File Name: brain glucose sensing and neural regulation of insulin and glucagon secretion .zip
The effects of stimulation of the mixed autonomic nerve to the dog pancreas has been studied under conditions in which both pancreaticoduodenal vein blood flow and insulin concentration were determined. Stimulation resulted in increased insulin output, which was blocked by prior administration of atropine. Blood flow was reduced by stimulation in proportion to the rate of stimulation.
Ever since Claude Bernards discovery in the mid 19th-century that a lesion in the floor of the third ventricle in dogs led to altered systemic glucose levels, a role of the CNS in whole-body glucose regulation has been acknowledged. However, this finding was later overshadowed by the isolation of pancreatic hormones in the 20th century. Since then, the understanding of glucose homeostasis and pathology has primarily evolved around peripheral mechanism. Due to scientific advances over these last few decades, however, increasing attention has been given to the possibility of the brain as a key player in glucose regulation and the pathogenesis of metabolic disorders such as type 2 diabetes. Studies of animals have enabled detailed neuroanatomical mapping of CNS structures involved in glucose regulation and key neuronal circuits and intracellular pathways have been identified. Furthermore, the development of neuroimaging techniques has provided methods to measure changes of activity in specific CNS regions upon diverse metabolic challenges in humans. In this narrative review, we discuss the available evidence on the topic.
Insulin and glucagon have opposite effects on glycaemia as well as on the metabolism of nutrients. Insulin acts mainly on muscle, liver and adipose tissue with an anabolic effect, inducing the incorporation of glucose into these tissues and its accumulation as glycogen and fat. By contrast, glucagon induces a catabolic effect, mainly by activating liver glycogenolysis and gluconeogenesis, which results in the release of glucose to the bloodstream. An abnormal function of these cells can generate failures in the control of glycaemia, which can lead to the development of diabetes Dunning et al. Actually, diabetes is associated with disorders in the normal levels of both insulin and glucagon. An excess of glucagon plasma levels relative to those of insulin can be determinant in the higher rate of hepatic glucose output, which seems to be critical in maintaining hyperglycaemia in diabetic patients Dunning et al.
Glucagon is a potent counterregulatory hormone that opposes the action of insulin in controlling glycemia. In this study, we examined hypoglycemia-induced glucagon secretion in vitro in isolated islets and in vivo using Sur1KO mice lacking neuroendocrine-type K ATP channels and paired wild-type WT controls. Sur1KO mice fed ad libitum have normal glucagon levels and mobilize hepatic glycogen in response to exogenous glucagon but exhibit a blunted glucagon response to insulin-induced hypoglycemia. WT islets increase glucagon secretion approximately fold when challenged with 0. Glibenclamide stimulated insulin secretion and reduced glucagon release in WT islets but was without effect on secretion from Sur1KO islets. In combination with insulin, glucagon determines the rate of gluconeogenesis and glycogenolysis in the liver and thus plays a key role in the counterregulatory response to hypoglycemia 1.
Glucagon is a potent counterregulatory hormone that opposes the action of insulin in controlling glycemia. In this study, we examined hypoglycemia-induced glucagon secretion in vitro in isolated islets and in vivo using Sur1KO mice lacking neuroendocrine-type K ATP channels and paired wild-type WT controls. Sur1KO mice fed ad libitum have normal glucagon levels and mobilize hepatic glycogen in response to exogenous glucagon but exhibit a blunted glucagon response to insulin-induced hypoglycemia.
It is increasingly apparent that the brain plays a central role in metabolic homeostasis, including the maintenance of blood glucose.
Metrics details. Diabetes is a disease caused by a breakdown in the glucose metabolic process resulting in abnormal blood glucose fluctuations. Traditionally, control has involved external insulin injection in response to elevated blood glucose to substitute the role of the beta cells in the pancreas which would otherwise perform this function in a healthy individual. The central nervous system CNS , however, also plays a vital role in glucose homoeostasis through the control of pancreatic secretion and insulin sensitivity which could potentially be used as a pathway for enhancing glucose control. In this review, we present an overview of the brain regions, peripheral nerves and molecular mechanisms by which the CNS regulates glucose metabolism and the potential benefits of modulating them for diabetes management. Development of technologies to interface to the nervous system will soon become a reality through bioelectronic medicine and we present the emerging opportunities for the treatment of type 1 and type 2 diabetes.
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Both branches of the autonomic nervous system stimulate glucagon secretion whereas the parasympathetic branch stimulates and the.
Increasing evidence suggests that, although pancreatic islets can function autonomously to detect and respond to changes in the circulating glucose level, the brain cooperates with the islet to maintain glycaemic control. Here, we review the role of the central and autonomic nervous systems in the control of the endocrine pancreas, including mechanisms whereby the brain senses circulating blood glucose levels. We also examine whether dysfunction in these systems might contribute to complications of type 1 diabetes and the pathogenesis of type 2 diabetes. Blood glucose levels are maintained within narrow physiological limits. Whenever glucose levels deviate from their defended level, adaptive metabolic responses are engaged to ensure glucose levels return to the normal range. Critical to these responses are the capacities of pancreatic islet alpha and beta cells to coordinately adjust glucagon and insulin secretion, respectively, in response to changes in blood glucose concentrations.
- Взгляни-ка на .
Особенно таких, как Хейл, - зеленых и наивных. Сьюзан посмотрела на него и подумала о том, как жаль, что этот человек, талантливый и очень ценный для АНБ, не понимает важности дела, которым занимается агентство. - Грег, - сказала она, и голос ее зазвучал мягче, хотя далось ей это нелегко.
В боковое зеркало заднего вида он увидел, как такси выехало на темное шоссе в сотне метров позади него и сразу же стало сокращать дистанцию. Беккер смотрел прямо перед. Вдалеке, метрах в пятистах, на фоне ночного неба возникли силуэты самолетных ангаров. Он подумал, успеет ли такси догнать его на таком расстоянии, и вспомнил, что Сьюзан решала такие задачки в две секунды.
Убивать Танкадо не было необходимости. Честно говоря, я бы предпочел, чтобы он остался жив. Его смерть бросает на Цифровую крепость тень подозрения. Я хотел внести исправления тихо и спокойно. Изначальный план состоял в том, чтобы сделать это незаметно и позволить Танкадо продать пароль.
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