Sunday, March 31, 2013

Skin Lipids

Sebum 

In addition to keeping the skin and hair supple, sebum also has antimicrobial properties.  The sebaceous glands are an important part of the innate immune system and function like an immune organ (they are regulated by things such as corticotrophin releasing hormone and vitamin D) [1].  The sebaceous gland also transports antioxidants in and onto the skin, regulates bacterial populations by having pro and anti-inflammatory functions and is involved in the wound healing process [2]

[3]

People with acne secrete 59% more sebum and the quality of sebum is also different.  The major differences are that people with acne secrete 120% more squalene, 84% more triglycerides and 21% less free fatty acids than controls [4] 

* The wax esters and squalene are unique to sebum and not found elsewhere in the body [3] 

Fatty Acids 

Fatty Acids in Sebum 

Triglycerides and free fatty acids make up about 57.5% of sebum.  Sebum has many of the usual but also some different fatty acids: 

  • Sapienic acid (16:1 cis n-10), which is unique to humans (hence the name).  Delta-6-desaturase converts palmitic acid (16:0) to sapienic acid
  • Sebaleic acid (18:2 cis n-10).  Elongase and desaturase enzymes convert sapienic acid to sebaleic acid [3]

* Humans are also the only animal that has triglycerides in their sebum and the only animal that normally gets acne [5] 

Linoleic Acid

People with acne may have a lower proportion of linoleic acid (LA) in their keratinocytes in the follicle wall. This may be because LA is an essential fatty acid and people with acne produce more sebum, which may dilute LA (sebum excretion is inversely correlated with LA). When sebaceous glands are deficient in LA they synthesise more sabeleic acid as an alternative PUFA. However, this leads to poor epidermal barrier function (remember that the skin is a barrier to the outside world), which can lead to water loss and then keratinocyte hyperproliferation*, pro-inflammatory cytokine release (from keratinocytes into the dermis), and allow P. acnes colonisation through barrier loss and increasing water [3] [5] [6] [7] [8] [9].

LA also inhibits ROS generation by neutrophils [10] and low LA may be a cause of the elevated IL-1 in people with acne, prior to comedone formation [5].

* Impaired water barrier function is also seen in diseases of hyperkeratosis [9] 

SFAs and MUFAs 

People with acne have a lower ratio of 16:0/16:1 ratio in triglycerides and wax esters [3] and from an acne point of view MUFAs aren’t that great for the following reasons: 

  • A higher proportion of MUFAs in sebum is associated with more sebum production and acne lesions, which is consistent with adolescents, who have a higher proportion of sapienic acid, produce more sebum and are more likely to get acne [11]
  • MUFA can alter keratinocyte proliferation and differentiation [2].  Topical application of MUFAs (oleic acid and palmitoleic acid) caused scaly skin, abnormal keratinization and epidermal hyperplasia whereas triglycerides and SFA didn’t have that effect [11]
  • A low glycemic load diet (but also better food quality) increases the SFA:MUFA ratio in sebum and improved acne (see picture below for mechanisms).  An increase in the SFA:MUFA ratio in sebum predicts improvement in acne [11] 

Lauric acid is one the free fatty acids found in sebum.  It has strong antimicrobial activity in vitro against skin bacteria including P. acnes and topical application or intradermal injection of lauric acid reduces inflammation caused by P. acnes and reduces the number of bacteria.  Palmitic acid, oleic acid and sapienic acid [1] also have some antimicrobial properties and increase antimicrobial peptides in sebocytes [2] 

* The SFAs in sebum are mainly palmitic acid while the MUFAs in sebum are mainly sapienic acid and palmitoleic acid.

[11]

No comments:

Post a Comment