Disequilibrium of polyunsaturated fatty acids status and its dual effect in modulating adipose tissue development and functions

Abstract

White adipocytes are storing energy under the form of triglycerides whereas brown adipocytes dissipate energy from triglycerides by producing heat. In rodents and possibly in humans both types of fat cells participate in the total energy balance. From a quantitative view point, a positive energy balance (energy intake > energy expenditure) is commonly regarded as a major factor contributing to obesity. Recent studies demonstrate that by altering rates of adipocyte differentiation and proliferation, differences in fatty acid composition of dietary fats may also contribute to adipose tissue development, in particular with respect to the relative intake of ω6 to ω3 poly-unsaturated fatty acids (PUFAs). The ω6/ω3 ratio determines the availability of ω6-arachidonic acid (ARA) within adipose tissue and thus the level of various prostaglandins derived from the cyclooxygenase-mediated pathway. We had shown earlier that prostacyclin (Prostaglandin I2) stimulates fat cell differentiation and this effect could be reversed by ω3-PUFA supplementation. Moreover, we had assessed that under conditions of genome stability a Western-like fat diet rich in ω6-PUFA was sufficient to induce a gradual fat mass enhancement across generations. Recently, we have characterized a second effect of some ARA metabolites (prostaglandins E2 and F2α) which appear to inhibit the formation of brown adipocytes within white adipose tissue. Altogether, our results demonstrate that, in addition to favoring white adipose tissue formation, dietary excess of ω6-PUFA prevents the “browning” process to take place in white adipose tissue depots, and strongly suggest a favorable role of ω3-PUFA supplementation in preventing both processes.

Keywords

• White adipocyte
• brite
• brown adipocyte
• arachidonic acid
• prostaglandin
• obesity