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{{For|the Doctor Who creatures|List of Doctor Who monsters and aliens#Adipose}} |
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[[Image:Illu connective tissues 1.jpg|thumb|390px|Adipose tissue is one of the main types of [[connective tissue]].]] |
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In Biology, '''adipose tissue''' ({{IPAc-en|ˈ|æ|d|ə|ˌ|p|oʊ|s}}) or '''body fat''' or '''fat depot''' or just '''fat''' is loose [[connective tissue]] composed of [[adipocyte]]s. It is technically composed of roughly only 80% fat; fat in its solitary state exists in the liver and muscles. Adipose tissue is derived from [[lipoblast]]s. Its main role is to store [[energy]] in the form of [[lipid]]s, although it also cushions and [[Thermal insulation|insulates]] the body. Far from hormonally inert, adipose tissue has in recent years been recognized as a major [[endocrine]] organ<ref>{{cite journal |author=Kershaw EE, Flier JS |title=Adipose tissue as an endocrine organ |journal=J. Clin. Endocrinol. Metab. |volume=89 |issue=6 |pages=2548–56 |year=2004 |pmid=15181022 |doi=10.1210/jc.2004-0395}}</ref>, as it produces [[hormone]]s such as [[leptin]], [[resistin]], and the [[cytokine]] [[TNF-alpha|TNFα]]. Moreover, adipose tissue can affect other organ systems of the body and may lead to disease. [[Obesity]] or being [[overweight]] in humans and most animals does not depend on body weight but on the amount of body fat—to be specific, adipose tissue{{Citation needed|date=January 2012}}. Two types of adipose tissue exist: [[white adipose tissue]] (WAT) and [[brown adipose tissue]] (BAT). The formation of adipose tissue appears to be controlled in part by the [[adipose gene]]. Adipose tissue was first identified by the Swiss naturalist [[Conrad Gessner]] in 1551.<ref>Cannon B, Nedergaard J. (2008). Developmental biology: Neither fat nor flesh. Nature. Aug 21;454(7207):947-8. {{PMID|18719573}}</ref> |
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== Anatomical features == |
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=== In humans === |
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In humans, adipose tissue is located beneath the [[human skin|skin]] ([[subcutaneous fat]]), around internal [[Organ (anatomy)|organ]]s ([[visceral fat]]), in bone marrow ([[yellow bone marrow]]) and in breast tissue. Adipose tissue is found in specific locations, which are referred to as ''adipose depots''. Adipose tissue contains several cell types, with the highest percentage of cells being [[adipocyte]]s, which contain fat droplets. Other cell types include [[fibroblast]]s, [[macrophage]]s, and [[endothelial cell]]s. Adipose tissue contains many small [[blood vessel]]s. In the [[integumentary system]], which includes the skin, it accumulates in the deepest level, the [[subcutaneous]] layer, providing insulation from heat and cold. Around organs, it provides protective padding. However, its main function is to be a reserve of lipids, which can be burned to meet the energy needs of the body. Adipose depots in different parts of the body have different biochemical profiles. Under normal conditions, it provides feedback for hunger and diet to the brain. |
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=== Mice === |
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In [[mouse|mice]], there are eight major adipose depots, four of which are within the [[abdominal cavity]]: The paired gonadal depots are attached to the [[uterus]] and [[ovary|ovaries]] in females and the [[epididymis]] and [[testes]] in males; the paired retroperitoneal depots are found along the [[Dorsum (biology)|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 [[intestine]]s, and the omental depot, which originates near the [[stomach]] and [[spleen]], and, when massive, extends into the ventral abdomen. Both the mesenteric and omental depots incorporate much [[lymphoid tissue]] as lymph nodes and [[milky spot]]s, respectively. The two superficial depots are the paired inguinal depots, which are found anterior to the upper segment of the hind limbs (underneath the skin) and the subscapular depots, paired medial mixtures of brown adipose tissue adjacent to regions of white adipose tissue, which are found under the [[skin]] 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 (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 heart, and the paired popliteal depots, between the major [[muscle]]s behind the knees, each containing one large [[lymph node]].