Adipose tissue
From Wikipedia, the free encyclopedia
Jump to: navigation, search
"Adipose" redirects here. For the fictional creature from Doctor Who, see List of Doctor Who
universe creatures and aliens (0–9, A–G)#Adipose.
See also: Fat
Adipose tissue is one of the main types of connective tissue.
In biology, adipose tissue /ˈædɨˌpoʊs/ or body fat or just fat is loose connective tissue
composed mostly of adipocytes. In addition to adipocytes, adipose tissue contains the stromal
vascular fraction (SVF) of cells including preadipocytes, fibroblasts, vascular endothelial cells
and a variety of immune cells (i.e. adipose tissue macrophages (ATMs)). Adipose tissue is
derived from preadipocytes. Its main role is to store energy in the form of lipids, although it also
cushions and insulates the body. Far from hormonally inert, adipose tissue has, in recent years,
been recognized as a major endocrine organ,[1] as it produces hormones such as leptin, estrogen,
resistin, and the cytokine 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]
The two types of adipose tissue are 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 – more specifically brown adipose tissue – was first identified by the Swiss
naturalist Conrad Gessner in 1551.[2]
Contents
[hide]

1 Anatomical features
o
1.1 Mice
o
1.2 Obesity
o
1.3 Abdominal fat
o
1.4 Epicardial fat
o
1.5 Subcutaneous fat
o
1.6 Ectopic fat

