scholarly journals Minireview: The Role of the Autonomic Nervous System in Mediating the Glucagon Response to Hypoglycemia

Endocrinology ◽  
2012 ◽  
Vol 153 (3) ◽  
pp. 1055-1062 ◽  
Author(s):  
Gerald J. Taborsky ◽  
Thomas O. Mundinger

In type 1 diabetes, the impairment of the glucagon response to hypoglycemia increases both its severity and duration. In nondiabetic individuals, hypoglycemia activates the autonomic nervous system, which in turn mediates the majority of the glucagon response to moderate and marked hypoglycemia. The first goal of this minireview is therefore to illustrate and document these autonomic mechanisms. Specifically we describe the hypoglycemic thresholds for activating the three autonomic inputs to the islet (parasympathetic nerves, sympathetic nerves, and adrenal medullary epinephrine) and their magnitudes of activation as glucose falls from euglycemia to near fatal levels. The implication is that their relative contributions to this glucagon response depend on the severity of hypoglycemia. The second goal of this minireview is to discuss known and suspected down-regulation or damage to these mechanisms in diabetes. We address defects in the central nervous system, the peripheral nervous system, and in the islet itself. They are categorized as either functional defects caused by glucose dysregulation or structural defects caused by the autoimmune attack of the islet. In the last section of the minireview, we outline approaches for reversing these defects. Such reversal has both scientific and clinical benefit. Scientifically, one could determine the contribution of these defects to the impairment of glucagon response seen early in type 1 diabetes. Clinically, restoring this glucagon response would allow more aggressive treatment of the chronic hyperglycemia that is linked to the debilitating long-term complications of this disease.

2016 ◽  
Vol 26 (7) ◽  
pp. 1383-1390 ◽  
Author(s):  
Naiara M. Souza ◽  
Thais R. Giacon ◽  
Francis L. Pacagnelli ◽  
Marianne P. C. R. Barbosa ◽  
Vitor E. Valenti ◽  
...  

AbstractBackgroundAutonomic diabetic neuropathy is one of the most common complications of type 1 diabetes mellitus, and studies using heart rate variability to investigate these individuals have shown inconclusive results regarding autonomic nervous system activation.AimsTo investigate the dynamics of heart rate in young subjects with type 1 diabetes mellitus through nonlinear and linear methods of heart rate variability.MethodsWe evaluated 20 subjects with type 1 diabetes mellitus and 23 healthy control subjects. We obtained the following nonlinear indices from the recurrence plot: recurrence rate (REC), determinism (DET), and Shanon entropy (ES), and we analysed indices in the frequency (LF and HF in ms2 and normalised units – nu – and LF/HF ratio) and time domains (SDNN and RMSSD), through analysis of 1000 R–R intervals, captured by a heart rate monitor.ResultsThere were reduced values (p<0.05) for individuals with type 1 diabetes mellitus compared with healthy subjects in the following indices: DET, REC, ES, RMSSD, SDNN, LF (ms2), and HF (ms2). In relation to the recurrence plot, subjects with type 1 diabetes mellitus demonstrated lower recurrence and greater variation in their plot, inter-group and intra-group, respectively.ConclusionYoung subjects with type 1 diabetes mellitus have autonomic nervous system behaviour that tends to randomness compared with healthy young subjects. Moreover, this behaviour is related to reduced sympathetic and parasympathetic activity of the autonomic nervous system.


Circulation ◽  
2009 ◽  
Vol 119 (22) ◽  
pp. 2886-2893 ◽  
Author(s):  
Rodica Pop-Busui ◽  
Phillip A. Low ◽  
Barbara H. Waberski ◽  
Catherine L. Martin ◽  
James W. Albers ◽  
...  

Vision ◽  
2022 ◽  
Vol 6 (1) ◽  
pp. 6
Author(s):  
Feipeng Wu ◽  
Yin Zhao ◽  
Hong Zhang

The autonomic nervous system (ANS) confers neural control of the entire body, mainly through the sympathetic and parasympathetic nerves. Several studies have observed that the physiological functions of the eye (pupil size, lens accommodation, ocular circulation, and intraocular pressure regulation) are precisely regulated by the ANS. Almost all parts of the eye have autonomic innervation for the regulation of local homeostasis through synergy and antagonism. With the advent of new research methods, novel anatomical characteristics and numerous physiological processes have been elucidated. Herein, we summarize the anatomical and physiological functions of the ANS in the eye within the context of its intrinsic connections. This review provides novel insights into ocular studies.


