Anyone understand gastric inhibitory polypeptide?

(Bob M) #1

I’ve been testing eating a high saturated fat diet, trying to maximize stearic acid (a long chain, even numbered saturated fat, 18:0). I am stunned at the lack of hunger this has given me and also the fact that I appear to be losing belly fat and gaining muscle. And I’ve been low carb/keto for 6 years. Never have I experienced this lack of hunger and body remodeling in all that time. This was also experienced by The Croissant Diet’s creator (Brad Marshall – Listen to the Biohacker’s Lab’s podcast if you want to hear it from Brad).

Part of what is happening is an increase in gastric inhibitory polypeptide (GIP). See this mouse study:

See this info on GIP:

Gabor Erdosi also said that eating a high butter croissant would “augment the GIP response profoundly”. He seems to think that’s bad.

However, I have experienced such a benefit from eating higher saturated fat (attempting to get as high in stearic acid as possible), that if stearic acid causes a high GIP response, there must be some “good” it does.

I can find information telling my what GIP does, but nothing that indicates whether a “high” GIP response is bad or good.

For instance, Wikipedia says:

In addition to its role as an incretin GIP is known to inhibit apoptosis of the pancreatic beta cells and to promote their proliferation. It also stimulates glucagon secretion and fat accumulation.

But this seems to be exactly the opposite in terms of fat for me. (I have NOT tested blood sugar; may have to get a CGM.)

Anyone have any theories?

(Bunny) #2

Also it stimulates (potentiates) the production of pancreatic beta cells if I’m not mistaken?

[1] “…Gastric inhibitory polypeptide (GIP), or gastric inhibitory peptide, also known as glucose - dependent insulinotropic polypeptide, is an inhibiting hormone of the secretin family of hormones. While it is weak inhibitor of gastric acid secretion, its main role is to stimulate insulin secretion. …More

[2] “… The therapeutic potential of glucose-dependent insulinotropic polypeptide (GIP) for improving glycemic control has largely gone unstudied. A series of synthetic GIP peptides modified at the NH2-terminus were screened in vitro for resistance to dipeptidyl peptidase IV (DP IV) degradation and potency to stimulate cyclic AMP and affinity for the transfected rat GIP receptor. In vitro experiments indicated that [d-Ala2]GIP possessed the greatest resistance to enzymatic degradation, combined with minimal effects on efficacy at the receptor. Thus, [d-Ala2]GIP1–42 was selected for further testing in the perfused rat pancreas and bioassay in conscious Wistar and Zucker rats. When injected subcutaneously in normal Wistar, Fa/?, or fa/fa Vancouver Diabetic Fatty (VDF) Zucker rats, both GIP and [d-Ala2] GIP significantly reduced glycemic excursions during a concurrent oral glucose tolerance test via stimulation of insulin release. The latter peptide displayed greater in vivo effectiveness, likely because of resistance to enzymatic degradation. Hence, despite reduced bioactivity in diabetic models at physiological concentrations, GIP and analogs with improved plasma stability still improve glucose tolerance when given in supraphysiological doses, and thus may prove useful in the treatment of diabetic states. …” …More

[3] “…The incretins are a class of hormones released from the small bowel that act on the endocrine pancreas to potentiate insulin secretion in a glucose-dependent manner. Due to the requirement for an elevated glucose concentration for activity, the incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1, have potential in the treatment of non-insulin-dependent diabetes mellitus. A series of synthetic peptide GIP fragments was generated for the purpose of elucidating the bioactive domain of the molecule. …” …More

(Jane) #3

Which fats have you been eating differently from the past?

(Jenna Ericson) #4

Hmm this doesn’t seem to fit, but why? It sounds like gastric inhibitory polypeptide’s main role is to stimulate insulin secretion, so the idea of more GIP being released in response to eating stearic acid seems off (at least in humans). It’s too bad that this study was on mice. I have a feeling this is one area where we might differ from rodents. We would have evolved to eat large game animals which have high amounts of longer chain saturated fats, whereas mice would have adapted to eating either plants or smaller prey, lower down on the food chain, which I assume would have higher PUFA content.

(Jenna Ericson) #5

@ctviggen I’ve really liked following your posts on this topic and I’ve been incorporating more stearic acid into my diet as well. I’m eating about 15 or 20 grams of cocoa butter each day and have been using beef and bison tallow a lot more. I noticed the same thing as far as hunger going way down. I don’t know exactly how long it’s been (maybe 3 or 4 weeks) but I’ve lost some weight and about an inch around my waist. I’ve also started strength training for an hour twice a week, though so that could have something to do with it.