2 Physiology
o
2.1 Brown fat
o
2.2 Genetics
o
2.3 Physical properties

3 Body fat meter

4 Additional images

5 See also

6 References

7 Further reading
Anatomical features[edit]
In humans, adipose tissue is located beneath the skin (subcutaneous fat), around internal organs
(visceral fat), in bone marrow (yellow bone marrow) and in the breast tissue. Adipose tissue is
found in specific locations, which are referred to as adipose depots. Apart from adipocytes,
which comprise the highest percentage of cells within adipose tissue, other cell types are present,
collectively termed stromal vascular fraction (SVF) of cells. SVF includes preadipocytes,
fibroblasts, adipose tissue macrophages, and endothelial cells. Adipose tissue contains many
small blood vessels. 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 and to protect it from excess glucose by storing
triglycerides produced by the liver from sugars, although some evidence suggests that most lipid
synthesis from carbohydrates occurs in the adipose tissue itself.[3] 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.
Mice[edit]
The obese mouse on the left has large stores of adipose tissue. For comparison, a mouse with a
normal amount of adipose tissue is shown on the right.
Mice have eight major adipose depots, four of which are within the abdominal cavity. 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
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 spots,
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 muscles behind the knees, each containing one large lymph
node.[4] Of all the depots in the mouse, the gonadal depots are the largest and the most easily
dissected,[5] comprising about 30% of dissectible fat.[6]
Obesity[edit]
In an 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 individual. It
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] Reconstructive surgery is
one method of treatment.
Abdominal fat[edit]
See also: Abdominal obesity
Visceral fat or abdominal fat[7] (also known as organ fat or intra-abdominal fat) is located inside
the abdominal cavity, packed between the organs (stomach, liver, intestines, kidneys, etc.).
Visceral fat is different from subcutaneous fat underneath the skin, and intramuscular fat
interspersed in skeletal muscles. Fat in the lower body, as in thighs and buttocks, is subcutaneous
and is not consistently spaced tissue, whereas fat in the abdomen is mostly visceral and semifluid.[8] Visceral fat is composed of several adipose depots, including mesenteric, epididymal
white adipose tissue (EWAT), and perirenal depots. Visceral fat is considered adipose tissue
whereas subcutaneous fat is not considered as such.
An excess of visceral fat is known as central obesity, or "belly fat", in which the abdomen
protrudes excessively. Excess visceral fat is also linked to type 2 diabetes,[9] insulin resistance,[10]
inflammatory diseases,[11] and other obesity-related diseases.[12]
Female sex hormone causes fat to be stored in the buttocks, thighs, and hips in women.[13][14]
Men are more likely to have fat stored in the belly due to sex hormone differences. When women
reach menopause and the estrogen produced by the ovaries declines, fat migrates from the
buttocks, hips and thighs to the waist;[15] later fat is stored in the abdomen.[16]
High-intensity exercise is one way to effectively reduce total abdominal fat.[17][18] One study
suggests at least 10 MET-hours per week of aerobic exercise is required for visceral fat
reduction.[19]
Epicardial fat[edit]
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.[20] Marked component differences have been observed in
comparing EAT with subcutaneous fat, suggesting a depot specific impact of stored fatty acids
on adipocyte function and metabolism.[21]
Subcutaneous fat[edit]
Abdominal fat on an overweight teenage boy's abdomen.
Most of the remaining nonvisceral fat is found just below the skin in a region called the
hypodermis.[22] This subcutaneous fat is not related to many of the classic obesity-related
pathologies, such as heart disease, cancer, and stroke, and some evidence even suggests it might
be protective.[23] 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.[24]
Like all other fat organs, subcutaneous fat is an active part of the endocrine system, secreting the
hormones leptin and resistin.[22]
The relationship between the subcutaneous adipose layer and total body fat in a person is often
modelled by using regression equations. The most popular of these equations was 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 an
inverse correlation between skinfolds and body density—as the sum of skinfolds increases, the
body density decreases.[25]
Factors such as sex, age, population size or other variables may make the equations invalid and
unusable, and, as of 2012, Durnin and Wormersley's equations remain only estimates of a
person's true level of fatness. New formulae are still being created.[25]
See also: Body fat percentage
Ectopic fat[edit]
Ectopic fat is the storage of triglycerides in tissues other than adipose tissue, that are supposed to
contain only small amounts of fat, such as the liver, skeletal muscle, heart, and pancreas. This
can interfere with cellular functions and hence organ function and is associated with insulin
resistance in type-2 diabetes.[26] It is stored in relatively high amounts around the organs of the
abdominal cavity, but is not to be confused as visceral fat.
The specific cause for the accumulation of ectopic fat is unknown. The cause is likely a
combination of genetic, environmental, and behavioral factors that are involved in excess energy
intake and decreased physical activity. Substantial weight loss can reduce ectopic fat stores in all
organs and this is associated with an improvement of the function of that organ.[26]
Physiology[edit]
Free fatty acids are liberated from lipoproteins by lipoprotein lipase (LPL) and enter the
adipocyte, where they are reassembled into triglycerides by esterifying it onto glycerol. Human
fat tissue contains about 87% lipids.
There is a constant flux of FFA (Free Fatty Acids) entering and leaving adipose tissue. The net
direction of this flux is controlled by insulin and leptin—if insulin is elevated 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 sugar, which results from consuming carbohydrates.
In humans, lipolysis (hydrolysis of triglycerides into free fatty acids) is controlled through the
balanced control of lipolytic B-adrenergic receptors and a2A-adrenergic receptor-mediated
antilipolysis.
Fat cells have an important physiological role in maintaining triglyceride and free fatty acid
levels, as well as determining insulin resistance. Abdominal 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 factor for
cardiovascular disease (even in the absence of diabetes mellitus and hypertension).[27] 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-andeffect 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.[28]
Recent advances in biotechnology have allowed for the harvesting of adult stem cells from
adipose tissue, allowing stimulation of tissue regrowth using a patient's own cells. In addition,
adipose-derived stem cells from both human and animals reportedly can be efficiently
reprogrammed into induced pluripotent stem cells without the need for feeder cells.[29] The use of
a patient's own cells reduces the chance of tissue rejection and avoids ethical issues associated
with the use of human embryonic stem cells.
Adipose tissue is the greatest peripheral source of aromatase in both males and females,[citation
needed]
contributing to the production of estradiol.
Adipose derived hormones include:

Adiponectin

Resistin

Plasminogen activator inhibitor-1 (PAI-1)

