Physical and Metabolic Constraints on Feed Intake in Ruminants

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The objective of this review article was to elucidate the main physical and metabolic constraints on feed intake in ruminants. Over the last 25 years, several major physical and metabolic regulators of feed intake in ruminants have been emphasized. Ruminal fill is one of the central regulators of Dry Matter Intake (DMI) under certain circumstances such as when feeds with low digestibility are fed. The dietary NDF, especially from forage, is a key contributor to reticulorumen fill. The greater NDF lowers the clearance rate of the rumen contents. Hence, the dietary NDF can be a key controller of feed intake in early and peak lactation cows that have not peaked in DMI or with limited rumen fiber pool. The NDF digestibility can significantly impact DMI. As NDF digestibility increases, the depressing effect of NDF on DMI weakens. Allen  stated that DMI rose by 0.17kg per unit rise in in vitro or in situ NDF digestibility. At higher NDF digestibility, the NDF will have a smaller impact on rumen distension. Thus, factors affecting NDF digestibility will affect DMI.

Among the important metabolic constraints of appetite are rumen concentrations of volatile fatty acids. Propionate injection into the portal vein has reduced feed intake in sheep. Propionate rather than acetate seems to cause hypophagia. Insulin secretion  and hepatic receptors have been proposed to mediate the hypophagic effects of propionate. In addition to the hepatic chemoreceptors, hepatic thermoreceptors may also control feed intake. Di Bella et al. heated the rat liver artificially and observed an increased chewing activity with reduced feed intake.

Feed intake is ultimately a psychological phenomenon integrating animal’s abilities to cope with changes in diet composition and metabolic demands. Thus, one must consider that the rumen or blood VFA is only one of many factors involved in feed intake. Illius and Jessop suggested that imbalances in nutrient supply both in the rumen, postrumen, and hepatic levels can reduce feed intake. They proposed that maximizing acetate use for lipogenesis needs a synchronous glucose supply. Glucose fuels lipogenesis by providing ATP and cofactors such as NADPH needed for fatty acid elongation. Thus, even the high production rate of acetate, if accompanied by adequate supply of other nutrients, May not necessarily down-regulate feed intake. The framework of Illius and Jessop  presumes that nutrient imbalances constrain feed intake via accumulation of excess metabolites such as acetate. Therefore, the animal targets a level of intake that minimizes nutrient imbalances. According to this framework, in the absence of adequate glucose, acetate will mount up and act as a hypophagic feedback.