<ref>{{cite book | last = Pond | first = Caroline M. | authorlink = Caroline M. Pond | title = The Fats of Life | publisher = Cambridge University Press | year = 1998 | isbn = 0-521-63577-2}}</ref> Of all the depots in the mouse, the gonadal depots are the largest and the most easily dissected,<ref>{{cite journal | last = Cinti | first = S | year = 2005 | month = July | title = The adipose organ | journal = Prostaglandins, leukotrienes, and essential fatty acids | volume = 73 | issue = 952–3278 | pages = 9–15 | publisher = Elsevier Science | pmid = 15936182 | doi = 10.1016/j.plefa.2005.04.010}}</ref> comprising about 30% of dissectible fat.<ref>{{cite journal | last= Bachmanov | first= Alexander | authorlink= Alexander Bachmanov | coauthors= D. R. Reed, M. G. Tordoff, R. A. Price | year= 2001 | month= March | title= Nutrient preference and diet-induced adiposity in C57BL/6ByJ and 129P3/J mice | journal= Physiology & Behavior | volume= 72 | issue= 31–9384 | pages= 603–613 | pmid=11282146 | doi= 10.1016/S0031-9384(01)00412-7}}</ref> |
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===Obesity=== |
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In a severely [[obese]] [[person]], excess adipose tissue hanging downward from the abdomen is referred to as a [[panniculus]] (or [[pannus]]). A panniculus complicates surgery of the morbidly obese. The panniculus may remain as a literal "apron of skin" if a severely obese person quickly loses large amounts of fat (a common result of [[gastric bypass surgery]]). This condition cannot be effectively corrected through diet and exercise alone, as the panniculus consists of adipocytes and other supporting cell types shrunken to their minimum volume and diameter.{{citation needed|date=January 2011}} Reconstructive surgery is one method of treatment. |
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===Abdominal fat=== |
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{{See also|Abdominal obesity}} |
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Visceral fat or ''abdominal fat''<ref>[http://lowfatcooking.about.com/od/healthandfitness/a/bodyfat.htm Fat on the Inside: Looking Thin is Not Enough], By Fiona Haynes, About.com</ref> also known as organ fat or ''intra-abdominal fat'', is located inside the [[abdominal cavity]], packed in between organs (stomach, liver, intestines, kidneys, etc.). Visceral fat is different than [[subcutaneous fat]] underneath the [[skin]], and [[intramuscular fat]] interspersed in [[skeletal muscle]]s. Fat in the lower body, as in thighs and buttocks, is subcutaneous, whereas fat in the [[abdomen]] is mostly visceral.<ref>[https://www.health.harvard.edu/fhg/updates/Abdominal-fat-and-what-to-do-about-it.shtml Abdominal fat and what to do about it], President & Fellows of Harvard College</ref> Visceral fat is composed of several adipose depots including [[mesenteric]], [[epididymal]] [[white adipose tissue]] (EWAT), and [[perirenal fat|perirenal]] depots. |
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An excess of visceral fat is known as [[central obesity]], or "belly fat", in which the abdomen protrudes excessively. There is a strong correlation between central [[obesity]] and [[cardiovascular disease]].<ref name=Yusuf2004>{{cite journal | author=Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L, INTERHEART Study Investigators. | title=Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study|journal=[[The Lancet|Lancet]] | year=2004 | pages=937–52 | volume=364 | pmid=15364185 | doi=10.1016/S0140-6736(04)17018-9 | issue=9438}}</ref> |
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Excess visceral fat is also linked to [[Diabetes mellitus type 2|type 2 diabetes]],<ref>C.T. Montague and S. O'Rahilly, "The perils of portliness: causes and consequences of visceral adiposity", ''Diabetes'' vol 49, pages 883-888 (2000)</ref> [[insulin resistance]]<ref>P.A. Kern, Ranganathan, et al, "Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance", ''Am J Physiol Endocrinol Metab'' vol 280 pages E745-E751 (2001),</ref> [[Inflammation#Inflammatory disorders|inflammatory diseases]],<ref>A. Marett, "Molecular mechanisms of inflammation in obesity-linked insulin resistance", ''Int J Obesity'' vol 27 pages S46-S48 (2003)</ref> and other obesity-related diseases.<ref>A.H. Mokdad, E.S. Ford, et al, "Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001", ''JAMA'' vol 289 pages 76-79 (2003)</ref> |