TNFα

IL-6

Leptin

Estradiol (E2)
Adipose tissues also secrete a type of cytokines (cell-to-cell signalling proteins) called
adipokines (adipocytokines), which play a role in obesity-associated complications. Perivascular
adipose tissue releases adipokines such as adiponectin that affect the contractile function of the
vessels that they surround.[30]
Brown fat[edit]
Main article: Brown adipose tissue
A specialized 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 specialized 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 ATP. This thermogenic process may be vital in neonates exposed to cold, which then
require this thermogenesis to keep warm, as they are unable to shiver, or take other actions to
keep themselves warm.[31]
Attempts to simulate this process pharmacologically have so far been unsuccessful. 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.
Until recently, brown adipose tissue was thought to be primarily limited to infants 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,[32] and the presence of brown adipose in human adults was later verified
histologically in the same anatomical regions.[33][34][35]
Genetics[edit]
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 original proponent of the idea himself.[36]
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.[37][38][39] Leptin is produced in the white adipose tissue and signals to the hypothalamus.
When leptin levels drop, the body interprets this as a loss of 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 signal.[40] However, 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.[41]
Gene defects in the leptin gene (ob) are rare in human obesity.[42] As of July, 2010, only 14
individuals from five families have been identified worldwide who 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[43][44][45][46][47]—and two other families have been found that carry a mutated ob
receptor.[48][49] 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.[50]
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.[51]
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.[52] Although its discoverers dubbed this gene the adipose gene,
it is not a gene responsible for creating adipose tissue.
Physical properties[edit]
Adipose tissue has a density of ~0.9 g/ml.[53] Thus, a person with more adipose tissue will float
more easily than a person of the same weight with more muscular tissue, since muscular tissue
has a density of 1.06 g/ml.[54]
Body fat meter[edit]
See also: Bioelectrical impedance analysis
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 to weight ratio. They tend
to under-read body fat percentage.[55]
In contrast with clinical tools, one relatively inexpensive type of body fat meter uses the
principle of bioelectrical impedance analysis (BIA) in order 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 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 percentage points depending on what has been eaten and how much water has
been drunk before the analysis.
Additional images[edit]

Diagrammatic sectional view of the skin (magnified).

White adipose tissue in paraffin section

Electronic instrument of body fat meter
See also[edit]

Adipose differentiation-related protein

Adiposopathy

Apelin

Bioelectrical impedance analysis – a method to measure body fat percentage.

Blubber – an extra thick form of adipose tissue found in some marine mammals.

Body fat percentage

Cellulite

Human fat used as pharmaceutical in traditional medicine

Obesity

Starvation

Steatosis (also called fatty change, fatty degeneration or adipose degeneration)

Stem cells

Subcutaneous fat

Bariatrics

Classification of obesity

Classification of childhood obesity

EPODE International Network The Worlds largest Obesity Prevention Network

World Fit A program of the United States Olympic Committee (USOC), and the United
States Olympians and Paralympians Association (USOP)

