Overexpression of uncoupling proteins in small rodents is an effective way to alter thermogenesis. This strategy prevents diet induced obesity and insulin resistance (link 1). There is now substantial interest in alternative methods of increasing thermogenesis as a means to treat obesity (links 2 and 3). However, due to the volume : surface ratio, small rodents have a high tolerance for elevated thermogenesis (link 4) as a result of UCP overexpression. Humans have a much lower surface area : volume ratio and therefore have a reduced capacity to dissipate heat. Therefore, will overweight humans have a sufficient tolerance for enhanced thermogenesis for this to be a safe and viable treatment option?
http://www.nature.com/nm/journal/v6/n10/full/nm1000_1115.html
http://www.nature.com/nrendo/journal/v10/n1/full/nrendo.2013.204.html
http://onlinelibrary.wiley.com/doi/10.1046/j.1467-789X.2001.00043.x/abstract;jsessionid=657E62D9AB4C75C16F9AB04FFC817917.f04t03
http://physiolgenomics.physiology.org/content/21/2/193.long
"Humans have a much lower surface area : volume ratio and therefore have a reduced capacity to dissipate heat. Therefore, will overweight humans have a sufficient tolerance for enhanced thermogenesis for this to be a safe and viable treatment option?"
Overweight people will have even lower surface area to volume ratio than normal people!
At the moment several groups are trying to develop strategies to increase the "browning" of fat. There exist several reviews:
Mol Cell Endocrinol. 2013 Oct 15;379(1-2):43-50.
Nat Rev Endocrinol. 2014 Jan;10(1):24-36.
This review provides a nice explanation:
http://www.ncbi.nlm.nih.gov/pubmed/10766252
In the 1930ies dinitrophenol, a protonophore which "leaks" the mitochondrial membrane, was used in the US as a diet-pill. There were several fatalities because of lethal hyperthermia, and chronic use led to blindness due to cataracts. I think adverse effects of even a slight hyperthermia, if it 's chronic, could be prohibitive in humans.
One can also take L-Thyroxine to push the levels closer to the upper end of normal spectrum, which is more than likely to use up reserve energy (provided the intake remains the same), just as wasting energy by fooling the normal thermogenesis. Both approaches have similar theoretical potential and both are dangerous in the long-run.
Rather than "promising", a sure way to control obesity has always been the "boring" consumption of balanced diet combined with exercise. ;)
Hi David!!. I think that at this moment this is hot topic in obesity field. Since several years ago that it was demonstrated that humans, under certain circumstances, could reactivate, the capacity to dissipate heat is fantastic by BAT. I remember you that scientific community thought for a long time that BAT dissapeared after birth in humans. Then, since 2009, BAT reactivation is one of the most exciting possibilities for burning fatty acids in mitochondria by increasing non-shivering thermogenesis
The nice article i have read recently
Moisan A, Lee Y-K, Zhang JD, Hudak CS, Meyer CA, Prummer M, et al. White-to-brown metabolic conversion of human adipocytes by JAK inhibition. Nature cell biology. 2014
Is a very interesting topic today. As per Herald, yes, we may not be able to measure the temperature rise but using K4B2, we may measure the energy expenditure , change in RQ and the diet Induced thermogenic effect of specific food or ingredient. BAT is related to mainly adoptive thermogenesis for cold.
Use of L-Thyroxine may be an easy way of loosing body wt for normal people but if the obesity is resistant type due to hypothyroidism, L-Thyroxine will not be effective .
Levothyroxine will lead to weight loss in Hypothyroidism primarily by facilitating weight loss by other means. Furthermore there are TH receptors in brown fat that suggests physiological role for thyroid hormone. In hypothyroid state weight loss induced by TH is not always related to thermognesis alone. Loss of retained fluid and better water clearance through improved renal blood flow are other reasons.
although most of research on obesity is concenrating on white adipose tissue and the development,differentiation ie hypertrophy and hyperplasia of adipocytes and pfeadipocyytes in WAT and role of inflammation and macrophage infiltration directly or conversion of preadi[ocytes,metabolic endotoxemia,gut microbiota lreading to increased LPS absorption from increased GIT permeability with altered gut microbiota is some of the aetiopathogenesis with infiltration of Treg cells,cdt4. CHT8 cellsiNKT CELLS th17 all have ben found but importance is being given simultaneously to the microrna which affect the differentiATION OF BRITE AND BROWN ADIPOCYTES AND IMPORTANCE OF MIrna'S 26,155,27a,b,130 a ,miR155 etc in adipocyte differentiation and how further roles of FGF21 may affect thermogenesis and natriureteic peptides
http://www.ncbi.nlm.nih.gov/pubmed/25408843
- Badges
- Science topic
- Similar topics
- Medicine
- Disease
- Metabolic Diseases