Fatty acids, dietary apoptosis

Avula, C.P., Zaman, A.K., Lawrence, R.A., and Fernandes, G. (1999) Induction of Apoptosis and Apoptotic Mediators in Balb/C Splenic Lymphocytes by Dietary n-3 and n-6 Fatty Acids, Lipids 34,921-927. 

A main part of the research on CLA is focused on its potential to reduce body adipose tissue. Many studies on CLA with mice models of different strains and some studies with hamsters demonstrated extreme adipose tissue loss after feeding CLA in the diet. For example, dietary intake of relatively low levels of CLA caused complete ablation of the adipose tissue in mice (6—8). Different modes of action of CLA on the decrease of adipose tissue have been su ested. Increased fatty acid oxidation via PPARa, a decrease in fat deposition in adipose tissue via the SREBP-1 or PPARy pathway, inhibition of adipocyte differentiation, an increase in lipolysis and apoptosis are all pathways that have been suggested as the underlying mechanism. The mechanisms are not mutually exclusive and may occur simultaneously in different tissues (9, 10). 

Increased fiber intake and the consumption of fruits and vegetables are well-known chemopreventive dietary strategies against colon carcinogenesis. It is reported that fiber intake reduces colonic transit time and increases the production of short chain fatty acids such as butyric acid. The latter is produced in the mammalian colon in mM concentrations as a by-product of anaerobic bacterial fermentation of dietary fiber. Butyric acid has been recognized as one candidates chemopreventive active against colon carcinogenesis because it induces apoptosis and differentiation in colon cancer cell lines. 

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