Oily skin, Skin lipids dysregulation

Sebaceous glands can be proinflammatory independent of p.acnes

Although lipogenesis and inflammation are induced by certain propionobactrium acnes strains, sebaceous glands also express proinflammatory cytokines and produce free fatty acids in the absence of bacteria [14]. This may explain a role independent from that of p.acnes for sebaceous gland hyperactivity in pathogenesis of oily skin in acne vulgaris. The same authors [14] suggest generation of antimicrobial peptides by p.acnes in absence of inflammation and proinflammatory cytokines. On the other hand, diets rich in docosahexaenoic acid/eicosapentaenoic acid (DHA/EPA) and gamma-linolenic acid (GLA) have been shown to incorporates metabolites of these fatty acids to epidermal phospholipids, which, in turn, leads to inhibition of leukotriens at the skin level [15].

Alpha linolenic acid activation of PPAR gamma

Another study by Strauss JS, et al substantiates inhibitory role of unsaturated essential fatty acids in sebum secretion. The oral administration of eicosa-5:8:11:14-tetrayonic acid, an unsaturated fatty acid, produced a 44% decrease in sebum production in each of 16 male subjects studied [16]. This may be due to impaired conversion of linoleate to pro-inflammatory-arachidonate as the same inhibition happens in hepatocytes [17]. These inflammatory molecules can be stimulatory to sebaceous glands and cause an oily skin. Another mechanism that may explain this is study by Zhao et al, suggesting that linoleic acid, alpha linolenic acid (ALA) and docosahexaenoic acid (DHA) attenuate the NF-kB mediated host immune defense via activation of peroxisome proliferator-activated receptor-gamma (PPAR gamma) [18]. Terminal sebocyte differentiation is assisted by PPAR-gamma [19].

Gamma linolenic acid inhibitor of 5-alpha-reductase

Increase in plasma androgen level induced by steroids cause an increase in cholesterol and free fatty acids in skin surface. Some essential fatty acids such as gamma linolenic acid are potent 5-alpha-reductase inhibitors, suggesting a linkage between unsaturated fatty acids and androgen action [20]. In adult skin androgen action is dependent to conversion of testosterone to five-alpha-dihydrotestosterone. This conversion takes place under enzymatic act of five-alpha-reductase. Cultured sebocytes strongly express 5-alpha-reducatase and 5-alpha-DHT [21]. Hypersensitivity of androgen receptors in pilosebaceous duct and the resulting increase in sebum production and oily skin appears to be associated with a significant increase in free fatty acids rather than other surface skin lipids.

Discussion and conclusion

High skin’s lipid production and the resulting low level of linoleic acid leads to hyperkeratosis, impaired epidermal barrier function and comedo formation. Stimulation of sebocyte proliferation by insulin, thyroid-stimulating hormone and hydrocortisone indicates that the hormonal control of the sebaceous gland is a complex mechanism [21]. Can providing the skin with essential linoleates prevent comedo formation and aid excessively-oil-forming skin to manage itself? A study reports that stratum corneum sphingolipids of adult acne patients is lower than that in control subjects. Decrease in sphingolipids content of cell walls contributes to diminished water barrier function which, in turn, leads to increased permeability to inflammatory substances and comedo formation . All these studies support use of unsaturated fatty acids in treatment of oily skin in acne vulgaris and call for a campaign against long-been-supported and conventionally-recommended oil-free products by physicians for acne patients.

Our hypothetical idea is that hypersensitive overworked sebaceous glands in an acne patient do not operate to produce their high-end products such as linoleates, rather, their overflow is associated with cheap secretions from less-differentiated sebocytes such as free fatty acids. There is an inverse relationship between secretion rates and the linoleate content of the surface wax esters. The question that whether local supply of essential fatty acids down regulate the overworked sebaceous glands is supported by studies of Letawe C, et al. Topical application of linoleic acid resulted in significant decrease in size of follicular casts and microcomedones [22]. Another study by Charakida ,et al indicates 53% in sebum production and significant improvement in lesions assessed by Leeds acne grading system by using ethyl linoleate for 4 weeks [23]. Moreover, linoleic acid significantly decreases phagocytosis and reactive oxygen species generated by neutrophils [24]. Thus, a practical role for lipid dysregulation in acne pathogenesis and its correction stays a demanding area for research in treatment and regulation of squalene peroxidation generated by neutrophils gland hyperactivity.

A supplementary note: Sebaceous gland localization, facial or body acne, testosterone or DHT

Stimulatory effect of androgens on sebocytes has been well known in vitro and in vivo. However, various species of androgens function differently on sebcacous glands locationwise. Facial sebocytes are under influence of testosterone and dihydrotestosterone (DHT) with later having the strongest effect while body sebocytes are up regulated by dihydrotestosterone (DHT) and their proliferation affected negatively by testosterone [25]. Inhibitory effect of acylceramide with linoleic acid on keratinocytes hyperplasia induced by UVB exposure [26].

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