Reply to Klevay, L.M. Comment on “Huang et al. Influence of Varied Dietary Cholesterol Levels on Lipid Metabolism in Hamsters. Nutrients 2024, 16, 2472”
Chung-Hsiung Huang, Hung-Sheng Hsu, Meng-Tsan Chiang

Abstract
Genes, proteins, chemicals, diseases, species, mutations and cell lines named across the full text — each resolved to its canonical identifier and authoritative record.
Peer Reviews
No public reviews on file for this paper yet. If you reviewed it on a platform where reviews are public (OpenReview, ICLR, NeurIPS, ICML), you can paste yours below so the community can read it here.
Videos
No videos yet. Explain this paper in a talk, walkthrough, or lecture? Add one.
Taxonomy
TopicsAdipose Tissue and Metabolism · Cancer, Lipids, and Metabolism · Adipokines, Inflammation, and Metabolic Diseases
Thank you for your insightful comments and suggestions [1]. We agree with your point that copper deficiency induced by cholesterol feeding has been well established in previous studies [2,3]. Our findings of decreased hepatic glutathione levels, which resemble those observed in copper-deficient models [4], highlight the potential role of oxidative stress in cholesterol-induced cardiovascular processes.
Regarding the observed decrease in lipid peroxidation despite the apparent copper deficiency, we acknowledge the complexity of this relationship. Variability in the effects of copper deficiency on lipid peroxidation has been noted, with reports of a wide range of metabolic changes [5]. This variability may suggest that lipid peroxidation is comparatively resistant to copper deficiency in certain contexts, which warrants further investigation.
We appreciate your suggestion to include a dietary copper supplementation group in our experiments. We agree that measuring copper status via markers such as serum copper, ceruloplasmin, and superoxide dismutase (SOD) would provide valuable insights into the role of copper in our observed changes. As noted, SOD, in particular, is an important antioxidant enzyme that may play a critical role in mitigating oxidative damage [6]. We will consider incorporating these measurements in future studies to better understand how copper status influences the outcomes in our cholesterol-fed hamster model.
Thank you again for your helpful feedback, which will inform our future research direction.
The reference list from the paper itself. Each links out to its DOI / PubMed record.
- 1Klevay L.M. Comment on Huang et al. Influence of Varied Dietary Cholesterol Levels on Lipid Metabolism in Hamsters. Nutrients 2024, 16, 2472 Nutrients 202517194410.3390/nu 17121944 PMC 1131402239125351 · doi ↗ · pubmed ↗
- 2Klevay L.M. Metabolic interactions among dietary cholesterol, copper, and fructose Am. J. Physiol. Endocrinol. Metab.2010298 E 138E 13910.1152/ajpendo.00591.200920009038 · doi ↗ · pubmed ↗
- 3Klevay L.M. Dietary cholesterol lowers liver copper in rabbits Biol. Trace Elem. Res.198816515710.1007/BF 027953332484535 · doi ↗ · pubmed ↗
- 4Wei T. Wang Q. Chen T. Zhou Z. Li S. Li Z. Zhang D. The possible association of mitochondrial fusion and fission in copper deficiency-induced oxidative damage and mitochondrial dysfunction of the heart J. Trace Elem. Med. Biol.20248512748310.1016/j.jtemb.2024.12748338878467 · doi ↗ · pubmed ↗
- 5Chhetri S.K. Mills R.J. Shaunak S. Emsley H.C. Copper deficiency BMJ 2014348 g 369110.1136/bmj.g 369124938531 · doi ↗ · pubmed ↗
- 6Linder M.C. Biochemistry of Copper Springer Science & Business Media Berlin, Germany 2013 Volume 10
