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Obesity's effects extend all through the body, and the liver is one of the more serious victims. Poor diet can cause fat to build up in the organ, leading to chronic liver disease and other serious health issues like diabetes and heart disease. Now a team from Saint Louis University has found that switching off a particular protein decreased the body fat and improved the blood sugar levels of mice.
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"When I think of fatty liver disease, I think of fatty hepatocytes – liver cells," explains Baldan. "Each cell has many lipid droplets, and those droplets contain triglycerides. The lipid droplets aren't skinny-dipping in the cells, though. They are coated by proteins. One such protein is called 'fat-specific protein 27,' or FSP27."The function of body fat is to store energy for later use. But what FSP27 does is prevent those lipids from mobilizing – being used – and instead encourages them to stay put in the cell. A high-fat diet increases the amount of FSP27 and, in turn, the amount of fat that builds up in the liver. Inversely, triglycerides can also accumulate as a result of fasting, which sees the body begin to process more stored fat, sending mobilized fat to the liver for processing.
Knowing this, the team hypothesized that shutting off FSP27 should reduce fat build-up. To test the idea, the researchers used two groups of obese mice, afflicted with high blood sugar and fatty liver disease. The difference was, one group was fed a high-fat diet, while the other mice were genetically modified. Some of each group were then treated with antisense oligonucleotides, polymers which essentially switch off FSP27.
Mice treated with a compound to shut off the fat-specific protein FSP27 showed significant declines in fat.
(Score: 3, Informative) by ikanreed on Wednesday December 21 2016, @04:32AM
Well, good news. There's a process to limit the ethical risks for treatments of exactly this sort.
Clinical trials are run in stages. First is proof of concept in vitro tests, wherein the underlying mechanisms are developed and understood and the most basic risks are assessed: what can this do to human cells. Then in vivo animal model(like this one) trials where the effectectiveness of the treatment and possible side effects can be detected. Then a follow up animal trial to assess dose-response curve to identify candidate levels of treatement.
Then all that is brought for ethical review, approximate risk-benefit tables are tabulated and if they're too close to 1:1 (Or worse) the whole thing is dropped.
Then a small sample size study with worst-case patients who haven't responded well to traditional treatment or who are considering high-risk procedures. For obesity the target group would probably be people who are considering surgery such as liposuction, "coolsculpting", or gastric bypass, all of which carry known risks. Then with placebo controls, the effectiveness and possible side effects are assessed in humans.
Then and only then, would a drug-based treatment for obesity be considered for wide-scale clinical trial, where regular people like you or I might be eligible. And at that point (if proper procedure were followed) you'd be informed by your doctor off all the side effects that previous trials showed. Ironically you'd be a lot more informed than what you'd likely get if it had already passed stage II clinical trials.
Anything goes wrong in any of those stages, it's over. This probably can't be sold as a supplement at GNC since it's an engineered drug to target a chemical pathway, and the FDA frowns on those shenanigans.
(Score: 0) by Anonymous Coward on Wednesday December 21 2016, @05:28AM
And at no stage do they make a prediction more precise than A is positively correlated with B- How strange.
(Score: 2) by ikanreed on Wednesday December 21 2016, @03:37PM
Other than, no, that's total bullshit due to the first stage of research that establish mechanisms, you're still full of shit because interventionary experiments establish causation in a way purely observational experiments don't.