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Barrier repair, regulation of cell membrane fluidity, effects on keratinization

Important Chemical Components:

Sterols, phospholipids

Origin Classification:

Naturally occurs in animal fats including cheese, egg yolks, beef, poultry, fish, and breast milk. Flaxseed and peanuts contain cholesterol-like components called phytosterols.1,2

Personal Care Category:

Emollient, occlusive, moisturizer

Recommended for the following Baumann Skin Types:



Cholesterol is found in all biologic membranes including keratinocytes, where it is organized into “lipid rafts.”3,4 Cholesterol sulfate is very abundant in the epidermis with the highest levels found in the granular layer. Amounts of cholesterol sulfate decline progressively from the granular layer to the outer stratum corneum (SC).5


Cholesterol is readily available in the diet and basal keratinocytes are capable of absorbing cholesterol from the circulation (Table 21-1). Cholesterol absorption by keratinocytes is regulated in part by peroxisome proliferator-activated receptors (PPARs) and retinoid X receptors. These have been found to play a role in transporting cholesterol across keratinocyte cell membranes by increasing expression of ATP-binding cassette transporter (ABCA1), a membrane transporter that regulates cholesterol efflux.6 Low-density lipoprotein (LDL) receptors may play a role in the absorption of cholesterol by skin cells. Although LDL receptors are not expressed on basal keratinocytes when the barrier is normal, when the barrier is first perturbed, LDL mRNA and protein levels and apolipoprotein E (ApoE) expression rise.7,8 In chronic barrier disruption, the keratinocytes express LDL receptors.9 Increased expression of LDL or ApoE can augment delivery of exogenously applied cholesterol to suprabasal keratinocytes. Most of the cholesterol in skin, however, is not derived from diet but, rather, is synthesized by skin cells.

TABLE 21-1Influence on Cholesterol Synthesis

Endogenous Synthesis

Most cholesterol in the skin is synthesized in keratinocytes by the enzyme cholesterol sulfotransferase type 2B isoform 1b, abbreviated as SULT2B1b (Table 21-2). The rate-limiting enzyme in this process is 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (see Figure 21-1 for the pathway of cholesterol synthesis). A group of transcription factors known as sterol regulatory element-binding proteins (SREBPs) also regulate cholesterol and fatty acid synthesis. When epidermal sterols decline, SREBPs are activated via proteolytic processes. The SREBPs enter the cell nucleus and activate genes leading to increased synthesis of cholesterol.10,11 There are three known types of SREBPs: SREBP-1a, SREBP-1c, and SREBP-2. In human keratinocytes, SREBP-2 has been shown to be the predominant type and is involved in regulating cholesterol production.11

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