This study was done in mice but has some interesting results, especially for fans of "calories in calories out"
We all know what happens when you feed mice a High-fat diet, they get obese and end up with metabolic syndrome. Nothing new. ( diet in this study was D12492, which is casein, surcrose, lard, soybean oil etc. )
But, what happens if you supplement thier diet with SCFA? They should gain even more weight, right? We've added calories to thier food, so you know, a calorie is a calorie yada yada, we know exactly what will happen, the mice will be even fatter!
Ok, now look at Figure 1 in the study.
If you cant be arsed, let me just spell it out for you. The result of adding SCFA to the diet completely prevented any weight gain on the HFD!
The mice eating the normal HFD preceeded to gain 40% of thier weight over 4 weeks, while the mice eating the HFD + butyrate gained........ nothing! Now, although they did reduce thier food intake slightly, this was only initially. Also, look at the acetate group, they ate the most calories but were still only half as fat as the control mice.
Actually, too add insult to injury, the mice eating butyrate actually LOST a very small amount of weight.
So what happened here, do calories vanish? *shrug* who knows. If your a calories in calories out fan you can enjoy your time trying to find out if the first law of thermodynamics is applicable here or not.
Hint : its not.
This is because the first law applies only to the organism as a whole, trying to apply it to predict changes in adiposity is incorrect because adipose tissue is an underlying sub-system of the over-laying top level system which is the organism as a whole.
Anyway, back to the study, the real reason the mice eating butyrate didnt gain weight was because thier incretin response was significantly higher. Infact the GLP-1 and PYY responses were pretty good predictors of the final increase in adiposity on the HFD, as in, butyrate, which produced the highest GLP-1 and PYY response, produced the leanest mice.
If your now sold on SCFA's ( and by inference, incretins ) being an important part of being lean, the question now becomes, does significant colon fermentation to produce SCFAs happen in humans?
And even if so, does SCFA manufacturing in the colon produce GLP-1? Luckily the answer to this second question appears to be yes. Also, I couldnt help but notice the picture of the portal vein in wikipedia, the portal vein actually innervates the whole colon, even the rectum! Whats the point of that? hhhmmmm
As for the first question, I found this study on inulin. I have to wonder though, would resistant starch do the same thing as inulin? Like, raw potato?
Getting lean and staying lean is all about maximising the incretin response. And SCFA's might be a critical component of that.