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Does Scar Tissue Register As Body Fat When Measured

Written By Sunday, 27 March 2022 Add Comment Edit

Loose connective tissue composed mostly past adipocytes

Run into also: Fat

Adipose tissue
Illu connective tissues 1.jpg

Adipose tissue is 1 of the main types of connective tissue.
Typy adipocytů.svg

Morphology of three different classes of adipocytes.
Pronunciation ( audio speaker icon listen )
Identifiers
MeSH D000273
FMA 20110
Anatomical terminology

[edit on Wikidata]

Adipose tissue, body fat, or simply fat is a loose connective tissue composed mostly of adipocytes.[ane] In add-on to adipocytes, adipose tissue contains the stromal vascular fraction (SVF) of cells including preadipocytes, fibroblasts, vascular endothelial cells and a variety of immune cells such as adipose tissue macrophages. Adipose tissue is derived from preadipocytes. Its chief role is to shop energy in the form of lipids, although it too cushions and insulates the body. Far from being hormonally inert, adipose tissue has, in contempo years, been recognized as a major endocrine organ,[two] equally information technology produces hormones such as leptin, estrogen, resistin, and cytokines (especially TNFα). In obesity, adipose tissue is also implicated in the chronic release of pro-inflammatory markers known as adipokines, which are responsible for the evolution of metabolic syndrome, a constellation of diseases including, but not express to, blazon two diabetes, cardiovascular affliction and atherosclerosis.[3] The two types of adipose tissue are white adipose tissue (WAT), which stores free energy, and brown adipose tissue (BAT), which generates torso heat. The formation of adipose tissue appears to be controlled in part by the adipose factor. Adipose tissue – more than specifically brown adipose tissue – was get-go identified by the Swiss naturalist Conrad Gessner in 1551.[4]

Anatomical features [edit]

Distribution of white adipose in the human body

In humans, adipose tissue is located: beneath the pare (subcutaneous fatty), around internal organs (visceral fat), in os marrow (yellow bone marrow), intermuscular (Muscular system) and in the chest (breast tissue). Adipose tissue is found in specific locations, which are referred to as adipose depots. Autonomously from adipocytes, which contain the highest percent of cells within adipose tissue, other cell types are nowadays, collectively termed stromal vascular fraction (SVF) of cells. SVF includes preadipocytes, fibroblasts, adipose tissue macrophages, and endothelial cells.

Adipose tissue contains many pocket-sized blood vessels. In the integumentary arrangement, which includes the pare, it accumulates in the deepest level, the subcutaneous layer, providing insulation from heat and common cold. Around organs, it provides protective padding. However, its main part is to be a reserve of lipids, which tin can be oxidised to meet the energy needs of the torso and to protect it from excess glucose past storing triglycerides produced by the liver from sugars, although some bear witness suggests that most lipid synthesis from carbohydrates occurs in the adipose tissue itself.[5] Adipose depots in different parts of the trunk accept different biochemical profiles. Under normal weather, it provides feedback for hunger and nutrition to the brain.

Mice [edit]

The obese mouse on the left has big stores of adipose tissue. Information technology is unable to produce the hormone leptin. This causes the mouse to be hungry and consume more than, which results in obesity. For comparison, a mouse with a normal amount of adipose tissue is shown on the right.

Mice have 8 major adipose depots, four of which are within the abdominal crenel.[1] The paired gonadal depots are attached to the uterus and ovaries in females and the epididymis and testes in males; the paired retroperitoneal depots are found along the dorsal wall of the abdomen, surrounding the kidney, and, when massive, extend into the pelvis. The mesenteric depot forms a glue-like web that supports the intestines and the omental depot (which originates near the tum and spleen) and - when massive - extends into the ventral abdomen. Both the mesenteric and omental depots incorporate much lymphoid tissue every bit lymph nodes and milky spots, respectively.

