Neural control of blood glucose level.

Abstract

It is well known that blood glucose is a major source of energy for cellular activities and the liver is an important organ for the storage of glucose in the form of glycogen. It is generally recognized that blood glucose level is maintained at a relatively constant level, and catecholamines (epinephrine and norepinephrine) released from the adrenal gland, and insulin and glucagon released from the pancreas play important roles in the regulation of the blood glucose level. Insulin is a key substance in controlling entry of glucose into the cell and utilization of glucose in the cell. Another insulin effect is to increase storage of glycogen in the liver and other tissues. These actions of insulin result in a fall in the blood glucose level. Glucagon, epinephrine, and norepinephrine cause release of glucose from the liver into the circulating blood by stimulating hepatic glycogenolysis. During starvation an increase in the rate of secretion of glucagon, epinephrine, and norepinephrine occurs. This facilitates release of glucose from the liver, thereby contributing to the maintenance of the blood glucose concentration above the lower limit of the physiological range. This is an important factor, guaranteeing reasonable utilization of glucose by the body and brain cells. It can be stated that insulin is an indispensable hormone for the utilization of glucose, and epinephrine, norepinephrine, and glucagon are the hormones which raise and maintain the glucose level in order to support utilization of the blood glucose. It has been reported that stimulation of the sympathetic nerve to the adrenal medulla causes release of epinephrine and norepinephrine into the circulating blood, resulting in release of glucose from the liver. Although it is generally accepted that the glucose concentration in the blood plasma has a direct effect on the islets of Langerhans in the pancreas in controlling the rate of insulin and glucagon secretion, the existence of an autonomic neural control mechanism for regulating the rate of secretion of these substances has been strongly suggested by WooDs and PoRTE [72]. This paper reviews the reports on the visceral afferents, glucose-responsive neurons in the central nervous system and autonomic outflows in relation to the regulation of blood glucose level.

Restoration of Euglycemia After Duodenal Bypass Surgery Is Reliant on Central and Peripheral Inputs in Zucker fa/fa Rats

“…On the basis of well-established effects of vagal inputs into glucose homeostasis (23), we examined the potential contribution of vagal signaling to the enhanced glucose metabolism after DJB. To account for potential contribution of all subbranches of the vagus nerve, we performed TSV in control ZF rats (TSV) (Supplementary Fig.…”

The fluctuation in sympathetic nerve activity around wake-up time was positively associated with not only morning but also daily glycemic variability in subjects with type 2 diabetes

“…Sympathetic nerve stimulation suppresses insulin secretion and increases glucagon secretion which leads to increase in blood glucose. Conversely, hyperglycemia suppresses sympathetic nerve activation, and insulin secretion is promoted by parasympathetic action, which could lead to a decrease in blood glucose [8,23]. These suggest that there would be a close relation among the fluctuation in sympathetic nerve activity around wake-up, insulin counterregulatory hormones, and GV around wake-up.…”

Review of the role of the nervous system in glucose homoeostasis and future perspectives towards the management of diabetes

“…Moreover, evidences of the interaction between the LHN region and the pancreas via the pancreatic parasympathetic branch are broadly found in different experiments in the literature (Oomura and Kita 1981;Niijima 1986). Stimulation of different areas within the LHN had different effects on the pancreatic vagus nerve activity (Oomura and Kita 1981).…”