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Review
. 2024 May 27;16(11):1641.
doi: 10.3390/nu16111641.

The Effects of Antioxidant Supplementation on the Pathologic Mechanisms of Metabolic Syndrome and Cardiovascular Disease Development

Hiva Sharebiani  1   2 , Mina Mokaram  2   3 , Melika Mirghani  1   2 , Bahare Fazeli  1   2 , Agata Stanek  1   4
Affiliations
Review

The Effects of Antioxidant Supplementation on the Pathologic Mechanisms of Metabolic Syndrome and Cardiovascular Disease Development

Hiva Sharebiani et al. Nutrients. .

Abstract

In people with obesity, diabetes, and hypertension, lipid and glucose metabolism and oxidative stress generation interact. This condition, known as a "metabolic syndrome" (MetS), presents a global challenge and appears to be the underlying mechanism for the development of cardiovascular diseases (CVDs). This review is designed based on evidence indicating the pathogenic mechanisms of MetS. In detail, we will look at the mechanisms of oxidative stress induction in MetS, the effects of elevated oxidative stress levels on the condition's pathophysiology, and matters related to endothelial function. According to different components of the MetS pathophysiological network, the effects of antioxidants and endothelial dysfunction are reviewed. After considering the strategic role of oxidative stress in the pathophysiology of MetS and its associated CVDs, oxidative stress management by antioxidant supplementation seems an appropriate therapeutic approach.

Keywords: antioxidant supplementation; hypertension; metabolic syndrome; obesity; oxidative stress.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Interactions of the MetS components, obesity, diabetes, and hypertension. FFA: free fatty acid; RAAS: renin–angiotensin–aldosterone system; ↑: increase; ↓: decrease.
Figure 2
Figure 2
The role of obesity, diabetes, and hypertension in inducing oxidative stress. FFA: free fatty acid; Ang II: angiotensin II; ET-1: endothelin-1; GSH: glutathione; AT: adipose tissue; ROS: reactive oxygen species; PKC: protein kinase C; NOX: NADPH oxidase; XO: xanthine oxidase; NF-κB: nuclear factor-κB; ↑: increase; ↓: decrease.
Figure 3
Figure 3
The effects of oxidative stress on obesity, diabetes, and the vascular system. FFA: free fatty acid; AT: adipose tissue; PKC: protein kinase C; NF-κB: nuclear factor-κB; NO: nitrite oxide; MAPK: nitrogen-activated protein kinase, PI3K: phosphoinositide 3-kinases; JNK: Jun N-terminal kinase; IRS-1: Insulin receptor substrate 1; ↑: increase; ↓: decrease.
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