ABSTRACT
In mammals, dietary linoleic acid (18:2n-6) is metabolized by ∆6-desaturase to form γ-linolenic acid (GLA, 18:3n-6), which is rapidly elongated to form dihomo-γlinolenic acid (DGLA, 20:3n-6). DGLA is then desaturated by ∆5-desaturase to form arachidonic acid (AA, 20:4n-6). DGLA and AA are precursors of 1-and 2-series of prostaglandins (PGs) and thromboxanes (TXs), respectively, which regulate a wide range of physiological functions. In this pathway, the desaturation of LA to GLA is considered to be the rate-limiting step (1). Thus, the essentiality of LA depends on the ability of animals to convert this acid to other long-chain polyunsaturated fatty acids (PUFAs). In humans, the activity of ∆6-desaturase is lower than many other mammals (2). It has been shown that this enzyme is further reduced by other factors such as aging, poor health (e.g., diabetes, viral infection), lifestyle factors (e.g., alcohol, stress), and certain dietary elements (e.g., intake of high levels of cholesterol, saturated fats, and trans fatty acids) (3). Under these circumstances, the formation of longchain PUFAs is reduced, and the nutritional value of dietary LA is significantly compromised. Clinical data have related the deficiency of PUFAs to the etiology of many degenerative chronic diseases (3). Indeed, direct consumption of GLA, bypassing the depressed ∆6-desaturase, has been shown to lower blood cholesterol, blood pressure and body fat. GLA also enhances the immune response, alleviates the neuropathic symptoms of diabetes and partially reverses the age-related abnormalities of tissue lipids (see review in reference 3).
