(I guess that we can all rest easy and double up on the cookies and hamburgers with this research under way!)
Wonder drug in development to let dieters eat whatever they want - without gaining a single pound
By Fiona MacraeLast updated at 8:07 AM on 04th September 2009
A pill that allows dieters to gorge on junk food without putting on a pound is being developed by scientists. The couch potato's dream, it would allow people to eat all their favourite foods without worrying about their waistline. The wonder drug would also protect against diabetes, liver disease and other debilitating conditions associated with unhealthy eating habits.
The breakthrough hinges on the discovery of a metabolism 'masterswitch' - a gene key to weight control. Mice lacking the gene, known as IKKE, stay slim despite being fed a lard-based diet.
The 'knock-out' mice also free of the liver problems associated with a junk food diet and appear to be protected against diabetes, the journal Cell reports.
Researcher Alan Saltiel said: 'We've studied other genes associated with obesity - we call them "obesogenes" - but this is the first one we've found that, when deleted, stops the animal from gaining weight. 'The fact that you can disrupt all the effects of the high fat diet by deleting this one gene in mice is pretty interesting and surprising.' It is thought that the gene makes enzymes called kinases that help regulate metabolism. Removing the gene - and the kinases - speeds up metabolism, leading to more calories being burnt.
Dr Saltiel said: 'Perhaps most interestingly, the mice burn more calories even though they aren't eating any less or exercising any more.' In the case of people, a drug that cuts kinase levels could allow people to eat fatty and sugary foods without putting on weight. It would also enable them to stay trim without going to the gym. The researchers, from the University of Michigan in the US, are now hunting for such a pill and predict that many others will join the search.
They said: 'The specificity of the apparent actions of IKKE, the nature of the enzyme, and the profound resistance of the knock-out mice to the high-fat diet, make it an especially appealing drug target for the treatment of metabolic disease.' If they do find the right formula, the drug could be on the market within a decade. But with suggestions that such a drug could increase vulnerability to infection, there are many hurdles to be crossed.
The rising tide of obesity has inspired a worldwide search for new weight loss drugs. Scientists at the Salk Institute in California are researching 'exercise in a pill' - drug that gives the benefits of exercise without leaving the sofa. In experiments, a medicine being developed to help heart bypass patients, boosted fat burning and stamina in inactive mice. The drug fooled the muscles into thinking they have exercised long and hard, rapidly burning fat and boosting fitness.
Others are trying to capitalise on the health benefits of red wine to create a fat-burning pill that protects against diabetes.
But obesity experts caution people against pinning their hopes on a quick fix, saying diet and exercise are key in the battle of the bulge.
Internet source:
http://www.dailymail.co.uk/health/article-1211021/Wonder-drug-development-let-dieters-eat-want--gaining-single-pound.html
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ReplyDeleteThis article is definitely interesting to read but I also foresee various downsides toward this new knowledge. I've seen shows on TV where people got so dangerously overweight and went through stomach bypass surgeries but many eventually died from it at young ages. If the technology mentioned in this article really benefit people from burning calories and no weigh gain, wouldn't it worsen our diet habit and evetually cause other chronic disease? In addition, will the "obesogenes" that get knocked out by the pills result in any other types of damage? (I have tried but not yet found any related article towards this pill)
ReplyDeleteI found this article very interesting and wanted to explore other things that the IKKE gene may be involved in or see if I could find anything related to the gene and how it affected obesity. Knocking out a gene that may have a good affect on one thing in its absence could be detrimental if its presence is important in another thing. I was researching and found an article from another UM lab that was pretty thorough. They seemed to make sure that the KO mice did not develop severe complications. An article by Chiang et. al. in the journal Cell stated:
ReplyDelete"IKKE is a direct transcriptional target of the NF-kB pathway, and is likely to amplify further inflammatory signals via phosphorylation
of other transcription factors. We show here that IKKE gene and protein expression and enzyme activity are increased in liver, adipocytes and ATMs after high-fat feeding, coincident with the activation of NFkB. IKKE KO mice are rendered resistant to the deleterious effects of HFD on insulin sensitivity, exhibiting normal glucose, pyruvate and insulin tolerance. Their circulating cholesterol levels are markedly reduced, and adiponectin is elevated while leptin is lowered. Interestingly, these mice do not gain as much weight as wild-type mice on HFD, due to
increased energy expenditure. Additionally, these mice do not develop hepatic steatosis, macrophage infiltration in adipose
tissue, or elevations in proinflammatory gene expression in fat and liver expected with an inflammatory state"(Chiang, et. al. 970).
What's even more interesting is that I read another article that links IKKE and cancer and how the KO of IKKE controls cell proliferation. An article by Adli and Baldwin in The Journal of Biological Chemistry stated:
"Furthermore, we have also shown that knockdown of IKKE or overexpression of mutated version of p65 (S536A) negatively effects the cell proliferation. These findings indicate an
important role of IKKE and p65 phosphorylation in cancer cell proliferation" (Adli 26983).
It will really be interesting to see how this research progresses because I actually found more pros than cons.
If you want to read more of the articles I mentioned, here is the info:
Adli and Baldwin Article:
http://www.jbc.org.ezproxy1.library.arizona.edu/cgi/reprint/281/37/26976
Shian -Huey Chiang et al Article in the journal Cell:
The link wouldn't work because I went through the UA library website and had to log into WebAuth. The title of the article is "The Protein Kinase IKKE Regulates Energy Balance
in Obese Mice".
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ReplyDeleteI also was interested in this. Found the same article by Chiang et al that you did.
ReplyDelete(link for reference: http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6WSN-4X4Y0RP-M-T&_cdi=7051&_user=99318&_coverDate=09%2F04%2F2009&_sk=%23TOC%237051%232009%23998619994%231484099%23FLA%23display%23Volume_138,_Issue_5,_Pages_809-1034_%284_September_2009%29%23tagged%23Volume%23first%3D138%23Issue%23first%3D5%23date%23%284_September_2009%29%23&view=c&_gw=y&wchp=dGLzVlz-zSkzS&_valck=1&md5=87e0932a564209bcd152190aac6245b1&ie=/sdarticle.pdf)
I think it will be interesting to see how this plays out. It would be really nice to see a development that treated both diabetes/metabolic syndrome and cancer. I think care still needs to be taken to ensure that this is thoroughly evaluated before it gets out into the public.
I also found another interesting article related. It involved knocking out a different gene that showed reduced blood levels of cholesterol and free fatty acids. XBP-1 (the gene involved) is vital in proper fetal development of the liver. The research indicated that there were no major abnormalities in knock out mice that had active XBP-1 in utero but then had the gene 'turned-off' as adults. The only visible result was the reduction in cholesterol and free fatty acids.
Article site: http://esciencenews.com/articles/2008/06/12/unexpected.finding.molecules.dual.role.mice.may.open.new.avenue.cholesterol.reduction XBP-1
Great discussion so far. Obviously we can't (or at least aren't going to) knock out this gene in humans. Any ideas on how to target IKKe with a pill like the original news article describes? Protein kinases (like IKKe) are notoriously difficult to inhibit specifically.
ReplyDelete