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Review
. 2024 Oct 10;29(20):4790.
doi: 10.3390/molecules29204790.

Research Progress on the Mechanism for Improving Glucose and Lipid Metabolism Disorders Using Phenolic Acid Components from Medicinal and Edible Homologous Plants

Affiliations
Review

Research Progress on the Mechanism for Improving Glucose and Lipid Metabolism Disorders Using Phenolic Acid Components from Medicinal and Edible Homologous Plants

Miao Sun et al. Molecules. .

Abstract

Glucose and lipid metabolism disorders are the core pathological mechanism of a variety of metabolic diseases, and the incidence of related diseases is increasing year by year, which seriously threatens human life and health. Traditional Chinese medicine with medicinal and edible properties refers to Chinese medicinal resources that have both medicinal and edible characteristics. Due to its safety and its health-promoting and medicinal functions, traditional Chinese medicine has received increasing attention in the development of functional health foods. Phenolic acids are important secondary metabolites that are ubiquitous in medicinal and edible homologous plants, and the regulation of glycolipid metabolism is an important activity and plays a key role in many diseases. In this paper, we focus on the alleviation of glycolipid disorders using MEHH phenolic acids, which regulate glucose metabolism and lipid metabolism, improve insulin resistance, inhibit inflammatory responses, alleviate oxidative stress, and regulate intestinal flora; additionally, we summarize the mechanism in order to provide a reference for MEHH phenolic acids in the treatment of glycolipid metabolism diseases.

Keywords: glycolipid metabolism; homology of medicine and food; plant phenolic acids.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
The structure of phenolic acid compounds in MEHHs.
Figure 2
Figure 2
A demonstration of MEHHs’ phenolic acids regulating pathways in glucose metabolism. The arrow (→) indicates enhancement, while the barred line (┤) signifies inhibition. Glucose metabolism encompasses the synthesis, cleavage, transport, and storage of glucose in living organisms, involving critical pathways such as glycolysis, the tricarboxylic acid cycle, and the processes of glycogen synthesis and breakdown, along with gluconeogenesis. MEHHs’ phenolic acids facilitate glucose uptake, inhibit gluconeogenesis, and enhance glycogen synthesis by increasing the expression or translocation of glucose transporters GLUT4 and GLUT2, thereby balancing blood glucose levels.
Figure 3
Figure 3
Illustration of MEHHs’ phenolic acids regulating lipid metabolism pathways. The arrow (→) indicates enhancement, while the barred line (┤) signifies inhibition. Lipid metabolism, a complex process, involves the synthesis, cleavage, transport, and storage of fats in living organisms. It includes the β-oxidation of fatty acids, cholesterol production, and lipoprotein metabolism, all finely regulated by hormones such as insulin and glucagon. These are crucial for maintaining energy balance, cellular structure, and function. The dysregulation of these pathways can lead to obesity, non-alcoholic fatty liver disease, and other metabolic disorders.
Figure 4
Figure 4
Depiction of how MEHHs phenolic acids regulate the insulin pathway. The arrow (→) indicates enhancement. The insulin signaling pathway plays a crucial role in regulating glucose and lipid metabolism within the body. MEHHs’ phenolic acids lower blood sugar levels by enhancing pancreatic β-cell secretion and promoting glucose uptake, glycogen synthesis, fatty acid synthesis, and storage. In the liver, muscle, and adipose tissue, these phenolic acids facilitate glucose utilization and glycogen synthesis through the activation of specific signal transduction pathways, such as the PI3K-Akt pathway, while concurrently inhibiting gluconeogenesis.
Figure 5
Figure 5
Illustration of MEHHs’ phenolic acids mitigating the inflammatory response by modulating various pathways. The arrow (→) indicates enhancement, while the barred line (┤) signifies inhibition. Disruptions in glycolipid metabolism can result in the accumulation of advanced glycation end products (AGEs) and free fatty acids, which may bind directly to cellular receptors and activate inflammatory signaling cascades. In conditions of insulin resistance, insulin signaling is compromised; however, insulin levels remain elevated, promoting hyperinsulinemia, which can further stimulate the production and release of inflammatory mediators. MEHHs’ phenolic acids counteract inflammatory responses and improve glucose and lipid metabolism disorders by inhibiting signaling pathways such as TLRs, NF-κB, NLRP3, and MAPK.
Figure 6
Figure 6
Illustration of MEHH phenolic acids mitigating oxidative stress by modulating various pathways. The arrow (→) indicates enhancement. Oxidative stress denotes the physiological and pathological responses of cells and tissues to the accumulation of reactive oxygen species (ROS) and reactive nitrogen radicals (RNS) stimulated by harmful internal and external environmental factors. MEHHs phenolic acids counteract oxidative stress and improve disorders in glucose and lipid metabolism by activating Nrf2, reducing ER stress, and regulating associated oxidative factors.
Figure 7
Figure 7
Illustration of the primary mechanisms through which MEHHs phenolic acids modulate intestinal microbiota. The arrow (→) indicates enhancement, while the barred line (┤) signifies inhibition. SCFAs activate GPR41 and GPR43 protein-coupled receptors in intestinal epithelial cells, inducing the production of YY peptide and GLP-1, and promoting the expression of intestinal tight junction proteins such as Zo-1 and occludin. By suppressing LPS expression, MEHHs phenolic acids increase the expression of ZO-1 and GLP-1, enhance the intestinal mucosal barrier, and mitigate disorders in glucose and lipid metabolism.

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