they had before.[15]
People who have been fat since childhood generally have an inflated number of fat cells. People who become fat as adults may have no more fat cells than their lean peers, but their fat cells are larger. In general, people with an excess of fat cells find it harder to lose weight and keep it off than the obese who simply have enlarged fat cells.[3]
Body fat cells have regional responses to the overfeeding that was studied in adult subjects. In the upper body, an increase of adipocyte size correlated with upper-body fat gain; however, the number of fat cells was not significantly changed. In contrast to the upper body fat cell response, the number of lower-body adipocytes did significantly increase during the course of experiment. Notably, there was no change in the size of the lower-body adipocytes.[16]
Approximately 10% of fat cells are renewed annually at all adult ages and levels of body mass index without a significant increase in the overall number of adipocytes in adulthood.[15]
Obesity is characterized by the expansion of fat mass, through adipocyte size increase (hypertrophy) and, to a lesser extent, cell proliferation (hyperplasia).[17][2] In thefatty tissue of obese individuals, there is increased production of metabolism modulators, such asglycerol,hormones,macrophage-stimulatingchemokines, andpro-inflammatory cytokines, leading to the development ofinsulin resistance.[18] Production of these modulators and the resultingpathogenesis of insulin resistance are probably caused by adipocytes as well asimmune system macrophages that infiltrate the tissue.[19]
Fat production in adipocytes is strongly stimulated byinsulin. By controlling the activity of thepyruvate dehydrogenase and theacetyl-CoA carboxylase enzymes, insulin promotes unsaturatedfatty acid synthesis. It also promotesglucose uptake and inducesSREBF1, which activates the transcription of genes that stimulatelipogenesis.[20]
SREBF1 (sterol regulatory element-bindingtranscription factor 1) is a transcription factor synthesized as an inactiveprecursor protein inserted into theendoplasmic reticulum (ER) membrane by two membrane-spanninghelices. Also anchored in the ER membrane isSCAP (SREBF-cleavage activating protein), which binds SREBF1. The SREBF1-SCAP complex is retained in the ER membrane byINSIG1 (insulin-induced gene 1 protein). When sterol levels are depleted, INSIG1 releases SCAP and the SREBF1-SCAP complex can be sorted into transportvesicles coated by thecoatomerCOPII that are exported to theGolgi apparatus. In the Golgi apparatus, SREBF1 is cleaved and released as a transcriptionally active mature protein. It is then free totranslocate to thenucleus and activate the expression of its target genes.[21]
Clinical studies have repeatedly shown that even though insulin resistance is usually associated with obesity, the membranephospholipids of the adipocytes of obese patients generally still show an increased degree of fatty acid unsaturation.[22] This seems to point to an adaptive mechanism that allows the adipocyte to maintain its functionality, despite the increased storage demands associated with obesity and insulin resistance.
A study conducted in 2013[22] found that, while INSIG1 and SREBF1mRNA expression was decreased in the adipose tissue of obese mice and humans, the amount of active SREBF1 was increased in comparison with normal mice and non-obese patients. This downregulation of INSIG1 expression combined with the increase of mature SREBF1 was also correlated with the maintenance of SREBF1-target gene expression. Hence, it appears that, by downregulating INSIG1, there is a resetting of the INSIG1/SREBF1 loop, allowing for the maintenance of active SREBF1 levels. This seems to help compensate for the anti-lipogenic effects of insulin resistance and thus preserve adipocyte fat storage abilities and availability of appropriate levels of fatty acid unsaturation in face of the nutritional pressures of obesity.
Adipocytes can synthesizeestrogens fromandrogens,[23] potentially being the reason why beingunderweight oroverweight are risk factors forinfertility.[24] Additionally, adipocytes are responsible for the production of the hormoneleptin. Leptin is important in regulation of appetite and acts as a satiety factor.[25]
Regular chow is composed of agricultural byproducts, such as ground wheat, corn, or oats, alfalfa and soybean meals, a protein source such as fish, and vegetable oil and is supplemented with minerals and vitamins. Thus, chow is a high fiber diet containing complex carbohydrates, with fats from a variety of vegetable sources. Chow is inexpensive to manufacture and is palatable to rodents.
Several factors derived not only from adipocytes but also from infiltrated macrophages probably contribute to the pathogenesis of insulin resistance.
