I was so amazed by this discovery that I just had to make a post about it. One of my favorite points of research is with insulin. And when insulin is low, the body releases free-fatty-acids (FFAs) into the bloodstream, which travels inside the organs and cells of the body to be used as energy (a process called lipolysis). The composition of these fats (saturated, monounsaturated, or polyunsaturated) has different effects on organs. For instance, when saturated FFAs (SFFAs) accumulate in cells (intracellular lipid) it produces a toxic reaction and induces insulin-resistance in that part of the body, it seems to be unable to properly oxidize SFFAs and the body must undergo a desaturation process called delta-9-desaturase, which converts saturated-fats into monounsaturated-fats, which are oxidized with ease and without problem. Saturated-fats are very attracted to adipocytes and it seems to me that that is where they belong, when saturated-fats are stored within the adipocyte, they are harmless and cannot induce metabolic dysfunction. Insulin is needed to not only store saturated-fats inside the adipocyte, but also to stimulate delta-9-desaturase within the adipocytes as well. However without insulin signaling in the adipocyte or with insulin-resistance within the adipocyte, these processes don't happen and out comes the saturated-fats which are so hard to oxidize. Basically these saturated-fats are liberated before having a chance to be converted into monounsaturated-fats, which the body burns with ease.
On the flipside polyunsaturated-fats are oxidized before monounsaturated-fats and the oxidation of these fats doesn't contribute to insulin-resistance (althou it can lead to an inflammatory prostaglandin cascade, but that is another story). The body has no problem at all oxidizing these fats, and the accumulation of them isn't prominent like SFFAs are because of their high oxidation rate. In other words they don't contribute to lipotoxicity as much as SFFAs.
But what I found really interesting is while it seems that polyunsaturated FFAs (PFFAs) are preferable and better for the body to burn than SFFAs because they do not induce insulin-resistance within the organs that are oxidizing them, I found that the ratio between the two, affects the amount of insulin the pancreas produces. I read some studies [1-2] where scientists artificially altered the type of FFAs in the blood of rats. One group of rats were made to have high levels of PFFAs and the other group was made to have high levels of SFFAs. The rats were then given glucose and they found that the body produced very little insulin in response to that glucose when their FFAs were mostly polyunsaturated and that the insulin response was much greater when the FFAs were mostly saturated.
Of course insulin is needed to not only inhibit lipolysis and stimulate delta-9-desaturase, but to prevent full-blown diabetes as well, so what does that tell us about polyunsaturated-fats? What are the implications of this knowledge? Since diabetes is characterized by impaired insulin-sensitivity combined with impaired glucose-stimulated insulin-secretion, would this not suggest that polyunsaturated-fats contribute to diabetes?
The human body contains a mixture of all three types of fats (saturated, monounsaturated and polyunsaturated), however the amount of polyunsaturated-fat in the human body has increased substantially since the early 1900s as the amount of this fat has increased in the diet since then. Since the ratio of saturated to polyunsaturated fat in the human body has increased, perhaps that would indicate that the release of PFFAs during lipolysis would impair insulin-secretion and contribute to diabetes. And that having a high ratio of SFFAs to PFFAs would produce more insulin-secretion which would prevent diabetes. Perhaps this is why milk, which contains a high ratio of saturated-fat to polyunsaturated-fat is one of the most insulinogenic foods known to man (besides the humble potato).
It seems to me that since SFFAs are so hard and toxic to oxidize, the pancreas secretes lots of insulin to ensure that these SFFAs will make it back inside the adipocyte where they belong.
I wanted to get some input on this and ask y'all if I'm interpreting these results correctly.
[1] J Clin Invest. 1997 Jul 15;100(2):398-403. The insulinotropic potency of fatty acids is influenced profoundly by their chain length and degree of saturation. Stein DT, Stevenson BE, Chester MW.
[2] Diabetes. 2002 Jun;51(6):1825-33. The composition of dietary fat directly influences glucose-stimulated insulin secretion in rats. Dobbins RL, Szczepaniak LS, Myhill J.
Edited by misterE, 09 May 2014 - 06:08 PM.