Faculty of Pharmacy, Université Laval, Québec City, QC G1V 0A6, Canada.
Quebec Heart and Lung Institute, Québec City, QC G1V 4G5, Canada.
Endocrinology. 2021 Nov 1;162(11). doi: 10.1210/endocr/bqab164.
The brain influences liver metabolism through many neuroendocrine and autonomic mechanisms that have evolved to protect the organism against starvation and hypoglycemia. Unfortunately, this effective way of preventing death has become dysregulated in modern obesogenic environments, although the pathophysiological mechanisms behind metabolic dyshomeostasis are still unclear. In this Mini-Review, we provide our thoughts regarding obesity and type 2 diabetes as diseases of the autonomic nervous system. We discuss the pathophysiological mechanisms that alter the autonomic brain-liver communication in these diseases, and how they could represent important targets to prevent or treat metabolic dysfunctions. We discuss how sympathetic hyperactivity to the liver may represent an early event in the progression of metabolic diseases and could progressively lead to hepatic neuropathy. We hope that this discussion will inspire and help to frame a model based on better understanding of the chronology of autonomic dysfunctions in the liver, enabling the application of the right strategy at the right time.
大脑通过许多神经内分泌和自主机制影响肝脏代谢,这些机制的进化是为了保护机体免受饥饿和低血糖的影响。不幸的是,尽管代谢失衡背后的病理生理机制尚不清楚,但这种预防死亡的有效方法在现代肥胖环境中已失调。在这篇迷你综述中,我们将肥胖和 2 型糖尿病视为自主神经系统疾病。我们讨论了改变这些疾病中自主脑-肝通讯的病理生理机制,以及它们如何成为预防或治疗代谢功能障碍的重要靶点。我们讨论了肝脏交感神经活性增加如何可能代表代谢疾病进展中的早期事件,并可能逐渐导致肝神经病。我们希望这一讨论将激发并有助于构建一个基于更好地理解肝脏自主功能障碍的时间顺序的模型,从而能够在适当的时间应用正确的策略。