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[[Estrogen|Female sex hormone]] causes fat to be stored in the [[buttocks]], [[thighs]], and [[Hip (anatomy)|hips]] in women.<ref>Estrogen causes fat to be stored around the pelvic region, hips, butt and thighs (pelvic region) [http://www.annecollins.com/obesity/reduce-abdominal-fat.htm]</ref><ref>[http://www.healthywomen.org/columns/drpeekescolumn/dbcolumn/waistlineworriesturningapplesbackintopears Waistline Worries: Turning Apples Back Into Pears]</ref> Men are more likely to have fat stored in the belly due to [[Sex differences in humans|sex hormone differences]]. When women reach [[menopause]] and the estrogen produced by ovaries declines, fat migrates from their buttocks, hips and thighs to their waists;<ref>Researchers think that the lack of estrogen at menopause play a role in driving our fat northward [http://health.yahoo.com/topic/nutrition/overview/article/womens-health/26287]</ref> later fat is stored in the [[abdomen|belly]].<ref>[http://www.health.harvard.edu/newsweek/Abdominal-fat-and-what-to-do-about-it.htm Abdominal fat and what to do about it]</ref> |
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High-intensity exercise is one way to effectively reduce total abdominal fat.<ref>{{cite pmid|18845966}}</ref><ref>{{cite pmid|19196080}}</ref> One study suggests at least 10 [[Metabolic equivalent|MET]]-hours per week of [[aerobic exercise]] is required for visceral fat reduction.<ref>{{cite pmid|17637702}}</ref> |
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===Epicardial fat=== |
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[[Epicardial]] adipose tissue (EAT) is a particular form of [[visceral fat]] deposited around the heart and found to be a metabolically active organ that generates various bioactive molecules, which might significantly affect cardiac function.<ref name="pmid14581396">Mazurek T, Zhang L, Zalewski A, Mannion JD, Diehl JT, Arafat H et al. (2003) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=14581396 Human epicardial adipose tissue is a source of inflammatory mediators.] ''Circulation'' 108 (20):2460-6. [http://dx.doi.org/10.1161/01.CIR.0000099542.57313.C5 DOI:10.1161/01.CIR.0000099542.57313.C5] PMID: [http://pubmed.gov/14581396 14581396]</ref> A marked component composition differences has been observed in comparing EAT with subcutaneous fat, suggesting a depot specific impact of stored fatty acids on adipocyte function and metabolism.<ref name="pmid19422139">Pezeshkian M, Noori M, Najjarpour-Jabbari H, Abolfathi A, Darabi M, Darabi M et al. (2009) [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=19422139 Fatty acid composition of epicardial and subcutaneous human adipose tissue.] ''Metab Syndr Relat Disord'' 7 (2):125-31. PMID: [http://pubmed.gov/19422139 19422139]</ref> |
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===Subcutaneous fat=== |
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Most of the remaining non-visceral fat is found just below the skin in a region called the hypodermis.<ref name="K Hoehn 2008">E Marieb and K Hoehn. Anatomy and Physiology, 3rd Edition. Benjamin Cummings 2008. ISBN 0-8053-0094-5</ref> This subcutaneous fat is not related to many of the classic obesity-related pathologies, such as heart disease, cancer, and stroke, and there is even some evidence to suggest that it might be protective.<ref>Porter SA, Massaro JM, Hoffmann U, Vasan RS, O'Donnel CJ, Fox CS. Abdominal subcutaneous adipose tissue: a protective fat depot? Diabetes Care. 2009 Jun;32(6):1068-75. Epub 2009 Feb 24</ref> The typically female (or gynecoid) pattern of body fat distribution around the hips, thighs, and buttocks, is subcutaneous fat, and therefore poses less of a health risk compared to visceral fat.<ref>Mayo Clinic staff. Belly fat in women: How to keep it off. MayoClinic.com. URL http://www.mayoclinic.com/health/belly-fat/WO00128/METHOD=print. Access date July 2, 2010</ref> |
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Like all other fat organs, subcutaneous fat is an active part of the endocrine system, secreting the hormones ''leptin'' and ''resistin''.<ref name="K Hoehn 2008"/> |