Obesity and walking

Social stigma of obesity
References[edit]
1.
Jump up ^ Kershaw EE, Flier JS (2004). "Adipose tissue as an endocrine organ". J. Clin. Endocrinol.
Metab. 89 (6): 2548–56. doi:10.1210/jc.2004-0395. PMID 15181022.
2.
Jump up ^ Cannon, B; Nedergaard, J (2008). "Developmental biology: Neither fat nor flesh". Nature 454
(7207): 947–8. doi:10.1038/454947a. PMID 18719573.
3.
Jump up ^ [1], Hepatic and whole-body fat synthesis in humans during carbohydrate overfeeding.
4.
Jump up ^ Pond, Caroline M. (1998). The Fats of Life. Cambridge University Press. ISBN 0-521-63577-2.
5.
Jump up ^ Cinti, S (July 2005). "The adipose organ". Prostaglandins, leukotrienes, and essential fatty
acids (Elsevier Science) 73 (952–3278): 9–15. doi:10.1016/j.plefa.2005.04.010. PMID 15936182.
6.
Jump up ^ Bachmanov, Alexander; D. R. Reed; M. G. Tordoff; R. A. Price (March 2001). "Nutrient
preference and diet-induced adiposity in C57BL/6ByJ and 129P3/J mice". Physiology & Behavior 72 (31–
9384): 603–613. doi:10.1016/S0031-9384(01)00412-7. PMC 3341942. PMID 11282146.
7.
Jump up ^ Fat on the Inside: Looking Thin is Not Enough, By Fiona Haynes, About.com
8.
Jump up ^ Abdominal fat and what to do about it, President & Fellows of Harvard College
9.
Jump up ^ Montague, CT; O'Rahilly, S (2000). "The perils of portliness: Causes and consequences of
visceral adiposity". Diabetes 49 (6): 883–8. doi:10.2337/diabetes.49.6.883. PMID 10866038.
10. Jump up ^ Kern, PA; Ranganathan, S; Li, C; Wood, L; Ranganathan, G (2001). "Adipose tissue tumor
necrosis factor and interleukin-6 expression in human obesity and insulin resistance". American journal of
physiology. Endocrinology and metabolism 280 (5): E745–51. PMID 11287357.
11. Jump up ^ Marette, A (2003). "Molecular mechanisms of inflammation in obesity-linked insulin
resistance". International journal of obesity and related metabolic disorders : journal of the International
Association for the Study of Obesity. 27 Suppl 3: S46–8. doi:10.1038/sj.ijo.0802500. PMID 14704744.
12. Jump up ^ Mokdad, AH; Ford, ES; Bowman, BA; Dietz, WH; Vinicor, F; Bales, VS et al. (2003).
"Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001". JAMA: the Journal of the
American Medical Association 289 (1): 76–9. doi:10.1001/jama.289.1.76. PMID 12503980.
13. Jump up ^ Estrogen causes fat to be stored around the pelvic region, hips, butt and thighs (pelvic region)
[2]
14. Jump up ^ Waistline Worries: Turning Apples Back Into Pears
15. Jump up ^ Researchers think that the lack of estrogen at menopause plays a role in driving our fat
northward. See: Andrews, Michelle (2006-12-01). "A Matter of Fat". Yahoo Health. Women's Health.
Archived from the original on 2007-03-15.
16. Jump up ^ Abdominal fat and what to do about it
17. Jump up ^ Irving; Davis, C.; Brock, D.; Weltman, J.; Swift, D.; Barrett, E.; Gaesser, G.; Weltman, A.
(2008). "Effect of exercise training intensity on abdominal visceral fat and body composition". Medicine
and science in sports and exercise 40 (11): 1863–1872. doi:10.1249/MSS.0b013e3181801d40.
PMC 2730190. PMID 18845966.
18. Jump up ^ Coker; Williams, R.; Kortebein, P.; Sullivan, D.; Evans, W. (2009). "Influence of Exercise
Intensity on Abdominal Fat and Adiponectin in Elderly Adults". Metabolic syndrome and related disorders
7 (4): 363–368. doi:10.1089/met.2008.0060. PMC 3135883. PMID 19196080.
19. Jump up ^ Ohkawara, K.; Tanaka, S.; Miyachi, M.; Ishikawa-takata, K.; Tabata, I. (2007). "A doseresponse relation between aerobic exercise and visceral fat reduction: systematic review of clinical trials".
