Year: 2010
Type: other
Abstract: introductionThe autonomic nervous system is the unconscious part of the peripheral nervous system and comprises the motor system for viscera, smooth muscles and exocrine glands.The scientific interest for the innervation of the liver by the autonomic nervous system and its function in the control of energy metabolism can be traced back to a time when the need to understand the pathophysiology of metabolic diseases like type 2 diabetes mellitus may have been less urgent than in our modern affluent society.The great French physiologist Claude Bernard was the first to discover and describe that the liver can store and release glucose, and he named this stored form of glucose glycogen.At that time in history the general assumption was that the body could not synthesize glucose de novo (gluconeogenesis).However, Claude Bernard believed that hepatic glucose production was under the control of autonomic nerves and carried out the earliest study on the autonomic innervation of the liver and glucose metabolism in 1848.He observed a decrease in hepatic glucose output after peripheral vagotomy, but failed to show increased glucose output by electrically stimulating the vagal nerves.He then tried to punch the floor of the fourth ventricle, i.e., the place of origin of the vagal nerves.The short-term "artificial diabetes" he induced in this way (the well-known piqûre diabetique) was not blocked by cutting the vagal nerves, but it could be blocked by transection of the spinal cord, i.e., the origin of the sympathetic nerves that innervate the liver.Although this earliest functional study did not mean he could distinguish the glucoregulatory function of the liver from that of other visceral organs, it was the first indication of a brain mechanism controlling peripheral glucose homeostasis and of the involvement of the autonomic nervous system.Despite this inspiring starting point, the role liver innervation plays in the control of energy metabolism is still not fully uncovered today, especially regarding metabolic sensing by the liver.After insulin was discovered by Banting and Macleod in the 1920s, physiologists and biochemists focused their attention on the control of liver metabolism by hormones, and in subsequent years only little attention was paid to the involvement of neuronal signaling in liver metabolism.In the 1950s Mayer put forward the "glucostatic theory", the "lipostatic theory" and the "glucoreceptor" conception [1][2][3] as explanatory brain mechanisms involved in the control of feeding behavior and glucose metabolism.Although these theories renewed interest in neuronal sensing mechanisms involved in the control of liver function, the "glucostatic theory" itself was soon rejected based on experimental studies by others 4 .In the early sixties the existence of glucose sensitive neurons in the ventromedial hypothalamus (VMH) and lateral hypothalamus (LH) was proven by Anand 5 and Oomura 6 .Russek then proposed the existence of glucose receptors in the liver 7 .Soon after, a change of vagal activity was recorded by Niijima upon glucose infusions into the portal vein 8 .Hepatic branch proper Common hepatic branch Gastroduodenal branch Hepatic artery proper Gastroduodenal artery Common hepatic artery
Author: Chun‐Xia Yi
Language: English
Subfield: Endocrine and Autonomic Systems
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2153611274