Thursday, September 25, 2014

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.
From a physiological perspective, the observation researchers from the Nakamura Gakuen University, the  Akita University, the Chiba University and the University of Copenhagen appear counter-intuitive, why should fat increase the insulin response to a meal. The presence of fat in a meal should slow down the absorption of glucose, right?

Obviously you haven't 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 today's SuppVersity article.
You can learn more about fat at the SuppVersity

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Don't worry, today's article still has something new to offer. While the previously reported data dealt with acute responses to high(er) fat meals, Itoh et al. (2014) whose study is available as an "ahead of print paper" on the website of Nutrition Research, looked at the effects of sub-chronic, not acute high saturated fat intakes.

Figure 1: Graphical overview of the procedure  (Itoh. 2014)
In that, they conducted an intervention study to investigate the insulin and plasma GIP responses in 11 healthy women, including a dietary control. Subjects were provided daily control meals (F-20; saturated fatty acids/monounsaturated fatty acids/polyunsaturated fatty acids [S/M/P] ratio, 3:4:3) with 20 energy (E) % fat, followed by 2 isoenergetic experimental meals for 7 days each. All meals were standard Japanese meals, the recipes for both experimental meals were identical, only a different cooking oil was used.
Muscular glucose uptake will be significantly reduced whenever free fatty acids are present in sign. amounts (Nuutila. 1992)
FFA = insulin resistance: The simple presence of an increased amount of fatty acids in the blood that will necessarily occur in response to the ingestion of high fat meals switches the bodies internal "fuel switch" to "burn fat" and reduces the uptake of glucose by fat and specifically muscle cells (Nuutila. 1992; Boden. 1994; Roden. 1996).

In the end that's 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 doesn't really have to worry about, if he works out regularly and does not live on twinkies & dingongs exclusively.
Talking about "test meals" (I don't like to call them thus, as they were consumed for a couple of days and not just for a "test), these meals comprised 60 E% carbohydrate, 15 E% protein, and 30 E% fat with the fat being distributed as follows:
  • 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
Tests were conducted after two days on the FB-20 meal (pre) and at the end of the FB-30 and F-30 phases (see Figure 1), before and 30, 60, and 120 minutes after a meal tolerance test.
Figure 2: Comparison of glucose, insulin, and C-peptide levels after the control, F-30, and FB-30 meals (Itoh. 2014)
Interestingly, the plasma glucose responses did not differ between F-20 and FB-30 or F-30. The insulin levels, on the other hand, were higher after the FB-30 than after the F-20 (P<.01).

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.

Figure 3: In contrast to the insulin spike, the GIP release was sign. higher in SFA vs. mixed fat (Itoh. 2014)
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 - that's a simple result of not eating glucose spiking foods | Comment on Facebook!
References:
  • 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.