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Review
. 2023 Feb 28;12(5):1023.
doi: 10.3390/foods12051023.

The Interplay of Dietary Fibers and Intestinal Microbiota Affects Type 2 Diabetes by Generating Short-Chain Fatty Acids

Muhammad Mazhar  1 , Yong Zhu  2 , Likang Qin  1   2
Affiliations
Review

The Interplay of Dietary Fibers and Intestinal Microbiota Affects Type 2 Diabetes by Generating Short-Chain Fatty Acids

Muhammad Mazhar et al. Foods. .

Abstract

Foods contain dietary fibers which can be classified into soluble and insoluble forms. The nutritional composition of fast foods is considered unhealthy because it negatively affects the production of short-chain fatty acids (SCFAs). Dietary fiber is resistant to digestive enzymes in the gut, which modulates the anaerobic intestinal microbiota (AIM) and fabricates SCFAs. Acetate, butyrate, and propionate are dominant in the gut and are generated via Wood-Ljungdahl and acrylate pathways. In pancreatic dysfunction, the release of insulin/glucagon is impaired, leading to hyperglycemia. SCFAs enhance insulin sensitivity or secretion, beta-cell function, leptin release, mitochondrial function, and intestinal gluconeogenesis in human organs, which positively affects type 2 diabetes (T2D). Research models have shown that SCFAs either enhance the release of peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) from L-cells (entero-endocrine), or promotes the release of leptin hormone in adipose tissues through G-protein receptors GPR-41 and GPR-43. Dietary fiber is a component that influences the production of SCFAs by AIM, which may have beneficial effects on T2D. This review focuses on the effectiveness of dietary fiber in producing SCFAs in the colon by the AIM as well as the health-promoting effects on T2D.

Keywords: dietary fibers; fermentation; intestinal microbiota; short-chain fatty acids; type 2 diabetes.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Dietary fiber classification based on water solubility/insolubility.
Figure 2
Figure 2
Schematic presentation of three pathways that contribute to disposing of excess reducing equivalents. (A) Reduction of pyruvate into lactate, thereby reducing NADH, pyruvate; ferredoxin oxidoreductase and hydrogenase/NADH; ferredoxin oxidoreductase and hydrogenase dispose of reducing equivalents into molecular hydrogen and NADH is reduced via electron transport chain. (B) Acetate is formed directly from acetyl CoA through the Wood–Ljungdahl pathway. Propionate is formed from PEP via succinate decarboxylation pathway or acrylate pathway while reducing propionate. (C) Butyrate is shaped by condensing acetyl CoA (two molecules) in the presence of butyrate kinase or by employing exogenously derived acetate through butyryl-CoA: acetate-CoA transferase. Abbreviations: NADH; nicotinamide adenine dinucleotide (NAD) + hydrogen (H): ACA; acetyl coenzyme A: H; Hydrogen: CO2; carbon dioxide: CH3; methyl radical: CH4; methane.
Figure 3
Figure 3
Gut microbiota ferments dietary fiber and produces short-chain fatty acids (SCFAs) acetate, propionate, and butyrate. These SCFAs may facilitate the production/release of GLP-1 and PYY from enteroendocrine (L-cells) and activate adipose tissue to release leptin hormone. These fatty acids also enhance insulin sensitivity and mitochondrial functions in muscle cells, promote pancreatic functions, including insulin secretion and beta cell activity, and promote intestinal gluconeogenesis. In the liver, lipid accumulation, and glucose production are reduced. Arrows pointing upwards indicate an increase, and arrows pointing downwards indicate a decrease. Abbreviations: PYY; peptide YY: GLP-1; glucagon-like peptide-1: GPR-41; G-protein receptors-41: GPR-43; G-protein receptors-43.
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