Cambridge Journals Online

Horizons in Nutritional Science

An emerging risk factor for obesity: does disequilibrium of polyunsaturated fatty acid metabolism contribute to excessive adipose tissue development?

Gérard Ailhauda1 c1, Philippe Guesneta2 and Stephen C. Cunnanea3 a1 ISDBC, Université de Nice Sophia-Antipolis, CNRS, 28 avenue Valrose, Nice 06100, France a2 Nu.Re.Li.Ce, INRA, UR909, Jouy-en-Josas cedex 78352, France a3 Research Center on Aging, Université de Sherbrooke, 1036 Belvedere Street South, Sherbrooke, Québec, Canada J1H 4C4

Article author query ailhaud g   guesnet p   cunnane sc

Abstract

A positive energy balance (energy intake>energy expenditure), in which total fat intake plays an important role, is commonly regarded as a major factor contributing to obesity. Adipose tissue development, i.e. both size (hypertrophy) and number (hyperplasia), is stimulated by high dietary fat intake during early postnatal development, a susceptibility that now appears to continue well into adulthood. Recent human and animal studies suggest that by altering rates of adipocyte differentiation and proliferation, differences in the composition of dietary fat may also contribute to adipose tissue development. At least in rodent models, the relative intake of n-6 to n-3 PUFA is clearly emerging as a new factor in this development. In these models, higher linoleate intake raises tissue arachidonic acid, which increases prostacyclin production and, in turn, stimulates signalling pathways implicated in adipogenesis. Signalling pathways stimulated by arachidonic acid probably include phospholipase and/or cyclo-oxygenase activation and may be linked as much to relatively low intake of n-3 PUFA as to excessive dietary linoleate. One factor potentially contributing to oversight about the apparent role of dietary n-6 PUFA (especially excess dietary linoleate) in adipose tissue development is the historical overestimation of linoleate requirements and the enthusiasm for higher intake of ‘essential fatty acids’. More research is needed to address whether disequilibration of dietary PUFA intake contributes to the risk of obesity in humans.

(Received April 26 2007)

(Revised December 07 2007)

(Accepted December 08 2007)

(Online publication February 28 2008)

Key Words:Obesity; Dietary fats; n-6 Fatty acids; Adipocyte; Linoleic acid; Arachidonic acid

Correspondence:

^c1 Corresponding author: Professor Gérard Ailhaud, fax +33 4 92 07 64 04, email ailhaud@unice.fr

Footnotes

Abbreviations: ARA, arachidonic acid; COX, cyclo-oxygenase; EFA, essential fatty acid; HFD, high-fat diet; IP-R, prostacyclin receptor; LA, linoleic acid; LC, long-chain; LNA, α-linolenic acid; PLA₂, phospholipase A₂