101 Intestinal Barrier Dysfunction: Causes and Metabolic Consequences

Abstract

Abstract The intestinal epithelium has two critical roles: nutrient absorption and protection against numerous pathogens and antigens present in the gastrointestinal tract (GIT). The GIT is thought to be the evolutionary developmental site of the original immune system which later progressed into adding more specialized tissues. The GIT contains an enormous surface area to defend against invading pathogens and contains the majority of the body’s immune cells. Poor gut health can be caused by a variety of stressors, and ruminant research has characterized the negative impacts of rumen acidosis, heat stress, and feed restriction (FR) on lower gut health. Recently, FR has been utilized as a model to study negative consequences of GIT health and strategies to ameliorate it. The mechanism by which FR causes barrier dysfunction is not known but could be due to a lack of luminal nutrients or associated psychological stress. If stress causes GIT health to be compromised to the point where pathogens/antigens cross into the host animal and if the insult is severe enough, systemic inflammation can ensue. Inflammation is energetically costly, in part because activated immune cells have a preferential appetite for glucose. Inflammation also alters basal and stimulated metabolism, likely to help support glucose sparing for immune system use. This is extremely costly to the producer, as an animal must mobilize valuable skeletal muscle stores or compromise milk (lactose) production to ensure adequate glucose for survival. In an intensely activated immune system, it has been estimated that ~1.0 g glucose / kg BW0.75 / hour is utilized to mount a response. Therefore, it is important for producers to minimize stresses known to compromise gut integrity and for nutritionists and allied industry personnel to understand and utilize nutritional strategies and interventions to protect GIT health.