The two superficial depots are the paired inguinal depots, which are institute anterior to the upper segment of the hind limbs (underneath the pare) and the subscapular depots, paired medial mixtures of brown adipose tissue adjacent to regions of white adipose tissue, which are found under the pare between the dorsal crests of the scapulae. The layer of brown adipose tissue in this depot is often covered by a "frosting" of white adipose tissue; sometimes these two types of fat (dark-brown and white) are hard to distinguish. The inguinal depots enclose the inguinal group of lymph nodes. Minor depots include the pericardial, which surrounds the center, and the paired popliteal depots, between the major muscles behind the knees, each containing one large lymph node.[half-dozen] Of all the depots in the mouse, the gonadal depots are the largest and the virtually easily dissected,[7] comprising well-nigh thirty% of dissectible fat.[8]

Obesity [edit]

In an obese person, excess adipose tissue hanging downwards from the abdomen is referred to as a panniculus. A panniculus complicates surgery of the morbidly obese individual. It may remain as a literal "apron of skin" if a severely obese person loses large amounts of fat (a mutual effect of gastric featherbed surgery). Obesity is treated through practice, diet, and behavioral therapy. Reconstructive surgery is ane aspect of treatment.[9]

Visceral fat [edit]

Visceral fatty or intestinal fat[10] (too known as organ fat or intra-abdominal fat) is located inside the abdominal cavity, packed between the organs (stomach, liver, intestines, kidneys, etc.). Visceral fatty is different from subcutaneous fat underneath the skin, and intramuscular fatty interspersed in skeletal muscles. Fat in the lower body, equally in thighs and buttocks, is subcutaneous and is not consistently spaced tissue, whereas fat in the abdomen is more often than not visceral and semi-fluid.[11] Visceral fat is equanimous of several adipose depots, including mesenteric, epididymal white adipose tissue (EWAT), and perirenal depots. Visceral fatty is oft expressed in terms of its area in cm2 (VFA, visceral fatty area).[12]

An excess of visceral fatty is known as central obesity, or "abdomen fatty", in which the abdomen protrudes excessively. New developments such every bit the Body Volume Index (BVI) are specifically designed to measure abdominal volume and abdominal fat. Excess visceral fat is too linked to type 2 diabetes,[thirteen] insulin resistance,[xiv] inflammatory diseases,[15] and other obesity-related diseases.[16] Also, the aggregating of cervix fat (or cervical adipose tissue) has been shown to exist associated with mortality.[17] Several studies have suggested that visceral fat tin be predicted from simple anthropometric measures,[eighteen] and predicts mortality more accurately than body mass alphabetize or waist circumference.[19]

Men are more likely to have fat stored in the abdomen due to sex activity hormone differences. Female sex hormone causes fatty to be stored in the buttocks, thighs, and hips in women.[20] [21] When women reach menopause and the estrogen produced by the ovaries declines, fat migrates from the buttocks, hips and thighs to the waist;[22] later fat is stored in the abdomen.[11]

Visceral fat tin be caused past excess cortisol levels.[23] At least 10 MET-hours per week of aerobic do leads to visceral fatty reduction in those without metabolic-related disorders.[24] Resistance grooming and caloric brake also reduce visceral fatty, although their effect may not be cumulative.[25] Both practise and hypocaloric nutrition cause loss of visceral fat, merely exercise has a larger consequence on visceral fat versus total fatty.[26] High-intensity exercise is one style to effectively reduce total abdominal fat.[27] [28] An free energy restricted diet combined with exercise will reduce full body fatty and the ratio of visceral adipose tissue to subcutaneous adipose tissue, suggesting a preferential mobilization for visceral fatty over subcutaneous fat.[29]

Epicardial fat [edit]

Epicardial adipose tissue (Consume) is a particular course of visceral fat deposited effectually the middle and establish to exist a metabolically agile organ that generates diverse bioactive molecules, which might significantly affect cardiac office.[30] Marked component differences take been observed in comparison EAT with subcutaneous fat, suggesting a location-specific touch of stored fat acids on adipocyte role and metabolism.[31]

Subcutaneous fat [edit]

Micro-anatomy of subcutaneous fat

Most of the remaining nonvisceral fatty is institute just below the peel in a region called the hypodermis.[32] This subcutaneous fat is not related to many of the classic obesity-related pathologies, such as heart illness, cancer, and stroke, and some evidence even suggests it might exist protective.[33] The typically female (or gynecoid) blueprint of trunk fat distribution effectually the hips, thighs, and buttocks is subcutaneous fatty, and therefore poses less of a wellness risk compared to visceral fat.[34] [35]

Like all other fatty organs, subcutaneous fatty is an agile part of the endocrine system, secreting the hormones leptin and resistin.[32]

The relationship between the subcutaneous adipose layer and total torso fat in a person is often modelled by using regression equations. The well-nigh popular of these equations was formed by Durnin and Wormersley, who rigorously tested many types of skinfold, and, every bit a event, created ii formulae to calculate the body density of both men and women. These equations present an changed correlation between skinfolds and body density—as the sum of skinfolds increases, the body density decreases.[36]

