Zinc is one of the most important trace elements that plays a vital role in many biological processes, and aberrant zinc metabolism has been implicated in lipid-related metabolic diseases. Previously, we showed that zinc antagonizes iron to regulate sterol regulatory element-binding proteins and stearoyl-CoA desaturase (SREBP-SCD) pathway in lipid metabolism in model organism Caenorhabditis elegans. Here, we further identified another cation diffusion facilitator CDF-1 in addition to SUR-7 in response to zinc to regulate lipid metabolism. Inactivation of SBP-1, the only homolog of SREBPs, leads to increased zinc level but decreased lipid accumulation reversely. However, either cdf-1(n2527) or sur-7(tm6523) mutation could successfully restore the altered fatty acid profile, fat content and zinc level of sbp-1(ep79) mutant. Furthermore, we found that CDF-1/SUR-7 may function bypass SBP-1 to directly affect the conversion activity of SCD in the biosynthesis of unsaturated fatty acids and lipid accumulation. Collectively, these results consistently support the link between zinc homeostasis and lipid metabolism via SREBP-SCD axis by cation diffusion facilitators CDF-1 and SUR-7.

中文翻译：

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阳离子扩散促进剂CDF-1在秀丽隐杆线虫脂质代谢中的作用

锌是最重要的微量元素之一，在许多生物过程中都起着至关重要的作用，异常的锌代谢与脂质相关的代谢性疾病有关。以前，我们显示了锌可拮抗铁，从而在模型生物秀丽隐杆线虫的脂质代谢中调节固醇调节元件结合蛋白和硬脂酰辅酶A去饱和酶（SREBP-SCD）途径。在这里，我们进一步确定了响应锌调节脂质代谢的SUR-7以外的另一种阳离子扩散促进剂CDF-1。SBP-1的唯一同源物SBP-1的失活导致锌水平升高，但脂质堆积反过来降低。但是，cdf-1（n2527）或sur-7（tm6523）突变可以成功地恢复sbp-1（ep79）突变体改变的脂肪酸谱，脂肪含量和锌水平。此外，我们发现CDF-1 / SUR-7可能通过旁路SBP-1直接影响SCD在不饱和脂肪酸的生物合成和脂质积累中的转化活性。总之，这些结果一致地支持了锌稳态和阳离子扩散促进剂CDF-1和SUR-7通过SREBP-SCD轴进行脂质代谢之间的联系。