Is Lipopolysaccharide-Induced Lipid Metabolism Disorder in Testis of Rats a Consequence of Plasma Lipid Changes?

Abstract

Purpose The systemic infection and inflammation can result in testes injury, whereas the exact mechanism is unknown. The lipid metabolism has a dual impact on controlling metabolism and inflammation, which is a potential pathway. The objective of this study was to determine if changes in plasma lipids during lipopolysaccharide (LPS)-induced systemic inflammation affect the dysregulation of testes lipid metabolism. Materials and Methods LPS (5 mg/kg) was used to induce systemic inflammation in rats after a single intraperitoneal injection. After 4 weeks, the rats were sacrificed, and the serum and testes were used for laboratory measurements and histology examination. Plasma and testis were used for lipidomics analysis based the liquid chromatography-mass spectrometry. Spearman rank correlation analysis was used to compare the correlation of differential lipids in phospholipids, glycerolipids, and sphingolipids between testis and plasma. Results LPS raised the levels of cytokines in serum and testis, decreased the activities of antioxidant enzymes, increased the levels of lipid peroxidation products, and damaged testis tissue. In testis and plasma, 146 and 401 differential lipids, mostly phosphatidylcholine, phosphatidylethanolamine an so on, were found in comparison to the control group. Correlation analysis produced a total of 2528 correlation coefficients, 1150 of which were P<0.05 and accounted for 45.49%. Conclusion The changes of lipid composition and content in the testis are related to cytokine overload and oxidative stress. Testis lipid metabolism disorders caused by LPS-induced systemic inflammation are lack of a correlation with plasma lipid changes, and are likely owing to interference with the testis itself.

Chronic oral LPS administration does not increase inflammation or induce metabolic dysregulation in mice fed a western-style diet

“…The metabolic syndrome and associated diseases are characterized by a state of dyslipidemia. Recent studies have proposed that LPS is an relevant regulator of areas in lipid metabolism such as modifying plasma lipid levels ( 76 ) and activating cholesterol metabolism processes ( 77 ), further connecting LPS to dyslipidemia and systemic inflammation. Even though our results point to little or no metabolic dysregulation, a limitation of this study is that we did not explore LPS’ effect on lipid metabolism or markers of sustained inflammation such as gene expression in the liver or relevant biomarkers in plasma.…”