Factors such as sexual activity, age, population size or other variables may make the equations invalid and unusable, and, every bit of 2012[update], Durnin and Wormersley'south equations remain only estimates of a person's true level of fatness. New formulae are nevertheless being created.[36]

Marrow fat [edit]

Marrow fat, besides known as marrow adipose tissue (MAT), is a poorly understood adipose depot that resides in the bone and is interspersed with hematopoietic cells as well equally bony elements. The adipocytes in this depot are derived from mesenchymal stem cells (MSC) which tin can give rise to fat cells, bone cells too as other prison cell types. The fact that MAT increases in the setting of calorie restriction/ anorexia is a feature that distinguishes this depot from other fat depots.[37] [38] [39] Exercise regulates MAT, decreasing MAT quantity and diminishing the size of marrow adipocytes.[forty] [41] [42] The practice regulation of marrow fat suggests that it bears some physiologic similarity to other white adipose depots. Moreover, increased MAT in obesity further suggests a similarity to white fat depots.[twoscore]

Ectopic fatty [edit]

Ectopic fat is the storage of triglycerides in tissues other than adipose tissue, that are supposed to incorporate simply small amounts of fatty, such as the liver, skeletal musculus, heart, and pancreas.[1] This can interfere with cellular functions and hence organ function and is associated with insulin resistance in type-ii diabetes.[43] It is stored in relatively high amounts effectually the organs of the abdominal cavity, but is not to be dislocated with visceral fat.

The specific crusade for the accumulation of ectopic fatty is unknown. The crusade is probable a combination of genetic, environmental, and behavioral factors that are involved in excess energy intake and decreased physical activeness. Substantial weight loss can reduce ectopic fat stores in all organs and this is associated with an improvement of the function of those organs.[43]

In the latter case, non-invasive weight loss interventions similar diet or exercise can decrease ectopic fat (especially in heart and liver) in overweight or obese children and adults.[44] [45]

Physiology [edit]

Complimentary fatty acids (FFAs) are liberated from lipoproteins past lipoprotein lipase (LPL) and enter the adipocyte, where they are reassembled into triglycerides by esterifying them onto glycerol. Human fatty tissue contains almost 87% lipids.[46]

There is a constant flux of FFAs inbound and leaving adipose tissue. The net direction of this flux is controlled by insulin and leptin—if insulin is elevated, then there is a net inward flux of FFA, and only when insulin is low can FFA leave adipose tissue. Insulin secretion is stimulated by high blood saccharide, which results from consuming carbohydrates.[47]

In humans, lipolysis (hydrolysis of triglycerides into gratuitous fatty acids) is controlled through the balanced command of lipolytic B-adrenergic receptors and a2A-adrenergic receptor-mediated antilipolysis.

Fat cells accept an important physiological office in maintaining triglyceride and free fat acid levels, as well as determining insulin resistance. Intestinal fat has a different metabolic profile—being more prone to induce insulin resistance. This explains to a large degree why central obesity is a marker of impaired glucose tolerance and is an independent risk gene for cardiovascular affliction (fifty-fifty in the absence of diabetes mellitus and hypertension).[48] Studies of female monkeys at Wake Forest University (2009) discovered that individuals suffering from higher stress have higher levels of visceral fat in their bodies. This suggests a possible cause-and-issue link between the 2, wherein stress promotes the aggregating of visceral fatty, which in plow causes hormonal and metabolic changes that contribute to heart disease and other health problems.[49]

Recent advances in biotechnology have allowed for the harvesting of adult stalk cells from adipose tissue, allowing stimulation of tissue regrowth using a patient's ain cells. In add-on, adipose-derived stem cells from both human being and animals reportedly can be efficiently reprogrammed into induced pluripotent stem cells without the demand for feeder cells.[l] The use of a patient's own cells reduces the chance of tissue rejection and avoids ethical issues associated with the use of man embryonic stalk cells.[51] A growing body of evidence too suggests that different fatty depots (i.e. abdominal, omental, pericardial) yield adipose-derived stem cells with different characteristics.[51] [52] These depot-dependent features include proliferation rate, immunophenotype, differentiation potential, gene expression, every bit well as sensitivity to hypoxic culture conditions.[53] Oxygen levels seem to play an important office on the metabolism and in full general the function of adipose-derived stem cells.[54]

Adipose tissue is a major peripheral source of aromatase in both males and females, contributing to the product of estradiol.[55]

Adipose derived hormones include:

  • Adiponectin
  • Resistin
  • Plasminogen activator inhibitor-1 (PAI-1)
  • TNFα
  • IL-6
  • Leptin
  • Estradiol (E2)

Adipose tissues as well secrete a type of cytokines (jail cell-to-prison cell signalling proteins) called adipokines (adipose cytokines), which play a office in obesity-associated complications. Perivascular adipose tissue releases adipokines such as adiponectin that touch on the contractile function of the vessels that they surroundings.[1] [56]

Brownish fat [edit]

Chocolate-brown fat or brown adipose tissue (BAT) is a specialized form of adipose tissue important for adaptive thermogenesis in humans and other mammals. BAT can generate heat by "uncoupling" the respiratory chain of oxidative phosphorylation inside mitochondria through tissue-specific expression of uncoupling protein 1 (UCP1).[57] BAT is primarily located effectually the neck and large blood vessels of the thorax, where it may effectively act in heat exchange. BAT is robustly activated upon common cold exposure by the release of catecholamines from sympathetic fretfulness that results in UCP1 activation. BAT activation may also occur in response to overfeeding.[58] UCP1 activity is stimulated by long chain fatty acids that are produced subsequent to β-adrenergic receptor activation.[57] UCP1 is proposed to function as a fatty acid proton symporter, although the exact mechanism has notwithstanding to be elucidated.[59] In contrast, UCP1 is inhibited by ATP, ADP, and GTP.[sixty]

Attempts to simulate this process pharmacologically have so far been unsuccessful. Techniques to manipulate the differentiation of "brown fat" could get a mechanism for weight loss therapy in the future, encouraging the growth of tissue with this specialized metabolism without inducing it in other organs. A review on the eventual therapeutic targeting of dark-brown fat to treat man obesity was published by Samuelson and Vidal-Puig in 2020.[61]

Until recently, brown adipose tissue in humans was idea to be primarily limited to infants, but new evidence has overturned that belief. Metabolically active tissue with temperature responses similar to chocolate-brown adipose was beginning reported in the neck and trunk of some man adults in 2007,[62] and the presence of brown adipose in human adults was after verified histologically in the aforementioned anatomical regions.[63] [64] [65]

Beige fat and WAT browning [edit]

Browning of WAT, also referred to as "beiging", occurs when adipocytes within WAT depots develop features of BAT. Beige adipocytes take on a multilocular appearance (containing several lipid droplets) and increment expression of uncoupling poly peptide ane (UCP1).[66] In doing and so, these normally energy-storing adipocytes become energy-releasing adipocytes.

The calorie-burning capacity of brownish and biscuit fat has been extensively studied as inquiry efforts focus on therapies targeted to treat obesity and diabetes. The drug 2,4-dinitrophenol, which also acts every bit a chemic uncoupler similarly to UCP1, was used for weight loss in the 1930s. Yet, it was quickly discontinued when excessive dosing led to adverse side effects including hyperthermia and death.[66] β3 agonists, like CL316,243, accept also been developed and tested in humans. However, the apply of such drugs has proven largely unsuccessful due to several challenges, including varying species receptor specificity and poor oral bioavailability.[67]

Common cold is a primary regulator of BAT processes and induces WAT browning. Browning in response to chronic cold exposure has been well documented and is a reversible process. A report in mice demonstrated that cold-induced browning can be completely reversed in 21 days, with measurable decreases in UCP1 seen within a 24-hour period.[68] A study by Rosenwald et al. revealed that when the animals are re-exposed to a cold environs, the aforementioned adipocytes will adopt a beige phenotype, suggesting that beige adipocytes are retained.[69]

Transcriptional regulators, besides as a growing number of other factors, regulate the consecration of beige fat. Four regulators of transcription are central to WAT browning and serve equally targets for many of the molecules known to influence this process.[70] These include peroxisome proliferator-activated receptor gamma (PPARγ), PRDM16,[71] peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α), and Early B-Cell Factor-two (EBF2).[72] [73] [74]

The listing of molecules that influence browning has grown in straight proportion to the popularity of this topic and is constantly evolving every bit more knowledge is acquired. Among these molecules are irisin and fibroblast growth factor 21 (FGF21), which accept been well-studied and are believed to exist important regulators of browning. Irisin is secreted from muscle in response to practise and has been shown to increase browning by interim on beige preadipocytes.[75] FGF21, a hormone secreted mainly past the liver, has garnered a not bad deal of interest subsequently being identified as a potent stimulator of glucose uptake and a browning regulator through its effects on PGC-1α.[66] Information technology is increased in BAT during common cold exposure and is thought to assist in resistance to diet-induced obesity[76] FGF21 may also be secreted in response to exercise and a low protein nutrition, although the latter has not been thoroughly investigated.[77] [78] Data from these studies propose that ecology factors similar diet and exercise may be important mediators of browning. In mice, it was found that beiging can occur through the production of methionine-enkephalin peptides past type 2 innate lymphoid cells in response to interleukin 33.[79]