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The relationship between a person's subcutaneous adipose layer and their total body fat is often modelled by using regression equations. The most popular of these equations were formed by Durnin and Wormersley, who rigorously tested many types of skinfold, and, as a result, created two formulae to calculate the body density of both men and women. These equations present a inverse correlation between skinfolds and body density – as the sum of skinfolds increases, the body density decreases.<ref name=Brodie>{{Cite doi|10.1016/S0899-9007(97)00474-7}}</ref> |
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Factors such as sex, age, population size or other variables may make the equations invalid and unusable, and, {{As of|2012|lc=y}}, Durnin and Wormersley's equations remain only estimates of a person's true level of fatness. New formulae are still being created to this day.<ref name=Brodie/> |
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{{See also|Body fat percentage}} |
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==Physiology== |
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{{Refimprove section|date=July 2007}} |
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[[Free fatty acid]] is liberated from [[lipoprotein]]s by [[Lipoprotein lipase]] (LPL) and enters the adipocyte, where it is reassembled into [[triglyceride]]s by [[ester]]ifying it onto [[glycerol]]. Human fat tissue contains about 87% lipids. |
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In humans, lipolysis is controlled through the balanced control of lipolytic B-adrenergic receptors and a2A-adrenergic receptor-mediated antilipolysis. |
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Fat is not laid down when there is surplus calories available and stored passively until it is needed; rather, it is constantly being stored in and released from the adipose tissue. |
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Storage in the adipose tissue is catalysed by insulin, the activity of which is stimulated by high blood sugar. |
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Fat cells have an important [[physiology|physiological]] role in maintaining triglyceride and [[free fatty acid]] levels, as well as determining [[insulin resistance]]. [[Abdomen|Abdominal]] fat has a different [[metabolism|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 factor for [[cardiovascular disease]] (even in the absence of [[diabetes mellitus]] and [[hypertension]]).<ref>Dhaliwal SS, Welborn TA. (May 2009) "Central obesity and multivariable cardiovascular risk as assessed by the Framingham prediction scores" ''Am J Cardiol.'' (American Journal of Cardiology) 103(10): pp. 1403-1407</ref> Studies of female monkeys at [[Wake Forest University]] (2009) discovered that individuals suffering from higher [[Stress (biological)|stress]] have higher levels of visceral fat in their bodies. This suggests a possible cause-and-effect link between the two, wherein stress promotes the accumulation of visceral fat, which in turn causes hormonal and metabolic changes that contribute to heart disease and other health problems.<ref name="Time2009">{{cite web |
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|url=http://www.time.com/time/health/article/0,8599,1915237,00.html |
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|title=Fat-Bellied Monkeys Suggest Why Stress Sucks |
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|publisher=[[Time magazine|Time]] |
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|author=Alice Park |
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|date=2009-08-08 |
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|accessdate=2009-08-08}}</ref> |
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Recent advances in biotechnology have allowed for the harvesting of [[adult stem cell]]s from adipose tissue, allowing stimulation of tissue regrowth using a patient's own cells. In addition, it was reported that adipose-derived stem cells from both human and animals can be efficiently reprogrammed into [[induced pluripotent stem cells]] without the need for feeder cells.<ref>Sugii et. al. (2010). [http://www.pnas.org/content/107/8/3558.abstract Human and mouse adipose-derived cells support feeder-independent induction of pluripotent stem cells]. Proc Natl Acad Sci USA. 107:3558-63. {{PMID| 20133714}}</ref> The use of a patient's own cells reduces the chance of tissue rejection and avoids the ethical issues associated with the use of human [[embryonic stem cell]]s. |
