Regulation and nutritional manipulation of milk fat: low-fat milk syndrome

Diet-induced low-fat milk syndrome, milk fat depression (MFD), was first de scribed 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. M any theories were based on the concept that reduced milk fat was a conseque nce of a limited supply of lipid precursors, e.g. the insulin-glucogenic th eory; experimental data provide little support for this concept as the basi s for diet-induced MFD. Other theories attributed MFD to a direct inhibitio n 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-C1 8:1 fatty acids in milk fat during MFD, and proposed these fatty acids inhi bited fat synthesis. We recently established the increase was specific for trans-10 C18:1 and its rumen precursor, trans-10, cis-12 conjugated linolei c 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 conten t of trans-10, cis-12 CLA. Furthermore, postruminal infusion of trans-10, c is-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 tha t cause MFD alter rumen biohydrogenation resulting in the production of tra ns-10, cis-12 CLA, and perhaps other unique fatty acids, that are potent in hibitors of milk fat synthesis. We refer to this as the biohydrogenation th eory of MFD and discuss the possibility that it may represent a unifying co ncept to explain diet-induced MFD. (C) 2001 Elsevier Science B.V. All right s reserved.