Genomics and bioinformatics tools to report browning [edit]

Due to the complex nature of adipose tissue and a growing list of browning regulatory molecules, great potential exists for the utilise of bioinformatics tools to meliorate written report within this field. Studies of WAT browning have profoundly benefited from advances in these techniques, as beige fat is rapidly gaining popularity every bit a therapeutic target for the handling of obesity and diabetes.

DNA microarray is a bioinformatics tool used to quantify expression levels of various genes simultaneously, and has been used extensively in the study of adipose tissue. One such study used microarray analysis in conjunction with Ingenuity IPA software to await at changes in WAT and BAT gene expression when mice were exposed to temperatures of 28 and vi °C.[lxxx] The most significantly upwardly- and downregulated genes were and so identified and used for analysis of differentially expressed pathways. Information technology was discovered that many of the pathways upregulated in WAT after common cold exposure are also highly expressed in BAT, such equally oxidative phosphorylation, fatty acid metabolism, and pyruvate metabolism.[lxxx] This suggests that some of the adipocytes switched to a beige phenotype at 6 °C. Mössenböck et al. also used microarray analysis to demonstrate that insulin deficiency inhibits the differentiation of beige adipocytes but does not disturb their capacity for browning.[81] These ii studies demonstrate the potential for the use of microarray in the study of WAT browning.

RNA sequencing (RNA-Seq) is a powerful computational tool that allows for the quantification of RNA expression for all genes within a sample. Incorporating RNA-Seq into browning studies is of great value, as information technology offers better specificity, sensitivity, and a more comprehensive overview of cistron expression than other methods. RNA-Seq has been used in both human being and mouse studies in an attempt narrate beige adipocytes according to their gene expression profiles and to identify potential therapeutic molecules that may induce the beige phenotype. One such study used RNA-Seq to compare cistron expression profiles of WAT from wild-type (WT) mice and those overexpressing Early B-Cell Factor-2 (EBF2). WAT from the transgenic animals exhibited a brown fat factor plan and had decreased WAT specific gene expression compared to the WT mice.[82] Thus, EBF2 has been identified as a potential therapeutic molecule to induce beiging.

Chromatin immunoprecipitation with sequencing (ChIP-seq) is a method used to identify poly peptide binding sites on DNA and assess histone modifications. This tool has enabled exam of epigenetic regulation of browning and helps elucidate the mechanisms by which poly peptide-Dna interactions stimulate the differentiation of biscuit adipocytes. Studies observing the chromatin landscapes of beige adipocytes accept found that adipogenesis of these cells results from the germination of cell specific chromatin landscapes, which regulate the transcriptional plan and, ultimately, control differentiation. Using Flake-seq in conjunction with other tools, recent studies accept identified over thirty transcriptional and epigenetic factors that influence beige adipocyte development.[82]

Genetics [edit]

The thrifty cistron hypothesis (also called the dearth hypothesis) states that in some populations the trunk would be more efficient at retaining fat in times of plenty, thereby endowing greater resistance to starvation in times of food scarcity. This hypothesis, originally avant-garde in the context of glucose metabolism and insulin resistance, has been discredited by physical anthropologists, physiologists, and the original proponent of the idea himself with respect to that context, although according to its developer it remains "every bit feasible as when [information technology was] start avant-garde" in other contexts.[83] [84]

In 1995, Jeffrey Friedman, in his residency at the Rockefeller University, together with Rudolph Leibel, Douglas Coleman et al. discovered the protein leptin that the genetically obese mouse lacked.[85] [86] [87] Leptin is produced in the white adipose tissue and signals to the hypothalamus. When leptin levels drop, the torso interprets this as a loss of free energy, and hunger increases. Mice lacking this protein eat until they are four times their normal size.

