The Diabetes Gut Connection
The microbiome has numerous functions including protecting against pathogens, shaping the immune system, regulating intestinal hormone secretion and GI nerve activity, nutrient absorption, and synthesizing certain vitamins1. In recent years, the gut microbiome, the term for the trillions of micro-organisms that inhabit the GI tract, has been shown to be involved in the development of metabolic diseases such as obesity, insulin resistance, and diabetes. Alterations in the abundance and diversity of the microbiome (dysbiosis) affect its functioning. A less diverse gut microbiome leads to more disease-causing bacteria, gut inflammation, and progression towards a diabetic state2. Larsen et al. found that those with type 2 diabetes had a lower abundance of Firmicutes with a higher proportion of Bacteroidetes and Proteobacteria compared to non-diabetics3.
Mechanisms by which microbes influence metabolism
Lipopolysaccharide (LPS) comes from the outer membrane of Gram-negative bacteria. They activate inflammatory pathways and induce intestinal permeability resulting in decreased insulin sensitivity1,4.
- Short-chain fatty acids (SCFAs)
SCFAs are produced by bacteria through fermentation of fiber. When bound to receptors, they signal different pathways which result in decreased inflammation and improved insulin sensitivity1. It’s also thought that SCFAs, specifically butyrate, induce satiety and strengthen the integrity of the gut2. There have been several studies showing that type 2 diabetics have significantly lower numbers of SCFA-producing bacteria5.
- Bile acids
Gut bacteria are capable of transforming primary bile acids to secondary bile acids, hindering their recirculation by the liver. These secondary bile acids can bind to specific receptors and the effects lead to improved insulin sensitivity1.
Intestinal permeability, commonly referred to as leaky gut, occurs when the tight junctions between the cells lining the GI tract become compromised, allowing foreign materials to pass from the intestine into the bloodstream. This increase in gut permeability activates the immune system, alters signaling pathways that affect lipid and glucose metabolism, creates systemic inflammation, and could even result in pancreatic beta-cell damage, all of which lead to insulin resistance1,5. The development of both type 1 (autoimmune) and type 2 (metabolic abnormalities) diabetes is connected to enhanced permeability2.
Influencing the microbiome for better blood sugar control
Probiotics seem to improve insulin sensitivity through multiple mechanisms4. Certain probiotics have been shown to reduce chronic inflammation, lower oxidative stress in pancreatic tissue, and reduce LDL and total cholesterol. Additionally, prebiotics can enrich the microbial population, improve intestinal permeability, reduce endotoxemia, and improve glucose tolerance2. Many foods are prebiotic and probiotic rich and it’s important to eat them regularly. These include garlic, onions, asparagus, berries, legumes, beans, and fermented foods. Supplementing with probiotics can also be beneficial. Here is a link to check out some of our favorite probiotic products.
Increase fiber intake
Fiber intake is associated with an increase in both abundance and diversity of gut microflora along with the production of SCFAs. Studies have shown that soluble fiber has a direct blood glucose lowering effect4. High-fiber foods include vegetables, fruits (eat the peel when possible), legumes and beans, whole grains, nuts and seeds. Make sure to increase fluid intake when increasing fiber in the diet.
The most profound way to affect the gut microbiome is through food. In order to establish a healthy, diverse microbiome, we must eat healthy, diverse foods. One strategy is to “eat the rainbow”. Aim to incorporate colorful foods into your meals and try new fruits and vegetables when possible. Shop mostly the perimeter of the grocery store where fresh foods are more prevalent. Limit highly processed, sugar-rich foods often found in the center of the grocery store.
Chronic stress can lead to dysbiosis and enhance intestinal permeability which are both linked to diabetes as mentioned above6. It’s imperative that we do things daily that help manage the inevitable stress that comes with living in today’s world. For more on simple ways to nurture the body and to download our free Breathing 101 guide, click here.
The health of the microbiome can’t be ignored when it comes to disease and chronic health conditions. Because of the connection between the gut and diabetes, improving gut health is a priority when working to prevent or reverse insulin resistance. Our pharmacists at PharmToTable specialize in functional medicine using a lifestyle-based approach and we also have health coaches on our team who can help you make changes towards improving your health. We’d be honored to help you on the journey of improving diabetes or other endocrine or metabolic condition. Book an appointment or schedule a free 15-minute discovery call today!
Written by Megan Morrison, PharmD
- Allin KH, Nielsen T, Pedersen O. Mechanisms in endocrinology: Gut microbiota in patients with type 2 diabetes mellitus. Eur J Endocrinol. 2015;172(4):R167-R177. doi:10.1530/EJE-14-0874
- Sharma S, Tripathi P. Gut microbiome and type 2 diabetes: where we are and where to go?. J Nutr Biochem. 2019;63:101-108. doi:10.1016/j.jnutbio.2018.10.003
- Larsen N, Vogensen FK, van den Berg FW, et al. Gut microbiota in human adults with type 2 diabetes differs from non-diabetic adults. PLoS One. 2010;5(2):e9085. Published 2010 Feb 5. doi:10.1371/journal.pone.0009085
- Li WZ, Stirling K, Yang JJ, Zhang L. Gut microbiota and diabetes: From correlation to causality and mechanism. World J Diabetes. 2020;11(7):293-308. doi:10.4239/wjd.v11.i7.293
- Aw W, Fukuda S. Understanding the role of the gut ecosystem in diabetes mellitus. J Diabetes Investig. 2018;9(1):5-12. doi:10.1111/jdi.12673
- Merabet N, Lucassen PJ, Crielaard L, et al. How exposure to chronic stress contributes to the development of type 2 diabetes: A complexity science approach. Front Neuroendocrinol. 2022;65:100972. doi:10.1016/j.yfrne.2021.100972