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Adipose tissue is the greatest [[peripheral]] source of [[aromatase]] in both males and females, contributing to the production of [[estradiol]]. |
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[[Adipose derived hormones]] include: |
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* [[Adiponectin]] |
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* [[Resistin]] |
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* [[Plasminogen activator inhibitor-1]] (PAI-1) |
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* [[TNF-alpha|TNFα]] |
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* [[Interleukin 6|IL-6]] |
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* [[Leptin]] |
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* [[Estradiol]] (E2) |
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Adipose tissues also secrete a type of [[cytokine]]s (cell-to-cell signalling proteins) called [[adipokine]]s (adipocytokines), which play a role in obesity-associated complications. |
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===Brown fat=== |
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{{Main|Brown adipose tissue}} |
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A specialised form of adipose tissue in humans, most rodents and small mammals, and some [[hibernating]] animals, is [[brown fat]] or [[brown adipose tissue]]. It is located mainly around the neck and large blood vessels of the [[thorax]]. This specialised tissue can generate heat by "uncoupling" the [[respiratory chain]] of [[oxidative phosphorylation]] within [[mitochondria]]. The process of uncoupling means that, when protons transit down the electrochemical gradient across the inner mitochondrial membrane, the energy from this process is released as heat rather than being used to generate [[Adenosine triphosphate|ATP]]. This thermogenic process may be vital in neonates exposed to the cold, which then require this thermogenesis to keep warm, as they are unable to [[shivering|shiver]], or take other actions to keep themselves warm.<ref>Himms-Hagen, J. (August 1990) "Brown adipose tissue thermogenesis: interdisciplinary studies" ''The FASEB Journal'' (Federation of American Societies for Experimental Biology) 4(11): pp. 2890-2898</ref> |
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Attempts to simulate this process [[pharmacology|pharmacologically]] have so far been unsuccessful (even lethal<ref name="pmid15487646">{{cite journal |author=McFee RB, Caraccio TR, McGuigan MA, Reynolds SA, Bellanger P |title=Dying to be thin: a dinitrophenol related fatality |journal=Veterinary and human toxicology |volume=46 |issue=5 |pages=251–4 |year=2004 |pmid=15487646 |doi = }}</ref><ref name="pmid16803658">{{cite journal |author=Miranda EJ, McIntyre IM, Parker DR, Gary RD, Logan BK |title=Two deaths attributed to the use of 2,4-dinitrophenol |journal=Journal of analytical toxicology |volume=30 |issue=3 |pages=219–22 |year=2006 |pmid=16803658 |doi = }}</ref>). Techniques to manipulate the differentiation of "brown fat" could become a mechanism for [[weight loss]] therapy in the future, encouraging the growth of tissue with this specialized metabolism without inducing it in other organs. |
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Until recently, it was thought that brown adipose tissue was primarily limited to [[infant]]s in humans, but new evidence has now overturned that belief. Metabolically active tissue with temperature responses similar to brown adipose was first reported in the neck and trunk of some human adults in 2007,<ref>Nedergaard J, Bengtsson T, Cannon B. (2007). [http://ajpendo.physiology.org/cgi/reprint/293/2/E444 Unexpected evidence for active brown adipose tissue in adult humans]. Am J Physiol Endocrinol Metab. 293:E444-52. {{PMID|17473055}}</ref> and the presence of brown adipose in human adults was later verified histologically in the same anatomical regions.<ref>Virtanen KA, Lidell ME, Orava J, Heglind M, Westergren R, Niemi T, Taittonen M, Laine J, Savisto NJ, Enerback S, Nuutila P. Functional brown adipose tissue in healthy adults. N Engl J Med 2009;360:1518–1525</ref><ref>van Marken Lichtenbelt WD, Vanhommerig JW, Smulders NM, Drossaerts JM, Kemerink GJ, Bouvy ND, Schrauwen P, Teule GJ. Cold-activated brown adipose tissue in healthy men. N Engl J Med 2009;360:1500–1508</ref><ref>Cypess AM, Lehman S, Williams G, Tal I, Rodman D, Goldfine AB, Kuo FC, Palmer EL, Tseng YH, Doria A, Kolodny GM, Kahn CR. Identification and importance of brown adipose tissue in adult humans. N Engl J Med 2009;360:1509–1517</ref> |
