Reference
Boss, Olivier and Stephen R. Farmer 2012. “Recruitment of Brown Adipose Tissue as a Therapy for Obesity-Associated Diseases” US National Library of Medicine: National Institute of Health. Accessed April 10, 2013. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356088/
http://ksj.mit.edu/sites/default/files/images/tracker/2009/brownadiposetissue.jp http://www.nature.com/ncb/journal/v14/n12/images/ncb2642-f1.jpg
The article, “Recruitment of Brown Adipose Tissue as a Therapy for Obesity-Associated Diseases” was well informing as it sought to present data on the effective use of brown adipose tissue in obesity and related diseases.
What is Brown adipose tissue?
According to the authors of the article, brown adipose tissue is a flexible tissue that can be recruited by stimuli, and deteriorates in the absence of a stimulus. Its has a major contribution in cold-induced non-shivering thermogenesis and body weight homeostasis in animals ana is closely related to UCP1.
What is UCP1? Thermogenin or uncoupling protein 1 ( UCP1) is an uncoupling protein found in the mitochondria of brown adipose tissue (BAT). It is used to generate heat by non-shivering thermogenesis. Non-shivering thermogenesis is the primary means of heat generation in hibernating mammals and in human infants.
The efficacy of increasing brown adipose tissue (BAT) recruitment (BAT mass and expression of UCP1) as a therapeutic approach for obesity and type 2 diabetes has been researched by many groups throughout the past 20 years.
Studies with rat specimens showed that agents which increase brown adipose tissue recruitment can effectively treat obesity and diabetes. In lean animals with normal brown adipose tissue amounts, enhancement of BAT recruitment or activity by drugs or cold exposure has no effect on body weight. While in obese animals, enhancement of energy spending by BAT recruitment is effective in decreasing body weight and improving metabolic status. Earlier results showed that over expression of UCP1 in white adipose tissue (WAT) of mice can prevent the development of obesity in genetic as well as dietary forms of diabetes. In contrast, lack of BAT or UCP1 stimulates obesity and diabetes in mice.
Some drugs were tested and it was revealed that induction of brown adipocyte formation with drugs in humans, in order to enhance or restore healthy levels of BAT recruitment, is possible to enhance energy expenditure.
Brown adipose tissue and white adipose tissue.
Studied also showed that primary preadipocytes isolated from white and brown adipose depots demonstrate in vitro (in an artificial environment outside the living organism) differentiation into white and brown adipocytes. There were many hypotheses that showed in WAT depots, brown adipocytes can emerge from differentiation of brown adipocyte precursors or preadipocytes or by transdifferentiation of the existing white adipocytes. It was shown that hyperleptinemia in rats induces the transformation of white adipocytes into so-called post-adipocytes (or fat-oxidizing machines), which have the phenotype of brown adipocytes. Several other effectors enhance brown adipocyte recruitment in white depots like synthetic PPARγ ligands. Brown adipocytes within the interscapular BAT depot of mice share an origin with skeletal myocytes that arise from the dermomyotome.
It is conceivable; therefore, that recruitment of WAT brown adipocytes is due to a selective activation of mural cells to progress along a brown lineage in response to effectors that are activated by the recruitment-associated stimulus. Possible effectors include BMP7, which has been shown to induce the conversion of mesenchymal stem cells to brown adipocytes in culture and is required for BAT formation in mice.
Infrared thermography provided data and proved that adult humans possess functional BAT that is activated by ephedrine.
The research showed that BAT can be recruited in humans just as in animals. Hence, brown adipose tissue could play an important role in human energy balance and body weight homeostasis and thus, has revived a concept that BAT is a therapeutic target for combating obesity-related metabolic disorders as there formerly existed a problem in identifying drug targets for brown adipocyte.
Studies found that stroma-vascular cell preparations from human BAT contained only very limited quantities of cells that can differentiate into brown adipocytes. Human brown adipocyte stem or progenitor cells, CD34+ are present in skeletal muscle and hMADs in subcutaneous WAT. These cells have self-renewal capability, differentiate, in response to specific agents, into functional brown adipocytes and are rich in mitochondria. These cell types are thus quite distinct, and each have the potential of generating relevant cell models for studying human brown adipocyte biology as well as screening for anti-obesity therapeutics. Such screens could identify agents that induce the differentiation of the cells into brown adipocytes.
Analysis of several functional features of BAT include quantitative phenotypic cellular screens, PCR, western blot analysis of brown-selective genes and measurement of cell respiration to determine the degree of uncoupling of oxidative phosphorylation.
Authors found that defective recruitment or activity of brown adipose tissue may contribute to weight gain and insulin resistance. The metabolic activity and energy expenditure, thermogenesis, in humans is activated by cold. The amount of BAT inversely correlates to body weight and is independent of age.
Brown adipocyte stem cells are present in skeletal muscle and subcutaneous WAT of humans. This suggests that enhancing BAT recruitment to restore BAT mass to a healthy level, is practicable.
The investigations supported the contention that activation of BAT formation in obese individuals is therapeutically powerful. We also propose that enhancement of brown adipocyte functions in white adipose tissue (WAT) will also regulate energy balance as well as reduce insulin resistance in obesity-associated inflammation in WAT.
Investigations proved that resistance to obesity and other related disorders in various rodent models resulted from increased BAT mass and the number of brown adipocytes or UCP1 expression. Readily accessible brown adipocyte stem/progenitor cellsthrough biopsy of human tissues encourages the development of transplantation procedures to treat obese and diabetic patients. The implants in mice proved to advance the metabolic condition of obese, insulin resistant mice. In addition, brown adipocytes have beneficial effects on glucose metabolism, insulin sensitivity and overall energy balance. we looked at the mechanism through which BAT affects the “adipostat.” BAT is quite different from WAT as BAT expresses significantly lower levels of resistin and other adipokines associated with insulin resistance.
Diagram showing the recruitment of brown adipose tissue.
In simpler words…brown adipose tissue helps adults burn more calories than white adipose tissue!!!
The most promising strategy for developing therapeutics for obesity and specifically, type two diabetes is to increase BAT mass. This allows the development of effective drugs for obesity, diabetes, and the metabolic syndrome that have very little side effects.
Juliana-Medicalpractitioner 
