Lin Shuhao, Jensen Michael D
Endocrine Research Unit, Mayo Clinic, Rochester, MN, USA.
J Obes Metab Syndr. 2025 Apr 30;34(2):105-119. doi: 10.7570/jomes25025. Epub 2025 Apr 8.
The scientific understanding of adipose tissue has advanced tremendously during the past decade. Once thought to be an inert fat storage organ, we now know that adipose tissue serves important functions in energy balance and endocrinology, as well as playing a central role in the development of metabolic diseases. Adipose tissue lipid storage and lipolysis are tightly controlled by hormones, such as insulin, in response to the body's energy needs. Adipose insulin sensitivity can be measured in humans using isotopic fatty acid tracers and the insulin clamp technique. These data allow investigators to calculate the plasma insulin concentration that results in a 50% suppression of lipolysis. In obesity, insulin's action on adipose tissue lipolysis is clearly impaired, resulting in excess free fatty acids in circulation, which can lead to metabolic dysfunction. However, the cause of this impairment is unclear. The chronic, low-grade adipose tissue inflammation seen in obesity was thought to be the cause of adipose tissue insulin resistance. In this review, we discuss the structure of adipose tissue, how normal and abnormal adipose tissue metabolism contributes to metabolic diseases, and how inflammation might or might not play a role in adipose tissue insulin resistance.
在过去十年中,对脂肪组织的科学认识有了巨大进展。脂肪组织曾被认为是一个惰性的脂肪储存器官,而我们现在知道,它在能量平衡和内分泌学中发挥着重要作用,并且在代谢性疾病的发展中起着核心作用。脂肪组织的脂质储存和脂解作用受到胰岛素等激素的严格控制,以响应身体的能量需求。在人类中,可以使用同位素脂肪酸示踪剂和胰岛素钳夹技术来测量脂肪组织对胰岛素的敏感性。这些数据使研究人员能够计算出导致脂解作用被抑制50%时的血浆胰岛素浓度。在肥胖症中,胰岛素对脂肪组织脂解作用的影响明显受损,导致循环中游离脂肪酸过多,进而可能导致代谢功能障碍。然而,这种损害的原因尚不清楚。肥胖症中出现的慢性、低度脂肪组织炎症被认为是脂肪组织胰岛素抵抗的原因。在这篇综述中,我们讨论了脂肪组织的结构、正常和异常的脂肪组织代谢如何导致代谢性疾病,以及炎症可能在或可能不在脂肪组织胰岛素抵抗中发挥作用。