http://www.eurekalert.org/pub_relea...o-sbe011106.php

In their latest finding on the brain's role in controlling appetite and weight, researchers at the Albert Einstein College of Medicine have shown that reducing levels of fatty acids in the hypothalamus causes rats to overeat and become obese. Their results suggest that restoring fatty-acid levels in the brain may be a promising way to treat obesity. The study, published in the January 15th on-line edition of Nature Neuroscience, was led by Dr. Luciano Rossetti, director of the Diabetes Research Center at Einstein. (The paper will appear in print in the February issue.) The brain's hypothalamus keeps track of the body's nutritional status by monitoring the blood levels of several different hormones and nutrients. Taking this information into account, the hypothalamus regulates our energy intake and metabolism.

In a study published last year in Science, Dr. Rossetti and his colleagues showed how the hypothalamus monitors and regulates glucose levels in the body. The present study shows that this brain region also monitors fatty acid levels and responds by controlling appetite.

The study focused on malonyl CoA, a molecule suspected of being one of the critical nutrients influencing hypothalamic regulation of eating behavior. Previous studies had shown that hypothalamic levels of malonyl CoA increase markedly after meals and are suppressed by fasting.

The Einstein researchers wanted to know whether sustained suppression of this nutrient within the hypothalamus could result in obesity. To find out, they piggybacked an enzyme known to degrade malonyl CoA onto an adeno-associated virus and injected the virus into the hypothalamus of rats. The injections caused a chronic decrease in malonyl CoA levels, which dramatically increased the rats' food intake and led to obesity that was maintained for at least four months.

"We showed in this study that disrupting malonyl-CoA levels in this region of the brain impairs the nutrient-sensing mechanism by which the hypothalamus modulates food intake to maintain normal weight," says Dr. Rossetti, who is also the Judy R. and Alfred A. Rosenberg Professor of Diabetes Research at Einstein. "Figuring out a way to re-adjust malonyl-CoA levels in the human hypothalamus could lead to innovative therapies not only to treat obesity but to help prevent diabetes and other consequences of being overweight."

Makes one wonder if maybe... oh say ... eating more fatty acids might help control hunger. Naw... couldn't be.

mike

I wonder if there are environmental things that are affecting this. Eating lots of fat doesn't help me out. I just eat more calories than ever.

Observation: eating fat suppresses appetite. The finding in rats is not surprising. *If* this also happens with humans, this could indicate that anything that reduces fatty acid levels in the blood (low fat diet?) would tend to lead to increased appetite and thus, perhaps, obesity.

Any time research indentifies one enzyme or biochemical as the cause of a disease state, you can be sure that they're looking for a designer molecule to make billions from. It's not serious research.

>>>restoring fatty-acid levels in the brain may be a promising way to treat obesity>>>

(Affecting Gomer Pyle-type smile)
Surprise, Surprise!!!

Eating more fat might not necessarily translate into higher levels of fatty acids in the hypothalamus. That's kind of like concluding that eating fat makes you fat. The body is very complex; you don't just eat something and then boom it's there (sorry guys, buying protein powder doesn't necessarily make you grow muscles, and sorry girls, eating low fat diets doesn't make you necessarily drop excess flab).

I would be inclined to think how much fat you're eating is a LOT less important than your overall metabolic state (balance of hormones/enzymes). Say you eat a big fatty meal but it messes up your blood sugar (because it was high in refined carbohydrate, or because it was so large that it made your body pour out insulin above and beyond necessary, or whatever reason). In 2 hrs you will be hypoglycemic which means your body's metabolism is basically in the crapper. Even though you consumed oodles of fat (and plenty of carbs to make fatty acids with) your body is in a low energy state similar to fasting. This would depress levels of fatty acids in the hypothalamus (in theory) which would trigger the pathways which increase hunger & food intake.

Again, the take home message is it's never This One Thing (fatty acid levels in the hypothalamus, or eating lots of fat). It's the big picture...
Obesity is a symptom. One of many.
The imbalance (syndrome-causing disease state) is the real issue.
Metabolic disease, caused by unhealthy lifestyle is the culprit.
Even if they do design a new appetite suppressing drug from this research, none of that will change... and you know what, in the long run, people will find out yet again they've been swindled and that you can't put a bandage and ignore the crumbling foundation.

Good point Wooo. My comment was kind of tongue in cheek but you are quit correct. The research does seem to be foolishly fixated on finding some micro-issue that can be used to develop a wonder drug rather than on understanding the how the entire system functions so that one can properly guide it to optimal health.

mike