Perspective: How to address the root cause of milk fat depression in dairy cattle.


Milk fat depression is a costly and complex disorder of mostly high-producing TMR fed dairy cows, with milk fat sometimes declining up to 50%. It occurs primarily on high carbohydrate fermentable diets and/or with unsaturated fat supplements. Although known and studied for many years, there is still no way to address the root cause directly; the problem being rumen microbes that synthesize so-called antilipogenic fatty acids on these diets. Briefly, the responsible rumen microbes form a number of unique fatty acids through biohydrogenation, taking dietary unsaturated fatty acids and isomerize these to double bonds and with further reduction forms saturated fatty acids. Collectively these fatty acids and associated intermediates are called antilipogenic fatty acids, since they result in less fatty acids being built in milk fat.

Milk fat depression is traditionally addressed by limiting the risk factors, but because of the availability of feed ingredients and feed cost, this is not always practical. For example, low fibre is a risk, but fibre needs to be kept low to meet energy demands. Rumen buffers such as sodium bicarbonate and other feed additives such as HMTBa (an analogue of the amino acid methionine) are used, but are only partly effective. As a result, the authors cited propose enzyme inhibitors to depress the biohydrogenation. One such compound could be polyethylene glycol (PEG) which has been shown to enter the active site of the enzymes producing antilipogenic fatty acids and it apparently also stops the usual substrate of linolenic acid from entering the active site. PEG has been successfully used in the past for other purposes, but it may have a role to play in milk fat depression. In addition, other inhibitors should be investigated as well as identification and elimination of specific antilipogenic-producing rumen microbial strains such as Cutibacterium acnes API. In these investigations, it is important that the inhibitors should be selective and not disrupt the normal pathways of lipogenic fatty acid formation.