Endotoxin-induced alterations of adipose tissue function:a pathway to bovine metabolic stress  

作　　者：Miguel Chirivi G.Andres Contreras 

机构地区：[1]Department of Large Animal Clinical Sciences,Michigan State University,East Lansing,MI,USA

出　　处：《Journal of Animal Science and Biotechnology》2024年第4期1391-1407,共17页畜牧与生物技术杂志（英文版）

基　　金：supported by USDA-National Institute of Food and Agriculture (Washington, DC) competitive grants 2019-67015-29443 and 202167015-34563;Department of Large Animal Clinical Sciences (East Lansing, MI), Office of the Associate Dean for Research and Graduate Studies of the College of Veterinary Medicine (East Lansing, MI);Michigan State University College of Veterinary Medicine Endowed Research Funds 2020 (East Lansing, MI;Robert and Janet Hafner Fund for Animal Health);the Michigan Alliance for Animal Agriculture (East Lansing, awards AA-21-154, AA-22-055)。

摘　　要：During the periparturient period, dairy cows exhibit negative energy balance due to limited appetite and increased energy requirements for lactogenesis. The delicate equilibrium between energy availability and expenditure puts cows in a state of metabolic stress characterized by excessive lipolysis in white adipose tissues(AT), increased production of reactive oxygen species, and immune cell dysfunction. Metabolic stress, especially in AT, increases the risk for metabolic and inflammatory diseases. Around parturition, cows are also susceptible to endotoxemia. Bacterial-derived toxins cause endotoxemia by promoting inflammatory processes and immune cell infiltration in different organs and systems while impacting metabolic function by altering lipolysis, mitochondrial activity, and insulin sensitivity. In dairy cows, endotoxins enter the bloodstream after overcoming the defense mechanisms of the epithelial barriers, particularly during common periparturient conditions such as mastitis, metritis, and pneumonia, or after abrupt changes in the gut microbiome. In the bovine AT, endotoxins induce a pro-inflammatory response and stimulate lipolysis in AT, leading to the release of free fatty acids into the bloodstream. When excessive and protracted, endotoxin-induced lipolysis can impair adipocyte's insulin signaling pathways and lipid synthesis. Endotoxin exposure can also induce oxidative stress in AT through the production of reactive oxygen species by inflammatory cells and other cellular components. This review provides insights into endotoxins' impact on AT function, highlighting the gaps in our knowledge of the mechanisms underlying AT dysfunction, its connection with periparturient cows' disease risk, and the need to develop effective interventions to prevent and treat endotoxemia-related inflammatory conditions in dairy cattle.

关 键 词：Adipose tissue dysfunction ENDOTOXIN INFLAMMATION Insulin resistance 

分 类 号：S823[农业科学—畜牧学]