Department of Animal Science, Cornell University, Ithaca, NY 14853.
Department of Animal Science, Cornell University, Ithaca, NY 14853.
J Dairy Sci. 2019 Sep;102(9):7619-7639. doi: 10.3168/jds.2018-16095. Epub 2019 Jul 10.
The physiological control of lactation through coordinated adaptations is of fundamental importance for mammalian neonatal life. The putative actions of reduced insulin sensitivity and responsiveness and enhanced adipose tissue lipolysis spare glucose for the mammary synthesis of milk. However, severe insulin antagonism and body fat mobilization may jeopardize hepatic health and lactation in dairy cattle. Interestingly, lipolysis- and dietary-derived fatty acids may impair insulin sensitivity in cows. The mechanisms are undefined yet have major implications for the development of postpartum fatty liver disease. In nonruminants, the sphingolipid ceramide is a potent mediator of saturated fat-induced insulin resistance that defines in part the mechanisms of type 2 diabetes mellitus and nonalcoholic fatty liver disease. In ruminants including the lactating dairy cow, the functions of ceramide had remained virtually undescribed. Through a series of hypothesis-centered studies, ceramide has emerged as a potential antagonist of insulin-stimulated glucose utilization by adipose and skeletal muscle tissues in dairy cattle. Importantly, bovine data suggest that the ability of ceramide to inhibit insulin action likely depends on the lipolysis-dependent hepatic synthesis and secretion of ceramide during early lactation. Although these mechanisms appear to fade as lactation advances beyond peak milk production, early evidence suggests that palmitic acid feeding is a means to augment ceramide supply. Herein, we review a body of work that focuses on sphingolipid biology and the role of ceramide in the dairy cow within the framework of hepatic and fatty acid metabolism, insulin function, and lactation. The potential involvement of ceramide within the endocrine control of lactation is also considered.
哺乳的生理调控通过协调适应对哺乳动物新生儿期具有重要意义。胰岛素敏感性和反应性降低以及脂肪组织脂解增强的推测作用可使葡萄糖保留用于乳腺合成乳汁。然而，严重的胰岛素拮抗和体脂动员可能危及奶牛的肝健康和泌乳。有趣的是，脂解和膳食来源的脂肪酸可能会损害奶牛的胰岛素敏感性。其机制尚未明确，但对产后脂肪肝疾病的发展具有重要意义。在非反刍动物中，鞘脂神经酰胺是饱和脂肪诱导的胰岛素抵抗的有力介质，部分定义了 2 型糖尿病和非酒精性脂肪肝疾病的机制。在反刍动物中，包括泌乳奶牛，神经酰胺的功能实际上尚未被描述。通过一系列以假设为中心的研究，神经酰胺已成为奶牛脂肪和骨骼肌组织胰岛素刺激葡萄糖利用的潜在拮抗剂。重要的是，牛数据表明，神经酰胺抑制胰岛素作用的能力可能取决于在泌乳早期依赖于脂解的肝合成和分泌神经酰胺。尽管这些机制似乎随着泌乳超过产奶高峰期而逐渐消失，但早期证据表明，棕榈酸喂养是增加神经酰胺供应的一种手段。在此，我们回顾了一系列关注鞘脂生物学和神经酰胺在奶牛肝和脂肪酸代谢、胰岛素功能和泌乳框架内作用的工作。还考虑了神经酰胺在哺乳的内分泌调控中的潜在作用。
