Quercetin Regulates Lipid Metabolism and Fat Accumulation by Regulating Inflammatory Responses and Glycometabolism Pathways: A Review

Abstract

Fat synthesis and lipolysis are natural processes in growth and have a close association with health. Fat provides energy, maintains physiological function, and so on, and thus plays a significant role in the body. However, excessive/abnormal fat accumulation leads to obesity and lipid metabolism disorder, which can have a detrimental impact on growth and even harm one's health. Aside from genetic effects, there are a range of factors related to obesity, such as excessive nutrient intake, inflammation, glycometabolism disease, and so on. These factors could serve as potential targets for anti-obesity therapy. Quercetin is a flavonol that has received a lot of attention recently because of its role in anti-obesity. It was thought to have the ability to regulate lipid metabolism and have a positive effect on anti-obesity, but the processes are still unknown. Recent studies have shown the role of quercetin in lipid metabolism might be related to its effects on inflammatory responses and glycometabolism. The references were chosen for this review with no date restrictions applied based on the topics they addressed, and the databases PubMed and Web of Sicence was used to conduct the references research, using the following search terms: "quercetin", "obesity", "inflammation", "glycometabolism", "insulin sensitivity", etc. This review summarizes the potential mechanisms of quercetin in alleviating lipid metabolism through anti-inflammatory and hypoglycemic signaling pathways, and describes the possible signaling pathways in the interaction of inflammation and glycometabolism, with the goal of providing references for future research and application of quercetin in the regulation of lipid metabolism.

Keywords: glycometabolism; inflammation; lipid metabolism; obesity; quercetin.

Figure 1

Molecular structure of quercetin, rutin, and its common derivatives.

Figure 2

Potential mechanisms of quercetin regulating inflammation. FFA, free fat acid; TLR4, Toll-like receptor 4; MyD88, myeloiddifferentiationfactor88; NF-κb, nuclear transcription factor-kappa B; MAPK, mitogen-activated protein kinase; ERK, extracellular regulated protein kinases; JNK, c-Jun n-terminal kinase; TNFR, tumor necrosis factor receptor; TNF-α, tumor necrosis factor α; IL-1β, interleukin-1β; IL-6, interleukin-6; AP-1, activator protein 1; and PPARγ, Peroxisome Proliferators-activated Receptor γ; MI, classically activated macrophage.

Figure 3

The possible mechanism of quercetin regulating glycolipid metabolism. FA, fat acid; FFA, free fat acid; ROS, reactive oxygen species; IRS2, insulin receptor substrate 2; Akt, protein kinase b; FOXO1, forkhead box transcription factor O1; Srebf1, sterol regulatory element binding transcription factor 1; Scd1, stearoyl-CoA desaturase 1; PPARγ, Peroxisome Proliferators-activated Receptor γ; GLUT1, recombinant glucose transporter 1; GLUT4, recombinant glucose transporter 4; ChREBP, carbohydrate response element-binding protein; TLR4, Toll-like receptor 4; AdipoR2, adiponectin receptor 2; AMPK, AMP-activated protein kinase; ACC, acetyl CoA carboxylase; PGC-1α, peroxisome proliferative activated receptor-gamma co-activator 1; and CREB, cAMP-response element binding protein; MI, classically activated macrophage.