International journal of obesity (2005) 31 (12): 1786–1797. doi:10.1038/sj.ijo.0803683. PMID 17637702.
20. Jump up ^ Mazurek T, Zhang L, Zalewski A, et al. (November 2003). "Human epicardial adipose tissue is
a source of inflammatory mediators". Circulation 108 (20): 2460–6.
doi:10.1161/01.CIR.0000099542.57313.C5. PMID 14581396.
21. Jump up ^ Pezeshkian M, Noori M, Najjarpour-Jabbari H, et al. (April 2009). "Fatty acid composition of
epicardial and subcutaneous human adipose tissue". Metab Syndr Relat Disord 7 (2): 125–31.
doi:10.1089/met.2008.0056. PMID 19422139.
22. ^ Jump up to: a b E Marieb and K Hoehn. Anatomy and Physiology, 3rd Edition. Benjamin Cummings
2008. ISBN 0-8053-0094-5
23. Jump up ^ 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
24. Jump up ^ "Belly fat in women: Taking — and keeping — it off". MayoClinic.com. 2013-06-08.
Retrieved 2013-12-02.
25. ^ Jump up to: a b Brodie, D.; Moscrip, V.; Hutcheon, R. (1998). "Body Composition Measurement: A
Review of Hydrodensitometry, Anthropometry, and Impedance Methods". Nutrition 14 (3): 296–310.
doi:10.1016/S0899-9007(97)00474-7. PMID 9583375.
26. ^ Jump up to: a b Snel M, Jonker JT, Schoones J, Lamb H, de Roos A, Pijl H et al. (2012). "Ectopic fat and
insulin resistance: pathophysiology and effect of diet and lifestyle interventions.". Int J Endocrinol 2012:
983814. doi:10.1155/2012/983814. PMC 3366269. PMID 22675355.
27. Jump up ^ 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
28. Jump up ^ Park, Alice (2009-08-08). "Fat-Bellied Monkeys Suggest Why Stress Sucks". Time. Retrieved
2013-12-19.
29. Jump up ^ Sugii, S; Kida, Y; Kawamura, T; Suzuki, J; Vassena, R; Yin, YQ et al. (2010). "Human and
mouse adipose-derived cells support feeder-independent induction of pluripotent stem cells". Proceedings
of the National Academy of Sciences of the United States of America 107 (8): 3558–63.
doi:10.1073/pnas.0910172106. PMC 2840462. PMID 20133714.
30. Jump up ^ Lohn, M; Dubrovska G, Lauterbach B, Luft FC, Gollasch M, Sharma (2002). "Periadventitial
fat releases a vascular relaxing factor". FASEB J 16 (9): 1057–1063. doi:10.1096/fj.02-0024com.
PMID 12087067.
31. Jump up ^ Himms-Hagen, J (1990). "Brown adipose tissue thermogenesis: Interdisciplinary studies".
FASEB journal : official publication of the Federation of American Societies for Experimental Biology 4
(11): 2890–8. PMID 2199286.
32. Jump up ^ Nedergaard, J.; Bengtsson, T.; Cannon, B. (2007). "Unexpected evidence for active brown
adipose tissue in adult humans". AJP: Endocrinology and Metabolism 293 (2): E444–52.
doi:10.1152/ajpendo.00691.2006. PMID 17473055.
33. Jump up ^ Virtanen, KA; Lidell, ME; Orava, J; Heglind, M; Westergren, R; Niemi, T et al. (2009).
"Functional brown adipose tissue in healthy adults". The New England Journal of Medicine 360 (15):
1518–25. doi:10.1056/NEJMoa0808949. PMID 19357407.
34. Jump up ^ Van Marken Lichtenbelt, WD; Vanhommerig, JW; Smulders, NM; Drossaerts, JM; Kemerink,
GJ; Bouvy, ND et al. (2009). "Cold-activated brown adipose tissue in healthy men". The New England
Journal of Medicine 360 (15): 1500–8. doi:10.1056/NEJMoa0808718. PMID 19357405.
35. Jump up ^ Cypess, AM; Lehman, S; Williams, G; Tal, I; Rodman, D; Goldfine, AB et al. (2009).
"Identification and importance of brown adipose tissue in adult humans". The New England Journal of
Medicine 360 (15): 1509–17. doi:10.1056/NEJMoa0810780. PMC 2859951. PMID 19357406.
36. Jump up ^ Speakerman, John R. (2007). "Genetics of Obesity: Five Fundamental Problems with the
