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Molecule Cuts Off Fat's Food Supply
hords writes "New Scientist reports a magic bullet that destroys the blood vessels that feed fat tissue enables mice to lose a third of their body weight. They first screened millions of peptides and identified one that binds to a membrane protein found only in the blood vessels supplying white fat. Then they hooked this up to another peptide that triggers cell suicide or apoptosis. Mice that had grown obese on a high-calorie diet were given daily injections of the combined peptide they lost 30 percent of their body weight in four weeks, whereas control mice given the two peptides separately grew even fatter."
These drugs work great for curing cancer in mice but don't work as well in humans. Given that, I wouldn't be surprised if they don't work well in humans for this either....
On the other hand, morbid obesity is probably the number one preventable health concern in America. I am doubtfull that this will ever be a useful drug (i.e. too many side effects, like DEATH), but if somehow it makes it's way onto the list of FDA approved drugs, this will have a MAJOR affect on the American lifestyle (even less exercising?). Whatever pharm company invents this will be filthy, filthy, filthy rich.
N.B. It usually takes about 10 years and close to a bilion dollars to go from a chemical/protein to an approved drug in America. Let's check back in a few years.
..........FULL STOP.
I'm not going to say this is a sure thing. However, it helps that they are merely using the presence of the protein in blood vessels supplying fat cells as a marker for attaching the cell death factor. They aren't trying to tweak a metabolic pathway, which would require the interplay of all the components to be preserved between mouse and human. Instead, they are just killing blood vessels that contain a particular protein. It seems like this is a little simpler and requires fewer caveats than a metabolism-altering drug. It is true that human fat cells may respond to the absence of blood vessels differently than mouse fat cells, but most parts of the body do poorly without oxygen or nutrients or waste removal.
"1. We don't know what else fat cells do in your body. They may have other roles than fat storage." For instance, fat contains stem cells that can heal fractures too large to heal by themselves. It seems likely that any reduction in blood flow would kill off the stem cells as quickly as the fat cells themselves. It would be unfortunate to be finally skinny, then break something because you lack your normal "fat cushion", then you are unable to heal yourself because you lack your fat derived stem cells!
Trust me being skinny is incredibly over rated. Where I work I am required to maintain a certain level of physical fitness and it isn't even all that high of a standard. Nonetheless I was a much happier individual when I was 40 to 60 pounds over weight according to the doctors. I do not see the theoretical extra years I may live, as a result of being uncomfortable for extended periods every week, as worth it. I would much rather live a happy and comfortable 40 to 60 years as a fatass than 100 years while regularly subjecting myself to exercising for nothing but the purpose of extending an uncomfortable lifestyle. That being said I used to ride mountain bikes a lot and am getting back to that as a hobby and I might get skinnier as a side affect. But I can not fully express my low opinion of exercising for the sake of being in shape.
But I can not fully express my low opinion of exercising for the sake of being in shape.
Amen to that. Most if not all the extra time you get to live (mind you, if any) is spent exercising. Heck, you might even live less when you subtract the exercising time, who knows *grin*
Fun stuff, by all means. But the 'just for the image' stuff is an ego trip.[*]
[*] geeks trying to get laid can qualify for an exemption
I also know how little we really understand on genomic-proteomic-metabolic pathways. In most cases the math needed to grok this isn't a common skill in the biological community. An organism's genomic-proteomic-metabolic pathways have similar complexity to the system of operating system, plus firmware/microcode, plus transistor-level circuit, plus process-level (e.g. doping) interactions of a Pentium processor-based computer, though:
There has been some interesting work but the heavy math and analysis required has only recently become common option for biology degrees, and then only those folks who do bioinformatics are going to have the education for 21st century biology. Biology will soon be part of the engineering school and/or part of the hard sciences like physics. It will not be a major you go into to avoid math like it has in the past.
I'm also remembering how slow and meticulous a process this research is and must be, and how uncertain the end result may be compared to initial hypotheses. Compare this to the scientifically illiterate mass-communication sound bite that type of research gets in the general media, and well, that tends to temper my enthusiasm when I see something like this outside the realm of a journal (my, how academically elitist of me :-) ).
Take asthma, for instance. There is a distinct set of pathologies associated with asthma, but there is no single etiology, nor is there a set of etiologies which acount fully for the disease state (i.e., two people exposed to the same conditions may or may not develop asthma, even apart from genetics). Type I diabetes is the same way. There is a set of symptoms (airway hyperresponsiveness for asthma, or low insulin for diabetes) with an unknown cause. As that we do not know the cause, we must treat only the symptoms. Oddly, with the primary diseases, controlling the symptoms makes the disease undectable.
If you treat all of the symptoms of a cold, the cold is still detectable as adenovirus in in lungs (Use Koch's postulates). If someone has cancer and it is forced into remission, there are still ways to detect the presence of an old cancer (exceptionally difficult sometimes, but possible).
Not so with things like asthma, diabetes and primary diseases. Unless the symptom reasserts itself, the syndrome/disease/etc is undectable. Keep in mind that total ablation of the symptoms is rarely possible. It is only a theorectical concept except in mild cases.
Back on topic, there are many known causes for obesity the most common of which are eating too much or sitting on your ass too much. Most commonly obesity is a result of a combination of the two. Therefore, it could be aruged that obesity is not a primary disease, because we know the cause. The opposing arguement is that because we do not understand the motivations which cause the self destructive behavior (which is regarded as a symptom), the disease is primary. That is, since we do not understand the cause of the "eating too much" symptom, we must call it a primary disease. I disagree, personally, because I do not see self-destructive behavior as a pathological state in Man. It may not be beneficial, but I don't think it's abnormal.
Obesity can however be described as a cyclical disease, in that the disease state causes worsening of the state after a certain point. It is these people that truly need help. They essentially dug a hole that is too deep for them to climb out of on their own. These are the people who need intervention.
There is a reason for everything. Sometimes that reason just sucks.
My health club recently installed individual 15" LCD screens on a whole bunch of treadmills and elliptical trainers... All have full cable access. Now, instead of sitting on the couch at home, I can watch Simpsons or Iron Chef and excersize while doing it. And if Simpsons isn't on, those screens are attached to a DVD/CD player, so I can bring a movie along. Makes my 30 min cardio session a breeze!