In biology, adipose tissue, body fat, or simply fat is a 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 such as adipose tissue
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 being hormonally inert,
adipose tissue has, in recent years, been recognized as a major
endocrine organ, as it produces hormones such as leptin, estrogen,
resistin, and the cytokine TNFα. The two types of adipose tissue are
white adipose tissue (WAT), which stores energy, and brown adipose
tissue (BAT), which generates body heat. 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.
1 Anatomical features
1.3 Visceral fat
1.4 Subcutaneous fat
1.5 Marrow fat
1.6 Ectopic fat
2.1 Brown fat
2.2 Beige fat and WAT browning
2.3 Genomics and bioinformatics tools to study browning
2.5 Physical properties
3 Body fat meter
4 Animal studies
6 See also
8 Further reading
9 External links
In humans, adipose tissue is located beneath the skin (subcutaneous
fat), around internal organs (visceral fat), in bone marrow (yellow
bone marrow), intermuscular (Muscular system) and in the breast
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 oxidised 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.
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.
The obese mouse on the left has large stores of adipose tissue. It is
unable to produce the hormone leptin, resulting in obesity. For
comparison, a mouse with a normal amount of adipose tissue is shown on
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. Of all the depots in the mouse, the gonadal depots are the
largest and the most easily dissected, comprising about 30% of
In an obese person, excess adipose tissue hanging downward 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 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.
Reconstructive surgery is one method of treatment.
See also: Abdominal obesity
Visceral fat or abdominal fat (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 semi-fluid.
Visceral fat is composed of several
adipose depots, including mesenteric, epididymal white adipose tissue
(EWAT), and perirenal depots.
Visceral fat is often expressed in terms
of its area in cm2 (VFA, visceral fat area).
An excess of visceral fat is known as central obesity, or "belly fat",
in which the abdomen protrudes excessively. New developments such as
Body Volume Index
Body Volume Index (BVI) are specifically designed to measure
abdominal volume and abdominal fat. Excess visceral fat is also linked
to type 2 diabetes, insulin resistance, inflammatory
diseases, and other obesity-related diseases. Likewise, the
accumulation of neck fat (or cervical adipose tissue) has been shown
to be associated with mortality. Several studies have suggested
that visceral fat can be predicted from simple anthropometic
measures, and predicts mortality more accurately than body mass
index or waist circumference.
Men are more likely to have fat stored in the abdomen due to sex
hormone differences. Female sex hormone causes fat to be stored in the
buttocks, thighs, and hips in women. When women reach
menopause and the estrogen produced by the ovaries declines, fat
migrates from the buttocks, hips and thighs to the waist; later
fat is stored in the abdomen.
High-intensity exercise is one way to effectively reduce total
abdominal fat. One study suggests at least 10 MET-hours per
week of aerobic exercise is required for visceral fat reduction.
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. 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.
See also: Body fat percentage
Micro-anatomy of subcutaneous fat
Most of the remaining nonvisceral fat is found just below the skin in
a region called the hypodermis. 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. 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.
Like all other fat organs, subcutaneous fat is an active part of the
endocrine system, secreting the hormones leptin and resistin.
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.
Factors such as sex, age, population size or other variables may make
the equations invalid and unusable, and, as of 2012[update], Durnin
and Wormersley's equations remain only estimates of a person's true
level of fatness. New formulae are still being created.
Marrow fat, also 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 as bony elements. The adipocytes in
this depot are derived from mesenchymal stem cells (MSC) which can
give rise to fat cells, bone cells as well as other 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. Exercise regulates MAT, decreasing MAT quantity
and diminishing the size of marrow adipocytes. The
exercise 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
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. 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.
In the latter case, non-invasive weight loss interventions like diet
or exercise have the ability to decrease ectopic fat (particularly in
heart and liver) in children and adults with overweight or
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, then there is a net
inward flux of FFA, and only when insulin is low can FFA leave adipose
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
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).
Studies of female monkeys at
Wake Forest University
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-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
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. 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. A growing body of evidence also
suggests that different fat depots (i.e. abdominal, omental,
pericardial) yield adipose-derived stem cells with different
characteristics. These depot-dependent features include
proliferation rate, immunophenotype, differentiation potential, gene
expression, as well as sensitivity to hypoxic culture conditions.
Adipose tissue is the greatest peripheral source of aromatase in both
males and females, contributing to the production of
Adipose derived hormones include:
Plasminogen activator inhibitor-1
Plasminogen activator inhibitor-1 (PAI-1)
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.
Main article: Brown adipose tissue
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 within mitochondria through
tissue-specific expression of uncoupling protein 1 (UCP1). BAT is
primarily located around the neck and large blood vessels of the
thorax, where may effectively act in heat exchange. BAT is robustly
activated upon cold exposure by the release of catecholamines from
sympathetic nerves that results in UCP1 activation. BAT activation may
also occur in response to overfeeding. UCP1 activity is stimulated
by long chain fatty acids that are produced subsequent to
β-adrenergic receptor activation. UCP1 is proposed to function as
a fatty acid proton symporter, although the exact mechanism has yet to
be elucidated. In contrast, UCP1 is inhibited by ATP, ADP, and
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, and the presence of brown adipose in human
adults was later verified histologically in the same anatomical
Beige fat and WAT browning
Morphology of three different classes of adipocytes
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 increase expression of uncoupling protein 1 (UCP1). In doing
so, these normally energy-storing adipocytes become energy-releasing
The calorie-burning capacity of brown and beige fat has been
extensively studied as research efforts focus on therapies targeted to
treat obesity and diabetes. The drug 2,4-dinitrophenol, which also
acts as a chemical uncoupler similarly to UCP1, was used for weight
loss in the 1930s. However, it was quickly discontinued when excessive
dosing led to adverse side effects including hyperthermia and
death. β3 agonists, like CL316,243, have also been developed and
tested in humans. However, the use of such drugs has proven largely
unsuccessful due to several challenges, including varying species
receptor specificity and poor oral bioavailability.
