Neuroendocrine and physiological regulation of intake with particular reference to domesticated ruminant animals

Abstract

The central nervous system undertakes the homeostatic role of sensing nutrient intake and body reserves, integrating the information, and regulating energy intake and/or energy expenditure. Few tasks regulated by the brain hold greater survival value, particularly important in farmed ruminant species, where the demands of pregnancy, lactation and/or growth are not easily met by often bulky plant-based and sometimes nutrient-sparse diets. Information regarding metabolic state can be transmitted to the appetite control centres of the brain by a diverse array of signals, such as stimulation of the vagus nerve, or metabolic 'feedback' factors derived from the pituitary gland, adipose tissue, stomach/abomasum, intestine, pancreas and/or muscle. These signals act directly on the neurons located in the arcuate nucleus of the medio-basal hypothalamus, a key integration, and hunger (orexigenic) and satiety (anorexigenic) control centre of the brain. Interest in human obesity and associated disorders has fuelled considerable research effort in this area, resulting in increased understanding of chronic and acute factors influencing feed intake. In recent years, research has demonstrated that these results have relevance to animal production, with genetic selection for production found to affect orexigenic hormones, feeding found to reduce the concentration of acute controllers of orexigenic signals, and exogenous administration of orexigenic hormones (i.e. growth hormone or ghrelin) reportedly increasing DM intake in ruminant animals as well as single-stomached species. The current state of knowledge on factors influencing the hypothalamic orexigenic and anorexigenic control centres is reviewed, particularly as it relates to domesticated ruminant animals, and potential avenues for future research are identified.

Models for estimating feed intake in small ruminants

“…Only recently, light has been shed on the key factors influencing the feeding behavior of animals and humans (de Araujo et al, 2006). A recent comprehensive review of the mechanism involved in the neuroendocrine and physiological control of feed intake in domesticated ruminants has been written by Roche et al (2008).…”

“…Searching for food is strategic for survival, and this mechanism is reinforced by two other neuropeptides that are secreted by the lateral hypothalamus in response to a decrease in blood leptine: the melanin-concentrating hormone (MCH) and orexin. All these mechanisms explain the long-term energy balance regulation of VFI (Baile & Della-Fera, 1981) which, based on the lipostatic theory, integrates via leptin another important signaling pathway represented by the insulin/ glucagon concentration in blood (Roche et al, 2008). The short-term action of insulin in ruminants, instead, is still unclear (Roche et al, 2008).…”

“…All these mechanisms explain the long-term energy balance regulation of VFI (Baile & Della-Fera, 1981) which, based on the lipostatic theory, integrates via leptin another important signaling pathway represented by the insulin/ glucagon concentration in blood (Roche et al, 2008). The short-term action of insulin in ruminants, instead, is still unclear (Roche et al, 2008).…”

“…All these hormones have a direct impact on the hypothalamus. After the beginning of the meal, its duration and intensity are controlled by a coordinated pool of stretch, chemical and hormonal stimuli going from the gut to the hindbrain, via the vagus nerve (Roche et al, 2008). Briefly, rumen and gastric vagal mechanoreceptors are excited by the degree of filling of rumen and abomasum.…”

“…Mechanoreceptors and chemoreceptors, together with the anorexic hormones, namely cholecystokinin (CCK) and the peptide YY 3-36 (PYY), signal the physical and chemical status of gut to the brain, causing the animal to stop eating. Cholecystokinin is produced mainly by the I cells of duodenal and jejuneal mucosa, whereas PYY is released by the enteroendocrine cells of the distal tract of the intestine (Roche et al, 2008). An additional powerful satiety signal comes to the brain from the hepatic glucoreceptors that, excited by the oxidation of a variety of fuels, reinforce the anorexic stimuli of the gut (Forbes, 1995).…”