Incretins 101
In the 1980s, scientists discovered a major difference in how the body responded to glucose ingested orally versus glucose administered intravenously. This finding led to the identification of the “incretin effect”—a process where hormones in the gastrointestinal (GI) tract play a crucial role in regulating insulin response and glucose levels (1).
This discovery paved the way for understanding incretin hormones like GLP-1 (Glucagon-like Peptide 1) and GIP (Glucose-dependent Insulinotropic Polypeptide), which together make up 90% of the body's incretin activity. (2,3)
The Role of Incretins in Insulin Secretion and Glucose Control
In conditions like pre-diabetes and Type 2 Diabetes, the body's ability to use glucose becomes impaired. One key factor in this is the decreased production of incretin hormones. Research has found that some individuals with Type 2 Diabetes produce only 30% of the normal amount of these hormones. (4,5)
So, how do incretins work?
After you eat, as glucose (the simplest form of carbohydrate) enters the small intestine, incretins like GLP-1 and GIP are released. These hormones help the pancreas secrete insulin, while simultaneously suppressing glucagon—a hormone that releases stored glucose into the bloodstream. Incretins also slow down the rate at which your stomach empties, giving insulin more time to manage blood sugar levels effectively.
Incretins and the Brain: A Complex Relationship
In addition to their role in insulin regulation, GLP-1 and GIP receptors are found in the brain and vagus nerve, which has led to widespread speculation about their effect on appetite. Despite common claims that incretins “tell the brain it's full,” research shows that the relationship is much more complex, and this oversimplification doesn't fully capture how incretins influence the nervous system. (6,7)
Medications Mimic Natural Hormones
In 2004, incretin mimetics were incorporated into effective therapeutic options for Type 2 Diabetes care. These medications “mimic” the effects of natural incretins. They are know as GLP-1 receptor agonists and Dual GLP-1/GIP receptor agonists.
For more information on this class of medications and how they fit into weight-inclusive care, check out our blog [link].
FAQs About Incretins
What are incretin hormones?
Incretin hormones, including GLP-1 and GIP, help regulate insulin secretion and blood sugar levels after eating.
How does GLP-1 affect diabetes and blood sugar?
GLP-1 stimulates insulin production, reduces glucagon secretion, and slows down stomach emptying.
Ready to care for your blood sugar and build a healthier relationship with food? Reach out to our team of expert Registered Dietitians at On the Brink Nutrition today. We’re here to support you with weight-inclusive, compassionate care.
Contact us now to book an appointment.
You might also like:
How the Human Body Uses Sugar: Understanding Normal Function vs. the Impact of Diabetes
What's the Deal with Carbohydrates? Debunking Myths and Embracing Facts
References
Nauck, M. K., et al. "Reduced incretin effect in type 2 (non-insulin-dependent) diabetes." Diabetologia 29.1 (1986): 46-52.
Seino Y, Fukushima M, Yabe D. “GIP and GLP-1, the two incretin hormones: Similarities and differences.” J Diabetes Investig. 2010 Apr 22;1(1-2):8-23. doi: 10.1111/j.2040-1124.2010.00022.x. PMID: 24843404; PMCID: PMC4020673.
Holst, J. J. "Glucagon-like peptide-1: from extract to agent. The Claude Bernard Lecture, 2005." Diabetologia 49.2 (2006): 253-260.
Nauck, Michael A., and Juris J. Meier. "The incretin effect in healthy individuals and those with type 2 diabetes: physiology, pathophysiology, and response to therapeutic interventions." The Lancet Diabetes & Endocrinology 4.6 (2016): 525-536.
Holst, Jens J., et al. "Loss of incretin effect is a specific, important, and early characteristic of type 2 diabetes." Diabetes Care 34.Supplement 2 (2011): S251-S257.
Harada, Norio, and Nobuya Inagaki. "Role of GIP receptor signaling in β-cell survival." Diabetology International 8 (2017): 137-138.
Kim SJ, Winter K, Nian C, Tsuneoka M, Koda Y, McIntosh CH. “Glucose-dependent insulinotropic polypeptide (GIP) stimulation of pancreatic beta-cell survival is dependent upon phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) signaling, inactivation of the forkhead transcription factor Foxo1, and down-regulation of bax expression.” J Biol Chem. 2005 Jun 10;280(23):22297-307. doi: 10.1074/jbc.M500540200. Epub 2005 Apr 6. PMID: 15817464.