GLP-1 secretion with Oral Prebiotics and Probiotics

Gut microbiota has been increasingly recognized to play a significant role in human health and disease by affecting the gastrointestinal tract's immune system, energy metabolism, and inflammatory responses. Recent advances in gut microbiota research have highlighted the link between oral prebiotics and probiotics and glucagon-like peptide-1(GLP-1) secretion.

GLP-1 is a hormone produced by the intestine that stimulates the release of insulin and inhibits the release of glucagon, which helps to lower blood sugar levels. GLP-1 medications, also known as glucagon-like peptide-1 receptor agonists (e.g. Wegovy, Ozempic, Saxenda, Victoza, etc.), are a type of drug used to treat type 2 diabetes by controlling blood sugar levels and reducing appetite. These medications are typically administered as an injection and have been shown to effectively control blood sugar levels and promote weight loss in individuals with type 2 diabetes. GLP-1 agonists mimic the effects of the natural hormone GLP-1 in the body and stimulate the GLP-1 receptor. This leads to increased glucose-dependent insulin secretion, reduced glucagon secretion, slowed gastric emptying, and increased satiety.

This article aims to provide an overview of the relationship between oral prebiotics and probiotics and GLP-1 secretion and how it can impact on metabolic and gastrointestinal health.

The human gut is a bustling metropolis of microorganisms that play a crucial role in our overall health, particularly in metabolic diseases like obesity and type 2 diabetes (T2D) (1). Recent research has shed light on the intricate dance between gut microbiota and the incretin glucagon-like peptide 1 (GLP-1), revealing potential pathways for innovative treatments.

Gut Microbiota: Our gut microbiota is tiny organisms inside us that do many important things for our bodies. They help with how our food is absorbed, how we digest fiber and break down bile acid. The gut microbiota even affects a substance called GLP-1 which helps us control our blood sugar after eating. This also helps with weight loss. 

The GLP-1 Connection. GLP-1 affects more than just blood sugar and is involved in how the gut bacteria works. Changes in the gut bacteria caused by diet, medicine, or obesity can contribute to T2D. GLP-1 drugs have been successful in treating T2D & obesity and show how important GLP-1 is.

Microbiota and Metabolites: A Symbiotic Relationship The microorganisms in our gut have a close relationship with the metabolites they produce. These metabolites can control the behavior of some cells, known as enteroendocrine cells, and affect hormone production and release. Some of these metabolites, like SCFAs and BAs, can induce the secretion of a hormone called GLP-1. This information suggests that certain dietary interventions, like consuming prebiotics and probiotics, may help fight obesity and Type 2 Diabetes.

The Future of Treatment: Personalized and Precise As we study the relationship between the bacteria in our gut and GLP-1, a hormone that helps regulate blood sugar levels, we're discovering that customized treatments may be the solution for managing metabolic diseases. By adjusting the bacteria in the gut through methods like bariatric surgery or medication, we can potentially improve metabolic health. This shows the potential of personalized medicine and targeting the gut microbiota for therapeutic purposes.

Closing Thoughts. The relationship between the gut microbiome and GLP-1 can be a promising way to treat metabolic diseases. With more research and advancements in technology, it opens up new opportunities for precision medicine where the gut microbiome is not only involved in our health but also becomes a target for treatment.

Kasivit's Gut Support Bundle provides the key ingredients that will help support the gut health, weight control, glucose control, immune support and improve health. 

References:

1. Zeng Y, Wu Y, Zhang Q, Xiao X.2024.Crosstalk between glucagon-like peptide 1 and gut microbiota in metabolic diseases. mBio15:e02032-23.https://doi.org/10.1128/mbio.02032-23