Matafome Paulo, Seiça Raquel
Institute of Physiology, Institute for Biomedical Imaging and Life Sciences-IBILI, Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
Department of Complementary Sciences, Coimbra Health School (ESTeSC), Instituto Politécnico de Coimbra, Coimbra, Portugal.
Adv Neurobiol. 2017;19:3-31. doi: 10.1007/978-3-319-63260-5_1.
Adipose tissue is an endocrine organ which is responsible for postprandial uptake of glucose and fatty acids, consequently producing a broad range of adipokines controlling several physiological functions like appetite, insulin sensitivity and secretion, immunity, coagulation, and vascular tone, among others. Many aspects of adipose tissue pathophysiology in metabolic diseases have been described in the last years. Recent data suggest two main factors for adipose tissue dysfunction: accumulation of nonesterified fatty acids and their secondary products and hypoxia. Both of these factors are thought to be on the basis of low-grade inflammatory activation, further increasing metabolic dysregulation in adipose tissue. In turn, inflammation is involved in the inhibition of substrate uptake, alteration of the secretory profile, stimulation of angiogenesis, and recruitment of further inflammatory cells, which creates an inflammatory feedback in the tissue and is responsible for long-term establishment of insulin resistance.
脂肪组织是一种内分泌器官，负责餐后葡萄糖和脂肪酸的摄取，从而产生多种脂肪因子，控制多种生理功能，如食欲、胰岛素敏感性和分泌、免疫、凝血以及血管张力等。近年来，人们对代谢性疾病中脂肪组织病理生理学的许多方面进行了描述。最新数据表明，脂肪组织功能障碍主要有两个因素：非酯化脂肪酸及其次级产物的积累和缺氧。这两个因素都被认为是低度炎症激活的基础，进而进一步加剧脂肪组织的代谢失调。反过来，炎症参与抑制底物摄取、改变分泌谱、刺激血管生成以及募集更多炎症细胞，这在组织中形成炎症反馈，并导致胰岛素抵抗的长期形成。
