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[作为代谢活跃组织的表皮:屏障功能对脂质合成的调节]

[The epidermis as metabolically active tissue: regulation of lipid synthesis by the barrier function].

作者信息

Proksch E

机构信息

Abteilung Dermatologie-Venerologie I, Georg-August-Universität Göttingen.

出版信息

Z Hautkr. 1990 Mar;65(3):296-300.

PMID:2187311
Abstract

Numerous investigations have shown that the lipids of the horny layer play an important role in the epidermal barrier function. These lipids consist of sphingolipids, cholesterol, and free fatty acids in nearly equimolar proportions. If the barrier function is disturbed--i.e. in case of lipid extraction or a diet deficient of essential fatty acids--we find an increased synthesis of free fatty acids, cholesterol, and non-saponifiable lipides in the epidermis. Covering the skin with a Latex wrap prevents an increased lipid synthesis. The synthesis of cholesterol depending on the barrier function is regulated by the enzyme HMG CoA reductase. The regulation process involves both the quantity and the activity (phosphorylation) of the enzyme. Acute disruption of the permeability barrier results in an increased synthesis of cholesterol in the lower epidermis, whereas in case of chronic barrier disorders, the specific increase takes place in the upper dermis. A reduction of the cholesterol synthesis by the HMG CoA reductase inhibitor Lovastatin leads to a disturbed permeability barrier and epidermal hyperplasia.

摘要

大量研究表明,角质层脂质在表皮屏障功能中起重要作用。这些脂质由鞘脂、胆固醇和游离脂肪酸组成,比例近乎等摩尔。如果屏障功能受到干扰——例如在脂质提取或必需脂肪酸缺乏的饮食情况下——我们会发现表皮中游离脂肪酸、胆固醇和非皂化脂质的合成增加。用乳胶包裹皮肤可防止脂质合成增加。依赖屏障功能的胆固醇合成由HMG CoA还原酶调节。调节过程涉及该酶的数量和活性(磷酸化)。通透性屏障的急性破坏导致下表皮胆固醇合成增加,而在慢性屏障紊乱的情况下,特定的增加发生在上真皮层。HMG CoA还原酶抑制剂洛伐他汀降低胆固醇合成会导致通透性屏障紊乱和表皮增生。

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