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===Genetics=== |
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The [[thrifty gene hypothesis]] (also called the Famine Hypothesis) states that in some populations the body would be more efficient at retaining fat in times of plenty, thereby endowing greater resistance to starvation in times of food scarcity. This hypothesis has been discredited by physical anthropologists, physiologists, and the [[James V. Neel|original proponent of the idea]] himself.<ref>Speakerman, John R. "Genetics of Obesity: Five Fundamental Problems with the Famine Hypothesis." Adipose Tissue and Adipokines in Health and Disease. 2007</ref> |
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In 1995 [[Jeffrey Friedman]], in his residency at [[Rockefeller University]], discovered the protein [[leptin]] that the genetically obese mouse lacked.<ref>Pelleymounter MA, Cullen MJ, Baker MB, Hecht R, Winters D, Boone T, Collins F. Effects of the obese gene product on body weight regulation in ob/ob mice. Science. 1995 Jul 28;269(5223):540-3.</ref> Leptin is produced in the white adipose tissue and signals to the [[hypothalamus]]. When leptin levels drop, the body interprets this as loss of energy, and hunger increases. Mice lacking this protein eat until they are four times their normal size. |
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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]] signal.<ref>Smith and Ravussin. "Role of the Adipocyte in Metabolism and Endocrine Function." Endocrinology. 2006.</ref> However, elevated leptin in obesity is known as [[Leptin#Leptin_resistance_and_obesity|leptin resistance]]. The changes that occur in the [[hypothalamus]] to result in leptin resistance in obesity are currently the focus of obesity research.<ref>Morris DL, Rui L. Recent advances in understanding leptin signaling and leptin resistance. Am J Physiol Endocrinol Metab. 2009 Dec;297(6):E1247-59. Epub 2009 Sep 1</ref> |
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Gene defects in the leptin gene (ob) are rare in human obesity.<ref>Obes Res. 1997 Jan;5(1):30-5.</ref> As of July, 2010, only fourteen individuals from five families have been identified worldwide that carry a mutated ''ob'' gene (one of which was the first ever identified cause of genetic obesity in humans) - two families of Pakistani origin living in the UK, one family living in Turkey, one in Egypt, and one in Austria<ref>Montague CT, Farooqi IS, Whitehead JP, Soos MA, Rau H, Wareham NJ, Sewter CP, Digby JE, Mohammed SN, Hurst JA, Cheetham CH, Earley AR, Barnett AH, Prins JB, O'Rahilly S. Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature. 1997 Jun 26;387(6636):903-8.</ref><ref>Strobel A, Issad T, Camoin L, Ozata M, Strosberg AD. A leptin missense mutation associated with hypogonadism and morbid obesity. Nat Genet. 1998 Mar;18(3):213-5.</ref><ref>Gibson WT, Farooqi IS, Moreau M, DePaoli AM, Lawrence E, O'Rahilly S, Trussell RA. Congenital leptin deficiency due to homozygosity for the Delta133G mutation: report of another case and evaluation of response to four years of leptin therapy. J Clin Endocrinol Metab. 2004 Oct;89(10):4821-6.</ref><ref>Mazen I, El-Gammal M, Abdel-Hamid M, Amr K. A novel homozygous missense mutation of the leptin gene (N103K) in an obese Egyptian patient. Mol Genet Metab. 2009 Aug;97(4):305-8. Epub 2009 Apr 9.</ref><ref>Fischer-Posovszky P, von Schnurbein J, Moepps B, Lahr G, Strauss G, Barth TF, Kassubek J, Mühleder H, Möller P, Debatin KM, Gierschik P, Wabitsch M. A new missense mutation in the leptin gene causes mild obesity and hypogonadism without affecting T cell responsiveness. J Clin Endocrinol Metab. 2010 Jun;95(6):2836-40. Epub 2010 Apr 9.</ref> - and two other families have been found that carry a mutated ''ob'' receptor.<ref>Clément K, Vaisse C, Lahlou N, Cabrol S, Pelloux V, Cassuto D, Gourmelen M, Dina C, Chambaz J, Lacorte JM, Basdevant A, Bougnères P, Lebouc Y, Froguel P, Guy-Grand B. A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction. Nature. 1998 Mar 26;392(6674):398-401.</ref><ref>Pankov YA. Adipose tissue as an endocrine organ regulating growth, puberty, and other physiological functions. Biochemistry (Mosc). 1999 Jun;64(6):601-9.</ref> Others have been identified as genetically partially deficient in leptin, and, in these individuals, leptin levels on the low end of the normal range can predict obesity.<ref>Farooqi IS, Keogh JM, Kamath S, Jones S, Gibson WT, Trussell R, Jebb SA, Lip GY, O'Rahilly S. Partial leptin deficiency and human adiposity. Nature. 2001 Nov 1;414(6859):34-5.</ref> |