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 study 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. A study
by Rosenwald et al. revealed that when the animals are re-exposed to a
cold environment, the same adipocytes will adopt a beige phenotype,
suggesting that beige adipocytes are retained.
Transcriptional regulators, as well as a growing number of other
factors, regulate the induction of beige fat. Four regulators of
transcription are central to WAT browning and serve as targets for
many of the molecules known to influence this process. These
include peroxisome proliferator-activated receptor gamma (PPARγ), PR
domain containing 16 (PRDM16), peroxisome proliferator-activated
receptor gamma coactivator 1 alpha (PGC-1α), and Early B-Cell
The list of molecules that influence browning has grown in direct
proportion to the popularity of this topic and is constantly evolving
as more knowledge is acquired. Among these molecules are irisin and
fibroblast growth factor 21 (FGF21), which have been well-studied and
are believed to be important regulators of browning. Irisin is
secreted from muscle in response to exercise and has been shown to
increase browning by acting on beige preadipocytes. FGF21, a
hormone secreted mainly by the liver, has garnered a great deal of
interest after being identified as a potent stimulator of glucose
uptake and a browning regulator through its effects on PGC-1α. It
is increased in BAT during cold exposure and is thought to aid in
resistance to diet-induced obesity
FGF21 may also be secreted in
response to exercise and a low protein diet, although the latter has
not been thoroughly investigated. Data from these studies
suggest that environmental factors like 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 by
type 2 innate lymphoid cells in response to interleukin 33.
Genomics and bioinformatics tools to study browning
Due to the complex nature of adipose tissue and a growing list of
browning regulatory molecules, great potential exists for the use of
bioinformatics tools to improve study within this field. Studies of
WAT browning have greatly benefited from advances in these techniques,
as beige fat is rapidly gaining popularity as a therapeutic target for
the treatment 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 look at changes
in WAT and BAT gene expression when mice were exposed to temperatures
of 28 and 6 °C. The most significantly up- and downregulated
genes were then identified and used for analysis of differentially
expressed pathways. It was discovered that many of the pathways
upregulated in WAT after cold exposure are also highly expressed in
BAT, such as oxidative phosphorylation, fatty acid metabolism, and
pyruvate metabolism. 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. These two 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
RNA-Seq into browning studies is of great value,
as it offers better specificity, sensitivity, and a more comprehensive
overview of gene expression than other methods.
RNA-Seq has been used
in both human and mouse studies in an attempt characterize 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 gene 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
gene program and had decreased WAT specific gene expression compared
to the WT mice. 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 protein binding sites on DNA and assess histone
modifications. This tool has enabled examination of epigenetic
regulation of browning and helps elucidate the mechanisms by which
protein-DNA interactions stimulate the differentiation of beige
adipocytes. Studies observing the chromatin landscapes of beige
adipocytes have found that adipogenesis of these cells results from
the formation of cell specific chromatin landscapes, which regulate
the transcriptional program and, ultimately, control differentiation.
Using ChIP-seq in conjunction with other tools, recent studies have
identified over 30 transcriptional and epigenetic factors that
influence beige adipocyte development.
Main article: Genetics_of_obesity § Genes
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, originally
advanced 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 "as viable as
when [it was] first advanced" in other contexts.
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
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. 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
Gene defects in the leptin gene (ob) are rare in human obesity. 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—and two
other families have been found that carry a mutated ob
receptor. 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.
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.
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. Although its discoverers dubbed this gene
the adipose gene, it is not a gene responsible for creating adipose
Pre-adipocytes are undifferentiated fibroblasts that can be stimulated
to form adipocytes. Recent studies shed light into potential molecular
mechanisms in the fate determination of pre-adipocytes although the
exact lineage of adipocyte is still unclear.
Adipose tissue has a density of ~0.9 g/ml. 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.
Body fat meter
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.
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.
Within the fat (adipose) tissue of
CCR2 deficient mice, there 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.
Diagrammatic sectional view of the skin (magnified).
White adipose tissue
White adipose tissue in paraffin section
Electronic instrument of body fat meter
Adipose differentiation-related protein
Bioelectrical impedance analysis – a method to measure body fat
Body Volume Index
Body Volume Index – a method to measure abdominal volume and
Blubber – an extra thick form of adipose tissue found in some marine
Body fat percentage
Human fat used as pharmaceutical in traditional medicine
Steatosis (also called fatty change, fatty degeneration or adipose
Classification of obesity
Classification of childhood obesity
EPODE International Network, the world's largest obesity-prevention
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
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Adipose tissue photomicrographs
Dense irregular connective tissue
Dense regular connective tissue