Leptin, however, plays a different role in diet-induced obesity in rodents and humans. Because adipocytes produce leptin, leptin levels are elevated in the obese. However, hunger remains, and—when leptin levels drop due to weight loss—hunger increases. The drop of leptin is better viewed as a starvation signal than the rise of leptin as a satiety betoken.[88] Notwithstanding, elevated leptin in obesity is known as leptin resistance. The changes that occur in the hypothalamus to result in leptin resistance in obesity are currently the focus of obesity research.[89]

Cistron defects in the leptin gene (ob) are rare in human obesity.[xc] Equally of July 2010[update], just xiv individuals from five families accept been identified worldwide who bear a mutated ob cistron (one of which was the first e'er identified cause of genetic obesity in humans)—ii families of Pakistani origin living in the United kingdom of great britain and northern ireland, one family living in Turkey, one in Arab republic of egypt, and one in Republic of austria[91] [92] [93] [94] [95]—and 2 other families have been found that acquit a mutated ob receptor.[96] [97] Others have been identified as genetically partially deficient in leptin, and, in these individuals, leptin levels on the low finish of the normal range can predict obesity.[98]

Several mutations of genes involving the melanocortins (used in brain signaling associated with appetite) and their receptors have also been identified as causing obesity in a larger portion of the population than leptin mutations.[99]

Physical properties [edit]

Adipose tissue has a density of ~0.ix grand/ml.[100] Thus, a person with more than adipose tissue volition float more hands than a person of the same weight with more than muscular tissue, since muscular tissue has a density of 1.06 g/ml.[101]

Body fat meter [edit]

A trunk fat meter is a tool used to measure out the body fatty to weight ratio in the man trunk. Unlike meters use various methods to determine the ratio. They tend to under-read torso fat percentage.

In contrast with clinical tools, one relatively cheap type of torso fat meter uses the principle of bioelectrical impedance analysis (BIA) in order to determine an individual's torso fat percentage. To achieve this, the meter passes a small-scale, harmless, electric current through the torso and measures the resistance, and then uses information on the person's weight, height, age, and sex activity to calculate an approximate value for the person's body fatty percent. The calculation measures the full volume of h2o in the body (lean tissue and muscle contain a higher pct of water than fat), and estimates the percentage of fat based on this information. The result can fluctuate several percentage points depending on what has been eaten and how much water has been drunkard earlier the analysis.

Before bioelectrical impedance assay machines were developed, there were many dissimilar ways in analyzing body composition such equally skin fold methods using calipers, underwater weighing, whole body air displacement plethysmography (ADP) and DXA.

Brute studies [edit]

Within the fatty (adipose) tissue of CCR2 scarce mice, at that place is an increased number of eosinophils, greater alternative Macrophage activation, and a propensity towards type 2 cytokine expression. Furthermore, this effect was exaggerated when the mice became obese from a high fat diet.[102]

Gallery [edit]

  • Diagrammatic exclusive view of the skin (magnified).

  • White adipose tissue in paraffin department

  • Electronic musical instrument of body fatty meter

See too [edit]

  • Adipose differentiation-related poly peptide
  • Adipocytes
  • Apelin
  • Bioelectrical impedance analysis – a method to measure body fatty percentage.
  • Blab – an extra thick form of adipose tissue found in some marine mammals.
  • Trunk fatty pct
  • Cellulite
  • Lipolysis
  • Lipodystrophy
  • Human fat used every bit pharmaceutical in traditional medicine
  • Obesity
  • Starvation
  • Steatosis (also chosen fatty modify, fatty degeneration or adipose degeneration)
  • Stem cells
  • Subcutaneous fatty
  • Bariatrics
  • Classification of obesity
  • Classification of childhood obesity
  • EPODE International Network, the world'due south largest obesity-prevention network
  • World Fit A program of the United States Olympic Committee (USOC), and the U.s.a. Olympians and Paralympians Association (USOP)
  • Obesity and walking
  • Social stigma of obesity

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Further reading [edit]

  • MeSH A10.165.114
  • Stock MJ, Cinti S (2003). "Adipose Tissue / Structure and Function of Brown Adipose Tissue". Encyclopedia of Food Sciences and Nutrition. pp. 29–34. doi:x.1016/B0-12-227055-X/00008-0. ISBN978-0-12-227055-0.
  • Vernon RG, Flint DJ (2003). "Adipose Tissue / Structure and Function of White Adipose Tissue". Encyclopedia of Food Sciences and Nutrition. pp. 23–29. doi:10.1016/B0-12-227055-X/00007-nine. ISBN978-0-12-227055-0.

External links [edit]

  • Adipose tissue photomicrographs

Source: https://en.wikipedia.org/wiki/Adipose_tissue

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