Friday, March 6, 2015
The Pro Insulinogenic Activity of Saturated Fat High Fat High GIP High Insulin After 6 Days on High SFA Diet
Asian foods are low in SFAs. So the researchers had to add it to the pan. |
Obviously you havent read my previous article on the fallacies of adding fat to glucose in the false believe that the reduced digestive speed would reduce the post-prandial insulin spike ("True or False? Adding Fat to A Carby Meal Lowers Insulin Response." | read more) - a highly suggested read you may want to read either, before or after you devour todays SuppVersity article.
You can learn more about fat at the SuppVersity
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Figure 1: Graphical overview of the procedure (Itoh. 2014) |
Muscular glucose uptake will be significantly reduced whenever free fatty acids are present in sign. amounts (Nuutila. 1992) |
In the end thats a physiologically sane reaction we developed in the days and age, where our meals were either high in fat or high in carbohydrates. In these days, however, it is one of the major obstacles to staying diabetes-free. An obstacle, however, the average healthy fitness enthusiast doesnt really have to worry about, if he works out regularly and does not live on twinkies & dingongs exclusively.
- in the high saturated fatty acid meal (FB-30): S/M/P, 5:4:1;
- in reduced saturated fatty acid meal (F-30): S/M/P, 3:4:3
Figure 2: Comparison of glucose, insulin, and C-peptide levels after the control, F-30, and FB-30 meals (Itoh. 2014) |
The GIP response, i.e. the response of the non-satiating non-fat burning insulin release triggering brother of GLP-1 (learn more) that does neither reduce hunger, not appetite nor improve glucose control (increased amount of insulin used to store away the same amount of glucose; cf. Edholm. 2010), after the FB-30 was higher than that after the F-30 (P< .05).
"In addition, the difference in the incremental GIP between FB-30 and F-30 correlated significantly and positively with that of the insulin." (Itoh. 2014)The scientists believe that their results clearly prove, what scientists have believed for quite some time, now: "a high saturated fatty acid content stimulates postprandial insulin release via increased GIP secretion." (Itoh. 2014)
So what do we make of these results? I guess my friend Alex who has been beaten up for posting the results of a similar study in the "Perfect Health" facebook group, will know why I point out that this does not mean that healthy individuals should no longer put butter on their potatoes.
What it does mean, though, is that the anti-hype around saturated fat is about as misplaced as the way saturated fats are still roasted by the media. They are not healthier than MUFAs and PUFAs (but not unhealthier, the insulin spike after the mixed fat meal was not sign. less pronounced), not "neutral" and not good for your glucose management, unless you eat only saturated fat and cut out the vast majority of carbs, i.e. go at least half-way keto. In that case, however, the SFA are just a means to provide you with the fuel you need, they are not the agent that will improve your glucose management - thats a simple result of not eating glucose spiking foods | Comment on Facebook!
References:Figure 3: In contrast to the insulin spike, the GIP release was sign. higher in SFA vs. mixed fat (Itoh. 2014) |
- Boden, Guenther, et al. "Mechanisms of fatty acid-induced inhibition of glucose uptake." Journal of Clinical Investigation 93.6 (1994): 2438.
- Edholm, T., et al. "Differential incretin effects of GIP and GLP‐1 on gastric emptying, appetite, and insulin‐glucose homeostasis." Neurogastroenterology & Motility 22.11 (2010): 1191-e315.
- Itoh, Kazue, et al. "High saturated fatty acid intake induces insulin secretion by elevating gastric inhibitory polypeptide levels in healthy individuals." Nutrition Research (2014).
- Nuutila, P., et al. "Glucose-free fatty acid cycle operates in human heart and skeletal muscle in vivo." Journal of Clinical Investigation 89.6 (1992): 1767.
- Roden, Michael, et al. "Mechanism of free fatty acid-induced insulin resistance in humans." Journal of Clinical Investigation 97.12 (1996): 2859.
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