2021 ◽  
pp. 158-168
Author(s):  
Jeremy K. Cutsforth-Gregory

The autonomic nervous system is involved in many important unconscious body functions. It is critical for maintaining the internal environment in response to changes in the external environment. The autonomic nervous system consists of peripheral components (sympathetic and parasympathetic nerves and ganglia) and central components (ventrolateral medulla, nucleus ambiguus, nucleus of the solitary tract, periaqueductal gray, anterior cingulate gyrus, insular cortex, amygdala, and hypothalamus). This chapter briefly reviews the anatomy and functional components of the autonomic nervous system and several anatomical clinical correlations.


Author(s):  
J. Z. Young

There are not sufficient data available to allow any general statements about the earlier stages of evolution of the autonomic nervous system and of its various transmitter mechanisms. In the previous paper (Young, 1980) it was shown that control of the stomach of elasmobranchs is largely by the inhibitory action of the sympathetic nerves, probably mediated by 5-HT. In teleostean fishes on the other hand control seems to be mainly by the cholinergic excitatory action of the vagus, especially in the more advanced (acanthopterygian) groups (Grove & Campbell, 1979a, b; Fänge & Grove, 1979).


1992 ◽  
Vol 70 (2) ◽  
pp. 167-206 ◽  
Author(s):  
Nobuharu Yamaguchi

Glucose homeostasis is maintained by complex neuroendocrine control mechanisms, involving three peripheral organs: the liver, pancreas, and adrenal gland, all of which are under control of the autonomic nervous system. During the past decade, abundant results from various studies on neuroendocrine control of glucose have been accumulated. The principal objective of this review is to provide overviews of basic adrenergic mechanisms closely related to glucose control in the three peripheral organs, and then to discuss the integrated glucoregulatory mechanisms in hemorrhage-induced hypotension and insulin-induced hypoglycemia with special reference to sympathoadrenal control mechanisms. The liver is richly innervated by sympathetic and parasympathetic nerves. The functional implication in glucoregulation of sympathetic nerves has been well-documented, while that of parasympathetic nerves remains less understood. More recently, hepatic glucoreceptors have been postulated to be coupled with capsaicin-sensitive afferent nerves, conveying sensory signals of blood glucose concentration to the central nervous system. The pancreas is also richly supplied by the autonomic nervous system. Besides the well documented adrenergic and cholinergic mechanisms, the potential implication of peptidergic neurotransmission by neuropeptide Y and neuromodulation by galanin has recently been postulated in the endocrine secretory function. Presynaptic interactions of these putative peptidergic neurotransmitters with the classic transmitters, noradrenaline and acetylcholine, in the pancreas remain to be clarified. It may be of particular interest that it was vagus nerve stimulation that caused a dominant release of neuropeptide Y over that caused by sympathetic nerve stimulation in the pig pancreas. The adrenal medulla receives its main nerve supply from the greater and lesser splanchnic nerves. Adrenal medullary catecholamine secretion appears to be regulated by three distinct local mechanisms: adrenoceptor-mediated, dihydropyridine-sensitive Ca2+ channel-mediated, and capsaicin-sensitive sensory nerve-mediated mechanisms. In response to hemorrhagic hypotension and insulin-induced hypoglycemia, the sympathoadrenal system is activated resulting in increases of adrenal catecholamine and pancreatic glucagon secretions, both of which are significantly implicated in glucoregulatory mechanisms. An increase in sympathetic nerve activity occurs in the liver during hemorrhagic hypotension and is also likely to occur in the pancreas in response to insulin-induced hypoglycemia. The functional implication of hepatic and central glucoreceptors has been suggested in the increased secretion of glucose counterregulatory hormones, particularly catecholamines and glucagon.Key words: sympathetic nerves, adrenal medulla, catecholamines, glucose, hypoglycemia, hemorrhage.


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