Obesity researchers are now focusing on getting rid of fat with brown adipose tissue. The good news is that you already possess this kind of fat. The bad news is that nobody knows how to make it work better. Here is what is happening in research on this topic right now.
Take a look at the summary abstract of a recent article in the journal, Drug News and Perspectives:
1. Drug News Perspect. 2010 Sep;23(7):409-17.
Brown adipose tissue: A promising target to combat obesity.
Vernochet C, McDonald ME, Farmer SR.
Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts, USA.
Obesity has now reached pandemic proportions leading to a collection of morbidities referred to as metabolic syndrome including insulin resistance, type 2 diabetes and cardiovascular disease. The expansion of adipose tissue is a direct cause of these comorbidities due to excessive accumulation of triglycerides within adipocytes, causing disruption of normal adipose function. There are two major types of adipose tissue, white and brown. The former stores energy as triglycerides within large droplets, whereas the latter catabolizes lipids to produce heat. A strategy to combat obesity-associated disorders, therefore, includes enhancement of brown adipose tissue activity by targeting the recently identified regulators of brown adipocyte development and function, including its master regulator, PRDM16.
Finding brown adipose tissue in adult humans was a surprise. Now all the research involving its role in obesity is scrambling to find a new drug to make it work better for optimizing the metabolism of fat. The article that I cite below points to where this should be going, and it is NOT the development of another unnecessary drug for what should be done naturally.
This is NOT a Surprise!
See what this review says, then take a look at my comment below it.
1. Curr Opin Endocrinol Diabetes Obes. 2010 Oct;17(5):446-52.
Mitochondrial dysfunction in obesity.
Bournat JC, Brown CW.
Departments of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA.
PURPOSE OF REVIEW: The review highlights recent findings regarding the functions of mitochondria in adipocytes, providing an understanding of their central roles in regulating substrate metabolism, energy expenditure, disposal of reactive oxygen species (ROS), and in the pathophysiology of obesity and insulin resistance, as well as roles in the mechanisms that affect adipogenesis and mature adipocyte function. RECENT FINDINGS: Nutrient excess leads to mitochondrial dysfunction, which in turn leads to obesity-related pathologies, in part due to the harmful effects of ROS. The recent recognition of ‘ectopic’ brown adipose in humans suggests that this tissue may play an underappreciated role in the control of energy expenditure. Transcription factors, PGC-1alpha and PRDM16, which regulate brown adipogenesis, and members of the TGF-beta superfamily that modulate this process may be important new targets for antiobesity drugs. SUMMARY: Mitochondria play central roles in ATP production, energy expenditure, and disposal of ROS. Excessive energy substrates lead to mitochondrial dysfunction with consequential effects on lipid and glucose metabolism. Adipocytes help to maintain the appropriate balance between energy storage and expenditure and maintaining this balance requires normal mitochondrial function. Many adipokines, including members of the TGF-beta superfamily, and transcriptional coactivators, PGC-1alpha and PRDM16, are important regulators of this process.
What we have based on these two articles, which are examples of many recent ones on this topic, are: 1) Brown adipose tissue is important for regulating fat metabolism; and, 2) the problem of how to make it work better involves the disposal of reactive oxygen species in mitochondria.
Translation: It is an antioxidant solution. In particular, it is a solution that entails enhancing your body’s own production of its best antioxidant, i.e., glutathione. Drug development will most likely not go in this direction, since you can boost glutathione levels naturally, without drugs. The best antioxidants will, of course, be of great value. Weight gain is, after all, an inflammatory (i.e., oxidative) problem as much as anything, and research on brown adipose tissue just confirms this observation.
By the way, taking glutathione as a supplement is not effective for boosting native glutathione synthesis. In fact, it is almost worthless.
Fun with brown adipose tissue,
- How to Eat to Reduce Visceral Fat (healthmad.com)
- Insulin Sensitive Obesity (drsharma.ca)
- Anti-Inflammatory and Metabolic Benefits of Resveratrol (gracemedeirosmj.wordpress.com)
You mention that glutathione is important, and that it’s better to stimulate your body’s own production of it, rather than taking it in supplement form, but I’m wondering _how_ to do that. How can I boost my body’s own production of glutathione?
Dr. Dennis Clark says
Great question, Adam. A lot of misinformation is out there regarding the usefulness of glutathione supplementation. It isn’t really all that useful. However, you can boost your native levels by: 1) making sure to eat enough meat, fish, poultry, and eggs to get an abundance of the sulfur-containing amino acids that are necessary for your body’s production of glutathione; 2) take 100-300 mg of alpha-lipoic acid daily, which helps recycle and regenerate glutathione; 3) be sure to get enough selenium (100 micrograms, 3 times per week is usually sufficient if you are also eating plenty of meat), which is a key cofactor in the enzyme that makes glutathione; 4) avoid consuming lipid peroxides (including cholesterol peroxide), which are formed by cooking unsaturated fats and oils too fast (such peroxides deplete glutathione faster than almost anything else); 5) avoid excessive exercise without sufficient periods of rest (exercise-induced inflammation soaks up a lot of glutathione). If you do all this, you should have a great glutathione level at all times.
All the best,