Adipose Tissue Biology

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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. High-intensity exercise is one way to effectively reduce total abdominal fat. 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.

Most of the remaining nonvisceral fat is found just below the skin in a region called the hypodermis. 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 [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. Moreover, increased MAT in obesity further suggests a similarity to white fat depots.

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. 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 obesity. 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.

The net direction of this flux is controlled by insulin and leptin—if insulin is elevated, then there is a net inward flux of FFA, and only when insulin is low can FFA leave adipose tissue. Insulin secretion is stimulated by high blood 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.

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. 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. 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:. 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. 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 robustly activated upon cold exposure by the release of catecholamines from sympathetic nerves that results in UCP1 activation.

Adipose tissue

BAT activation may also occur in response to overfeeding. 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 , [50] and the presence of brown adipose in human adults was later verified histologically in the same anatomical regions. Beige adipocytes take on a multilocular appearance containing several lipid droplets and increase expression of uncoupling protein 1 UCP1. 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 s. However, it was quickly discontinued when excessive dosing led to adverse side effects including hyperthermia and death. However, the use of such drugs has proven largely unsuccessful due to several challenges, including varying species receptor specificity and poor oral bioavailability.


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 hour period. 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.

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. 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 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. 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. Incorporating 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. WAT from the transgenic animals exhibited a brown fat gene program and had decreased WAT specific gene expression compared to the WT mice.

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.

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Using ChIP-seq in conjunction with other tools, recent studies have identified over 30 transcriptional and epigenetic factors that influence beige adipocyte development. 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.

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. The changes that occur in the hypothalamus to result in leptin resistance in obesity are currently the focus of obesity research. Gene defects in the leptin gene ob are rare in human 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.

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.

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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.

Adipose tissue dysregulation in patients with metabolic syndrome. Adipokine inflammation and insulin resistance: Chemerin is associated with metabolic syndrome phenotypes in a Mexican-American population. Increased chemerin and decreased omentin-1 in both adipose tissue and plasma in nascent metabolic syndrome. Omentin plasma levels and gene expression are decreased in obesity. Omentin, fat and heart: Serum omentin-1 levels are inversely associated with the presence and severity of coronary artery disease in patients with metabolic syndrome.

Adipose tissue in metabolic syndrome: Plasma resistin levels correlate with determinants of the metabolic syndrome. Old and new findings on lipopolysaccharide-binding protein: Increased adipose tissue secretion of fetuin-A, lipopolysaccharide-binding protein and high-mobility group box protein 1 in metabolic syndrome. A role for adipocyte-derived lipopolysaccharide-binding protein in inflammation and obesity associated adipose tissue dysfunction.

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The role of hepatokines in metabolism. Adipocyte fetuin-A contributes to macrophage migration into adipose tissue and polarization of macrophages. Factors that promote macrophage homing to adipose tissue in metabolic syndrome. Increased fibrosis and angiogenesis in subcutaneous gluteal adipose tissue in nascent metabolic syndrome.

Immunological contributions to adipose tissue homeostasis. Molecular mechanisms underlying metabolic syndrome: Jialal I, Rajamani U. Endotoxemia of metabolic syndrome: The conducted research is not related to either human or animals use. Here you can find all Crossref-listed publications in which this article is cited. User Account Log in Register Help. My Content 1 Recently viewed 1 Subcutaneous adipose t Hormone Molecular Biology and Clinical Investigation.

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