upvotes for the cuteness of the picture and the awesomeness of the experiment

"Solo! Come out of there, Solo!"

Now that I see it, I can't unsee it.

Since the previous posts have winged their way right
over my head and out the window, I will comment on the story. (Which is not to say that I don't find the pudgy widdow mouse pic very cute.)

So, human beings have been taking ACE inhibitors for high blood pressure for decades now. If this works, why aren't they losing weight and not developing diabetes? What the heck, in other words, is the relevance of another mouse study to human health, especially in light of the fact that the drugs are already in human use and show no sign of having the same effects? In scientific terms, WTF?

Do you know for certain that the people taking it haven't been losing weight and not developing diabetes?

At a guess I would say that it is to try to understand the demonstrable mechanism in on type of mammal and ultimately to see if that effect could be recreated in another. Really not that far fetched.

Quite substantial, I'd say.

These mice have no ACE at all (my bad in the description), whereas the humans concerned are taking drugs that inhibit ACE. The article doesn't say to what degree - it may just be reducing the action.

Viagra, as an example off the top of my head, was a drug developed for treating blood pressure and angina (admittedly not very well) but adjusting the dosage produced markedly different effects.

So just because these drugs have been taken in one way for one purpose doesn't mean that they can't be counted out for any other treatments that haven't yet been observed.

Finally, even if it doesn't lead to any tangible treatment for weight issues, at the very least it will increase the overall understanding of adipose tissue and it's functions beyond fat storage.

(Oh, and theshirtpocket was saying the photo I chose looks like Jabba the Hutt).

If ACE inhibitors helped humans lose weight and avoid diabetes, I would have heard about it, and so would you. (But particularly me, since I teach pharmacology.)

There is no need to demonstrate the mechanism in mice when we can already down-regulate ACE in humans with drugs. I do agree that down-regulating is not the same as knocking out. This could be a key difference, but one could reasonably expect to see some changes related to the miraculous murine weight loss and diabetes prevention in humans even without completely knocking out ACE production.

It baffles me that the media think one mouse study is newsworthy. It's also a bit troubling; are we so ignorant of the scientific process that we think a mouse study is only a couple of steps away from a human cure? That frightens me.