Lipid metabolism during lactation: a review of adipose tissue-liver interactions and the development of fatty liver

摘要

Fatty acids are the major source of energy for most tissues during periods of negative energy balance; however, fatty acids can, in some circumstances, have pathological effects. Fatty acids are stored as triacylglycerols (TAG), mostly in the various adipose tissue depots of the body. However, if blood unesterified fatty acid (NEFA) levels are elevated for prolonged periods, as may occur during lactation or obesity, TAG can accumulate in other tissues including liver and muscle cells (myocytes), and this can have pathological consequences such as the development of ketosis (Grummer, 1993; Drackley et al. 2001) or type 2 diabetes (Boden & Shulman, 2002; McGarry, 2002). Adipose tissues, however, are not just stores of fatty acids, or to be precise TAG; they are now known to secrete a wide variety of substances, some of which have endocrine functions, acting on the hypothalamus to influence appetite and modulating the metabolism of various tissues including the liver and muscle (Arner, 2003; Vernon, 2003; Havel, 2004; Kershaw & Flier, 2004; Pittas et al. 2004; Steppan & Lazar, 2004; Tomas et al. 2004). It is now thought that some of these hormones, collectively called adipocytokines, secreted by adipose tissue are involved in the development of fatty liver, which occurs in conditions such as obesity and type 2 diabetes. The possibility of adipocytokines being involved in the development of fatty liver during lactation is considered in this review. Adipocytokines do not act in isolation, but function against a background of classical hormones such as insulin, catecholamines and growth hormone, which have major roles in lipid metabolism.