Dipartimento di Scienze e Tecnologie Ambientali, Biologiche e Farmaceutiche, Università degli studi della Campania "Luigi Vanvitelli", Caserta, Italy.
Dipartimento di Scienze e Tecnologie, Università degli studi del Sannio, Benevento, Italy.
J Exp Zool A Ecol Integr Physiol. 2022 Dec;337(9-10):1025-1038. doi: 10.1002/jez.2646. Epub 2022 Aug 4.
The Harderian gland (HG) of Rattus norvegicus is an orbital gland secreting lipids that accumulate in excess under condition of increased lipid metabolism. To study the response elicitated by lipid overload in rat HG, we housed the animals in thermoneutral conditions (28-30°C) in association to high fat diet (HFD). In HFD rats alterated blood lipid levels result in lipid accumulation in HG as demonstrated by the increased gland weight and histochemical/ultrastructural analyses. The HFD-caused oxidative stress forces the gland to trigger antioxidant defense mechanisms and autophagic process, such as lipophagy and mitophagy. Induction of mitochondrial DNA (mtDNA) damage and repair was stronger in HFD-rat HGs. An increase in marker expression levels of mitochondrial biogenesis, fission, and fusion occurred to counteract mtDNA copy number reduction and mitophagy. Therefore, the results demonstrate that rat HG activates autophagy as survival strategy under conditions of increased lipid metabolism and suggest a key role for mitophagy and membrane dynamics in the mitochondrial adaptive response to HFD.
大鼠的哈德氏腺（HG）是一种眶内腺体，分泌脂质，在脂质代谢增加的情况下会过量积累。为了研究脂质过载在大鼠 HG 中引发的反应，我们将动物饲养在温度适中的条件下（28-30°C），并给予高脂肪饮食（HFD）。在 HFD 大鼠中，改变的血脂水平导致 HG 中的脂质积累，如增加的腺体重量和组织化学/超微结构分析所示。HFD 引起的氧化应激迫使腺体触发抗氧化防御机制和自噬过程，如脂自噬和线粒体自噬。HFD-大鼠 HG 中的线粒体 DNA（mtDNA）损伤和修复诱导更强。线粒体生物发生、分裂和融合的标志物表达水平增加，以抵消 mtDNA 拷贝数减少和线粒体自噬。因此，这些结果表明，大鼠 HG 在脂质代谢增加的情况下激活自噬作为生存策略，并表明线粒体自噬和膜动力学在 HFD 适应反应中起关键作用。