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Several [[mutation]]s of genes involving the [[melanocortin]]s (used in brain signaling associated with appetite) and their [[Receptor (biochemistry)|receptors]] have also been identified as causing obesity in a larger portion of the population than leptin mutations.<ref>Farooqi IS, O'Rahilly S. Mutations in [[ligand]]s and receptors of the [[leptin]]-[[melanocortin]] pathway that lead to obesity. Nat Clin Pract Endocrinol Metab. 2008 Oct;4(10):569-77. Epub 2008 Sep 9.</ref> |
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In 2007, researchers isolated the ''adipose'' gene, which those researchers hypothesize serves to keep animals lean during times of plenty. In that study, increased adipose gene activity was associated with slimmer animals.<ref>Suh, Jae Myoung ''et al.'' (September 2007) "Adipose Is a Conserved Dosage-Sensitive Antiobesity Gene" ''Cell Metabolism'' 6(3): pp. 195-207 {{PMID|17767906}}</ref> Although its discoverers dubbed this gene the ''adipose'' gene, it is not a gene responsible for creating adipose tissue. |
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===Physical properties=== |
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Adipose tissue has a density of ~0.9 g/ml <ref name=fatvsmuscle>[http://answers.google.com/answers/threadview?id=576481 Google Answers: Muscle Density vs. Fat Density]</ref> [0.9 kg/l]. Thus, a person with much adipose tissue will float more easily than a person with a lot of [[muscular tissue]], since muscular tissue has a density of 1.06 g/ml<ref name=fatvsmuscle/> [1.06 kg/l]. |
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==Body fat meter== |
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{{See also|Bioelectrical impedance analysis}} |
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A '''body fat meter''' is a widely available tool used to measure the percentage of fat in the human body. Different meters use various methods to determine the [[Body fat percentage|body fat to weight ratio]]. They tend to under-read body fat percentage.<ref>{{cite web|url=http://www.choice.com.au/Reviews-and-Tests/Food-and-Health/Diet-and-exercise/Weight-loss/Body-fat-scales-review-and-compare.aspx|title=Body fat scales review and compare|date=10 January 2010|accessdate=11 January 2010| archiveurl= http://web.archive.org/web/20100117183041/http://www.choice.com.au/Reviews-and-Tests/Food-and-Health/Diet-and-exercise/Weight-loss/Body-fat-scales-review-and-compare.aspx| archivedate= 17 January 2010 <!--DASHBot-->| deadurl= no}}</ref> |
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In contrast with clinical tools, one relatively inexpensive type of body fat meter uses the principle of [[bioelectrical impedance analysis]] (BIA) to determine an individual's body fat percentage. To achieve this, the meter passes a small, harmless, [[electric current]] through the body and measures the [[Ohm|resistance]], then uses information on the person's weight, height, age, and sex, to calculate an approximate value for the person's body fat percentage. The calculation measures the total volume of water in the body (lean tissue and muscle contain a higher percentage of water than fat), and estimates the percentage of fat based on this information. The result can fluctuate several percent depending on what one has eaten and how much water one has consumed prior to the analysis. |
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==Additional images== |
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<gallery> |
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Image:Gray940.png|Diagrammatic sectional view of the skin (magnified). |
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Image:Yellow adipose tissue in paraffin section - lipids washed out.jpg|White adipose tissue in paraffin section |
