In histology, adipose tissue or body fat or fat depot or just fat is loose connective tissue composed of adipocytes. 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 lipoblasts. 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, as it produces hormones such as leptin, 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. 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.
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. Excess visceral fat is also linked to type 2 diabetes, insulin resistance inflammatory diseases, and other obesity-related diseases.
Female sex hormone causes fat to be stored in the buttocks, thighs, and hips in women. 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 ovaries declines, fat migrates from their buttocks, hips and thighs to their waists; later fat is stored in the belly.
High intensity exercise is one way to effectively reduce total abdominal fat. One study suggests at least 10 METs x hours per week of aerobic exercise is required for visceral fat reduction.
Like all other fat organs, subcutaneous fat is an active part of the endocrine system, secreting the hormones ''leptin'' and ''resistin''.
In humans, lipolysis is controlled through the balanced control of lipolytic B-adrenergic receptors and a2A-adrenergic receptor-mediated antilipolysis.
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 .
Storage in the adipose tissue is catalysed by insulin, the activity of which is stimulated by high blood sugar
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 (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 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, 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. 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 cells.
Adipose tissue is the greatest peripheral source of aromatase in both males and females 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.
Attempts to simulate this process pharmacologically have so far been unsuccessful (even lethal). 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, it was thought that brown adipose tissue was 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 regions.
In 1995 Jeffrey Friedman, in his residency at Rockefeller University, discovered the protein leptin that the genetically obese mouse lacked. 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.
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 currently the focus of obesity research.
Gene defects in the leptin gene (ob) are rare in human obesity. 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 - 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 tissue.
Excess adipose tissue on a human can lead to medical problems. For a discussion of the aesthetic and medical significance of body shape, see dieting and obesity.
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 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.
Category:Tissues Category:Obesity
ar:نسيج دهني ca:Teixit adipós cs:Tuková tkáň da:Fedtvæv de:Fettgewebe el:Λιπώδης ιστός es:Tejido adiposo eu:Gantz ehun fa:بافت چربی fr:Tissu adipeux gl:Tecido adiposo it:Tessuto adiposo he:רקמת שומן kk:Май ұлпасы lt:Riebalinis audinys hu:Zsírszövet arz:نسيج دهنى nl:Vetweefsel ja:脂肪組織 no:Fettvev pag:Taba pl:Tkanka tłuszczowa pt:Tecido adiposo ru:Жировая ткань simple:Adipose tissue fi:Rasvakudos sv:Fettvävnad ta:கொழுப்பிழையம் tr:Yağ doku uk:Жирова тканина zh:脂肪組織This text is licensed under the Creative Commons CC-BY-SA License. This text was originally published on Wikipedia and was developed by the Wikipedia community.
The World News (WN) Network, has created this privacy statement in order to demonstrate our firm commitment to user privacy. The following discloses our information gathering and dissemination practices for wn.com, as well as e-mail newsletters.
We do not collect personally identifiable information about you, except when you provide it to us. For example, if you submit an inquiry to us or sign up for our newsletter, you may be asked to provide certain information such as your contact details (name, e-mail address, mailing address, etc.).
When you submit your personally identifiable information through wn.com, you are giving your consent to the collection, use and disclosure of your personal information as set forth in this Privacy Policy. If you would prefer that we not collect any personally identifiable information from you, please do not provide us with any such information. We will not sell or rent your personally identifiable information to third parties without your consent, except as otherwise disclosed in this Privacy Policy.
Except as otherwise disclosed in this Privacy Policy, we will use the information you provide us only for the purpose of responding to your inquiry or in connection with the service for which you provided such information. We may forward your contact information and inquiry to our affiliates and other divisions of our company that we feel can best address your inquiry or provide you with the requested service. We may also use the information you provide in aggregate form for internal business purposes, such as generating statistics and developing marketing plans. We may share or transfer such non-personally identifiable information with or to our affiliates, licensees, agents and partners.
We may retain other companies and individuals to perform functions on our behalf. Such third parties may be provided with access to personally identifiable information needed to perform their functions, but may not use such information for any other purpose.
In addition, we may disclose any information, including personally identifiable information, we deem necessary, in our sole discretion, to comply with any applicable law, regulation, legal proceeding or governmental request.
We do not want you to receive unwanted e-mail from us. We try to make it easy to opt-out of any service you have asked to receive. If you sign-up to our e-mail newsletters we do not sell, exchange or give your e-mail address to a third party.
E-mail addresses are collected via the wn.com web site. Users have to physically opt-in to receive the wn.com newsletter and a verification e-mail is sent. wn.com is clearly and conspicuously named at the point of
collection.If you no longer wish to receive our newsletter and promotional communications, you may opt-out of receiving them by following the instructions included in each newsletter or communication or by e-mailing us at michaelw(at)wn.com
The security of your personal information is important to us. We follow generally accepted industry standards to protect the personal information submitted to us, both during registration and once we receive it. No method of transmission over the Internet, or method of electronic storage, is 100 percent secure, however. Therefore, though we strive to use commercially acceptable means to protect your personal information, we cannot guarantee its absolute security.
If we decide to change our e-mail practices, we will post those changes to this privacy statement, the homepage, and other places we think appropriate so that you are aware of what information we collect, how we use it, and under what circumstances, if any, we disclose it.
If we make material changes to our e-mail practices, we will notify you here, by e-mail, and by means of a notice on our home page.
The advertising banners and other forms of advertising appearing on this Web site are sometimes delivered to you, on our behalf, by a third party. In the course of serving advertisements to this site, the third party may place or recognize a unique cookie on your browser. For more information on cookies, you can visit www.cookiecentral.com.
As we continue to develop our business, we might sell certain aspects of our entities or assets. In such transactions, user information, including personally identifiable information, generally is one of the transferred business assets, and by submitting your personal information on Wn.com you agree that your data may be transferred to such parties in these circumstances.