Un nouveau système de production et un nouvel aspect pour la Revue des Maladies Respiratoires: A new production system and a new presentation for the Journal

Abstract

Diet-induced low-fat milk syndrome, milk fat depression (MFD), was first described over a century ago. It continues to be an active research area and we reviewed theories that have been proposed to explain diet-induced MFD. Many theories were based on the concept that reduced milk fat was a consequence of a limited supply of lipid precursors, e.g. the insulin-glucogenic theory; experimental data provide little support for this concept as the basis for diet-induced MFD. Other theories attributed MFD to a direct inhibition of lipid synthesis in the mammary gland. Davis and Brown (In: Phillipson, A.T. (Ed.), Physiology of Digestion and Metabolism in the Ruminant. Oriel Press, Newcastle upon Tyne, UK, 1970, pp. 545–565) noted increased trans-C18:1 fatty acids in milk fat during MFD, and proposed these fatty acids inhibited fat synthesis. We recently established the increase was specific for trans-10 C18:1 and its rumen precursor, trans-10, cis-12 conjugated linoleic acid (CLA). Across a range of diets there was a curvilinear relationship between the reduction in milk fat yield and the increase in milk fat content of trans-10, cis-12 CLA. Furthermore, postruminal infusion of trans-10, cis-12 CLA resulted in a marked inhibition of milk fat synthesis and a shift in fatty acid pattern similar to dietary-induced MFD. Therefore, diets that cause MFD alter rumen biohydrogenation resulting in the production of trans-10, cis-12 CLA, and perhaps other unique fatty acids, that are potent inhibitors of milk fat synthesis. We refer to this as the biohydrogenation theory of MFD and discuss the possibility that it may represent a unifying concept to explain diet-induced MFD.