The Relationship Between Metabolic Syndrome Development and Tissue Trace Elements Status and Inflammatory Markers
Sevginur Akdas1, Belma Turan1,2, Aysegul Durak2
1Institute of Health Sciences, Interdisciplinary Food, Metabolism and Clinical Nutrition Department, Ankara University, Ankara, Turkey.
Metabolic syndrome (MetS) is linked to altered zinc and copper levels, impacting inflammatory markers. This study reveals significant tissue-specific changes in zinc and copper, correlating with inflammation in MetS rats.
Area of Science:
- Biochemistry
- Physiology
- Metabolic Disorders
Background:
- Metabolic syndrome (MetS) is characterized by insulin resistance, dyslipidemia, inflammation, and hypertension.
- Trace elements like zinc (Zn) and copper (Cu), along with cytokines, play crucial roles in inflammation and glucose metabolism.
Purpose of the Study:
- To investigate the relationship between cytokine responses and trace element concentrations (Zn and Cu) in various tissues of sucrose-induced MetS rats.
- To compare these levels with those in healthy control rats.
Main Methods:
- Sucrose-induced metabolic syndrome model in rats (n=7 per group).
- Measurement of zinc and copper concentrations in serum and specific tissues (liver, pancreas, kidney, heart).
- Analysis of inflammatory cytokine levels (TNF-α, IL-6) in MetS tissues.
Main Results:
- MetS rats showed decreased Zn in liver and pancreas, and increased Zn in kidney and heart tissues compared to controls.
- Serum Zn levels were lower in MetS rats; serum Cu levels showed no significant difference.
- Kidney tissues in MetS rats exhibited decreased Cu concentration and an increased Zn/Cu ratio. Inflammatory markers TNF-α and IL-6 were elevated in MetS tissues.
Conclusions:
- This study is the first to report Zn and Cu concentrations and their relationship with inflammation in different tissues in MetS.
- Tissue-specific Zn levels, more so than Cu levels, significantly impact MetS pathogenesis.
- A clear relationship exists between Zn and Cu concentrations and inflammatory markers within the pathophysiology of MetS.
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