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Review
. 2024 Oct 11;16(20):3447.
doi: 10.3390/nu16203447.

Harnessing Prebiotics to Improve Type 2 Diabetes Outcomes

Oana C Iatcu  1 , Sevag Hamamah  2   3 , Mihai Covasa  1   2
Affiliations
Review

Harnessing Prebiotics to Improve Type 2 Diabetes Outcomes

Oana C Iatcu et al. Nutrients. .

Abstract

The gut microbiota, a complex ecosystem of microorganisms in the human gastrointestinal tract (GI), plays a crucial role in maintaining metabolic health and influencing disease susceptibility. Dysbiosis, or an imbalance in gut microbiota, has been linked to the development of type 2 diabetes mellitus (T2DM) through mechanisms such as reduced glucose tolerance and increased insulin resistance. A balanced gut microbiota, or eubiosis, is associated with improved glucose metabolism and insulin sensitivity, potentially reducing the risk of diabetes-related complications. Various strategies, including the use of prebiotics like inulin, fructooligosaccharides, galactooligosaccharides, resistant starch, pectic oligosaccharides, polyphenols, β-glucan, and Dendrobium officinale have been shown to improve gut microbial composition and support glycemic control in T2DM patients. These prebiotics can directly impact blood sugar levels while promoting the growth of beneficial bacteria, thus enhancing glycemic control. Studies have shown that T2DM patients often exhibit a decrease in beneficial butyrate-producing bacteria, like Roseburia and Faecalibacterium, and an increase in harmful bacteria, such as Escherichia and Prevotella. This review aims to explore the effects of different prebiotics on T2DM, their impact on gut microbiota composition, and the potential for personalized dietary interventions to optimize diabetes management and improve overall health outcomes.

Keywords: inulin; oligosaccharides; polyphenols; resistant starch; β-glucan.

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Conflict of interest statement

The authors declare no conflicts of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of the data; in the writing of the manuscript; or in the decision to publish the results.

Figures

Figure 1
Figure 1
Suggested daily intake of inulin and the richest food sources. Inulin content is listed per 100 g of product.
Figure 2
Figure 2
Suggested daily intake of resistant starch and the richest food sources. Resistant starch content is listed per 100 g of product. RS, resistant starch.
Figure 3
Figure 3
Suggested daily intake of fructooligosaccharides and the richest food sources. Fructooligosaccharide content is listed per 100 g of product. FOS, fructooligosaccharide.
Figure 4
Figure 4
Suggested daily intake of galactooligosaccharides and the richest food sources. Galactooligosaccharide content is listed per 100 g of product. GOS, galactooligosaccharide.
Figure 5
Figure 5
Schematic representation of gut microbiota composition in T2DM patients following administration of inulin, fructooligosaccharides, galactooligosaccharides, resistant starch, pectic oligosaccharides, polyphenols, β-glucans, and Dendrobium officinale. A green arrow indicates an increase or decrease in the abundance of bacteria that are typically less or more abundant in the gut microbiota of T2DM patients, contributing to a balanced microbial composition. A red arrow indicates potential increases in bacteria whose abundance is associated with T2DM patients or a decrease in beneficial bacteria that are typically less abundant in these patients. PP, polyphenol; RS, resistant starch; POS, pectic oligosaccharide; FOS, fructooligosaccharide; GOS, galactooligosaccharide; DO, Dendrobium officinale; Bif., Bifidobacterium; ↑, increase; ↓, decrease.
Figure 6
Figure 6
Microbiota-related mechanisms by which prebiotics improve glycemic indices. Short-chain fatty acids: Butyrate, propionate, and acetate enhance AMPK signaling in hepatic cells which inhibits gluconeogenesis through downstream signaling pathways. AMPK improves glucose oxidation for better uptake into tissue. These changes contribute to decreased blood glucose and improve insulin resistance. Anti-inflammatory: Inflammatory states in T2DM are associated with harmful bacterial overgrowth, leading to compromised intestinal barrier integrity and endotoxemia, where lipopolysaccharides (LPSs) leak into the bloodstream, causing metabolic inflammation. This process negatively impacts insulin resistance. Conversely, prebiotics enhance gut microbial composition, promoting better barrier integrity. These positive changes reduce the phosphorylation of insulin receptor substrate 1 (IRS1), improving downstream signaling and enhancing insulin sensitivity. Lipid profile: Prebiotics downregulate acetyl-CoA carboxylase (ACC) and fatty acid synthase (FASs), as well as peroxisome proliferator-activated receptor gamma (PPARγ). This promotes reduced total cholesterol and LDL while improving glucose control. Incretin Hormones: Prebiotics increase colonic microbial composition promoting the density of GPR43 receptors in the distal gastrointestinal tract. GPR43 activation leads to the induction of glucagon-like receptor 1 (GLP-1) and peptide YY (PYY) secretion, which improve postprandial insulin release and reduce postprandial glucose. Antioxidant properties: Prebiotics promote nuclear factor erythroid 2-related factor (Nrf2) transcription which induces the release of antioxidases. Antioxidases reduce reactive oxygen species (ROS) to reduce IRS1 phosphorylation and improve pancreatic β-cell survival, collectively improving insulin sensitivity. Abbreviations: AMPK, AMP-activated protein kinase; IRS1, insulin receptor substrate 1; p-IRS1, phosphorylated IRS1; PI3K, phosphoinositide 3 kinase; ACC, acetyl-CoA carboxylase; FAS, fatty acid synthase; PPARγ, peroxisome proliferator-activated receptor gamma; TC, total cholesterol; LDL, low-density lipoprotein; EECs, enteroendocrine cells; GLP-1, glucagon-like peptide 1; PYY, peptide YY; GPR43, G-coupled receptor 43; Nrf2, nuclear factor erythroid 2-related factor; ROS, reactive oxygen species.
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