Abstract

Hydroxycinnamic acid derivatives are important class of polyphenolic compounds originated from the Mavolanate-Shikimate biosynthesis pathways in plants. Several simple phenolic compounds such as cinnamic acid, p-coumaric acid, ferulic acid, caffeic acid, chlorgenic acid, and rosmarinic acid belong to this class. These phenolic compounds possess potent antioxidant and anti-inflammatory properties. These compounds were also showed potential therapeutic benefit in experimental diabetes and hyperlipidemia. Recent evidences also suggest that they may serve as valuable molecule for the treatment of obesity related health complications. In adipose tissues, hydroxycinnamic acid derivatives inhibit macrophage infiltration and nuclear factor κB (NF-κB) activation in obese animals. Hydroxycinnamic acid derivatives also reduce the expression of the potent proinflammatory adipokines tumor necrosis factor-α (TNFα), monocyte chemoattractant protein-1 (MCP-1), and plasminogen activator inhibitor type-1 (PAI-1), and they increase the secretion of an anti-inflammatory agent adiponectin from adipocytes. Furthermore, hydroxycinnamic acid derivatives also prevent adipocyte differentiation and lower lipid profile in experimental animals. Through these diverse mechanisms hydroxycinnamic acid derivatives reduce obesity and curtail associated adverse health complications.

Highlights

  • Metabolic syndrome is a cluster of non-communicable diseases includes central obesity, diabetes, insulin resistance, hypertension and dyslipidemia

  • Recent research has provided the scientific benefit of these phenolic acids and confirmed the important role of phenolic acids in the prevention and treatment of obesity, diabetes and associated disorders

  • Phenolic acids could favourably affect most of the leading aspects of obesity including diabetes, including insulin resistance, hyperglycemia, hyperlipidemia, and adepocyte dysfunction and inflammation (Fig. 3)

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Summary

Background

Metabolic syndrome is a cluster of non-communicable diseases includes central obesity, diabetes, insulin resistance, hypertension and dyslipidemia. AMPK regulated PPAR-γ and PGC1α activation stimulated most of the transcriptional signal to increase fatty acid oxidation and mitochondrial function [30,31,32]. Resveratrol increased insulin sensitivity, reduced insulin-like growth factor-1 (IGF-I) levels, increased AMP-activated protein kinase (AMPK) and peroxisome proliferatoractivated receptor-gamma co-activator-1α (PGC-1α) activity, increased mitochondrial number, and improved motor function in middle-aged mice fed a high-calorie diet [62]. Ferulic acid prevented the production of TNF-alpha and decreased Macrophage inflammatory protein-2 (MIP-2) levels in lipopolysaccharide (LPS)-stimulated RAW264.7 cells [82]. - Lowered plasma cholesterol by reducing the activity of fatty acid synthase and HMG-CoA reductase and increased the fatty acid beta oxidation. Caffeic acid supplementation reduced the inflammatory cytokines interleukin (IL)-beta, IL-6, tumor necrosis factor (TNF)-alpha and monocyte chemoattractant protein (MCP)-1 concentration in diabetic mice [16]. - o-coumaric acid inhibited GPDH activity and the expression of PPARγ, C/EBPα and leptin and up-regulated expression of adiponectin

T3-L1 adipocytes
Conclusion
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