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Review
. 2018 Jan;68(1):19-31.
doi: 10.1007/s12576-017-0571-7. Epub 2017 Sep 30.

"VSports在线直播" Zinc status is associated with inflammation, oxidative stress, lipid, and glucose metabolism

Affiliations
Review

Zinc status is associated with inflammation, oxidative stress, lipid, and glucose metabolism

J Olechnowicz (VSports注册入口) et al. J Physiol Sci. 2018 Jan.

Abstract

A number of studies have reported that zinc plays a substantial role in the development of metabolic syndrome, taking part in the regulation of cytokine expression, suppressing inflammation, and is also required to activate antioxidant enzymes that scavenge reactive oxygen species, reducing oxidative stress. Zinc also plays a role in the correct functioning of lipid and glucose metabolism, regulating and forming the expression of insulin. In numerous studies, zinc supplementation has been found to improve blood pressure, glucose, and LDL cholesterol serum level. Deeper knowledge of zinc's properties may help in treating metabolic syndrome, thus protecting against stroke and angina pectoris, and ultimately against death VSports手机版. .

Keywords: Glucose metabolism; Inflammation; Lipid metabolism; Oxidative stress; Zinc. V体育安卓版.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
The influence of zinc on oxidative stress and inflammation. Zinc prevents the generation of reactive oxygen species through a number of mechanisms. Zn is a cofactor of Cu,Zn-SOD, which catalyzes the dismutation of superoxide. It up-regulates Nrf2, being the principal regulator of antioxidant system functioning, thus increasing GSH synthesis, GPx activity, and other mechanisms of detoxification. Zinc also affects the generation of reactive oxygen species through modulation of prooxidant pathways. Zn-induced decrease in NADPH oxidase activity results in decreased superoxide production. Through induction of metallothionein synthesis, Zn may decrease the availability of redox metals and their participation in Fenton reaction. Susceptibility of proteins to free radical oxidation is also inhibited by zinc through protection of thiol groups. Zn-induced inhibition of redox-sensitive proinflammatory transcription factors is accompanied by decreased production of proinflammatory cytokines, enzymes, and adhesion molecules, thus resulting in the prevention of inflammatory response
Fig. 2
Fig. 2
Functions of ZAG in adipose tissue. Expression of ZAG is down- or up-regulated by the negative or positive stimuli. In adipose tissue, ZAG inhibits FAS and ACC1 activity, thus resulting in decreased fatty acid synthesis. Lower level of free fatty acids together with ZAG-induced increase in adiponectin expression may significantly reduce insulin resistance. Depression of DGAT1 activity suppresses triglyceride synthesis. Together with up-regulation of HSL the latter results in lower lipid deposition in adipose tissue
Fig. 3
Fig. 3
The role of zinc finger proteins and zinc transporters in the regulation of adipogenesis

References

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