Famine Hypothesis". Adipose Tissue and Adipokines in Health and Disease.
37. Jump up ^ Shell E (January 1, 2002). "Chapter 4: On the Cutting Edge". The Hungry Gene: The Inside
Story of the Obesity Industry. Atlantic Monthly Press. ISBN 978-1422352434.
38. Jump up ^ Shell E (January 1, 2002). "Chapter 5: Hunger". The Hungry Gene: The Inside Story of the
Obesity Industry. Atlantic Monthly Press. ISBN 978-1422352434.
39. Jump up ^ Pelleymounter, MA; Cullen, MJ; Baker, MB; Hecht, R; Winters, D; Boone, T et al. (1995).
"Effects of the obese gene product on body weight regulation in ob/ob mice". Science 269 (5223): 540–3.
doi:10.1126/science.7624776. PMID 7624776.
40. Jump up ^ Smith; Ravussin (2006). "Role of the Adipocyte in Metabolism and Endocrine Function".
Endocrinology.[page needed]
41. Jump up ^ Morris, DL; Rui, L (2009). "Recent advances in understanding leptin signaling and leptin
resistance". American journal of physiology. Endocrinology and metabolism 297 (6): E1247–59.
doi:10.1152/ajpendo.00274.2009. PMC 2793049. PMID 19724019.
42. Jump up ^ Carlsson, B; Lindell, K; Gabrielsson, B; Karlsson, C; Bjarnason, R; Westphal, O et al. (1997).
"Obese (ob) gene defects are rare in human obesity". Obesity research 5 (1): 30–5. doi:10.1002/j.15508528.1997.tb00280.x. PMID 9061713.
43. Jump up ^ 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.
44. Jump up ^ 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.
45. Jump up ^ 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.
46. Jump up ^ 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.
47. Jump up ^ 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.
48. Jump up ^ 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.
49. Jump up ^ Pankov YA. Adipose tissue as an endocrine organ regulating growth, puberty, and other
physiological functions. Biochemistry (Mosc). 1999 Jun;64(6):601–9.
50. Jump up ^ 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.
51. Jump up ^ Farooqi IS, O'Rahilly S. Mutations in ligands 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.
52. Jump up ^ Suh, JM; Zeve, D; McKay, R; Seo, J; Salo, Z; Li, R et al. (2007). "Adipose is a conserved
dosage-sensitive antiobesity gene". Cell metabolism 6 (3): 195–207. doi:10.1016/j.cmet.2007.08.001.
PMC 2587167. PMID 17767906.
53. Jump up ^ Farvid, MS; Ng TW; Chan DC; Barret PH; Watts GF (July 2005). "Association of adiponectin
and resistin with adipose tissue compartments, insulin resistance and dyslipidaemia". Diabetes, Obesity and
Metabolism 7 (4): 406–413. doi:10.1111/j.1463-1326.2004.00410.x. PMID 15955127.(registration required)
54. Jump up ^ Urbanchek, MG; Picken EB; Kalliainen LK; Kuzon WM Jr. (May 2001). "Specific force
deficit in skeletal muscles of old rats is partially explained by the existence of denervated muscle fibers". J
Gerontol a Biol Sci Med Sci 56 (5): 191–197. doi:10.1093/gerona/56.5.B191. PMID 11320099.
55. Jump up ^ "Body fat scales review and compare". 10 January 2010. Archived from the original on 17
January 2010. Retrieved 11 January 2010.
Further reading[edit]

MeSH A10.165.114

Stock, M. J.; Cinti, S. (2003). "ADIPOSE TISSUE | Structure and Function of Brown
Adipose Tissue". Encyclopedia of Food Sciences and Nutrition. p. 29. doi:10.1016/B012-227055-X/00008-0. ISBN 9780122270550.

Vernon, R. G.; Flint, D. J. (2003). "ADIPOSE TISSUE | Structure and Function of White
Adipose Tissue". Encyclopedia of Food Sciences and Nutrition. p. 23. doi:10.1016/B012-227055-X/00007-9. ISBN 9780122270550.