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Image:Body Fat meter.jpg|Electronic instrument of ''body fat meter'' |
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</gallery> |
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==See also== |
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* [[Apelin]] |
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* [[Bioelectrical impedance analysis]]: a method to measure body fat percentage. |
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* [[Blubber]]: an extra thick form of adipose tissue found in some marine mammals. |
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* [[Body fat percentage]] |
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* [[Cellulite]] |
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* [[Human fat]] used as pharmaceutical in traditional medicine |
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* [[Obesity]] |
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* [[Starving]] |
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* [[Steatosis]] (Also called ''fatty change'', ''fatty degeneration'' or ''adipose degeneration''). |
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* [[Stem Cells]] |
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* [[Subcutaneous fat]] |
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* [[Adipose differentiation-related protein]] |
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* [[Adiposopathy]] |
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==References== |
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{{Reflist|colwidth=30em}} |
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==External links== |
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* {{MeshNumber|A10.165.114}} |
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{{Connective tissue}} |
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{{DEFAULTSORT:Adipose Tissue}} |
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[[Category:Tissues]] |
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[[Category:Obesity]] |
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[[ar:نسيج دهني]] |
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[[ca:Teixit adipós]] |
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[[cs:Tuková tkáň]] |
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[[da:Fedtvæv]] |
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[[de:Fettgewebe]] |
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[[el:Λιπώδης ιστός]] |
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[[es:Tejido adiposo]] |
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[[eu:Gantz ehun]] |
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[[fa:بافت چربی]] |
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[[fr:Tissu adipeux]] |
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[[gl:Tecido adiposo]] |
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[[it:Tessuto adiposo]] |
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[[he:רקמת שומן]] |
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[[kk:Май ұлпасы]] |
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[[lt:Riebalinis audinys]] |
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[[hu:Zsírszövet]] |
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[[arz:نسيج دهنى]] |
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[[nl:Vetweefsel]] |
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[[ja:脂肪組織]] |
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[[no:Fettvev]] |
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[[pag:Taba]] |
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[[pl:Tkanka tłuszczowa]] |
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[[pt:Tecido adiposo]] |
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[[ru:Жировая ткань]] |
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[[simple:Adipose tissue]] |
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[[fi:Rasvakudos]] |
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[[sv:Fettvävnad]] |
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[[ta:கொழுப்பிழையம்]] |
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[[tr:Yağ doku]] |
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[[uk:Жирова тканина]] |
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[[zh:脂肪組織]] |
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Revision as of 19:54, 15 April 2012
Liam Gilheany