Diabetic autonomic neuropathy

Freeman, Roy

doi:10.1016/b978-0-444-53480-4.00006-0

Cited by 112 publications

(70 citation statements)

References 214 publications

(177 reference statements)

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“…Although this initial observation may have merely been a physiological response to inflammation—it none the less sparked a curiosity in characterising the ANS responses of this patient population. Generally, symptoms of autonomic dysfunction include those of orthostatic hypotension and tachycardia, but can involve bowel and bladder dysfunction along with sweating irregularities and abnormal pupillary reactions . Multiple assessment methods used to evaluate the function of the ANS (Table ) have been applied to several cohorts of patients with IBD who did not manifest classical symptoms of autonomic dysfunction.…”

Section: Evidence Of Autonomic Dysfunction In Ibd and Proposed Mechanmentioning

confidence: 99%

Review article: the role of the autonomic nervous system in the pathogenesis and therapy of IBD

Mogilevski

Burgell

Aziz

et al. 2019

Aliment Pharmacol Ther

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Summary Background There is a growing body of evidence implicating a role for the brain‐gut axis in the pathogenesis of inflammation in patients with IBD. Aims To perform a narrative review of published literature regarding the association of the autonomic nervous system and intestinal inflammation and to describe the rationale for and emerging use of autonomic manipulation as a therapeutic agent Methods Current relevant literature was summarised and critically examined. Results There is substantial pre‐clinical and clinical evidence for a multifaceted anti‐inflammatory effect of the vagus at both systemic and local intestinal levels. It acts via acetylcholine‐mediated activation of α‐7‐acetylcholine receptors involving multiple cell types in innate and adaptive immunity and the enteric nervous system with subsequent protective influences on the intestinal barrier, inflammatory mechanisms and the microbiome. In patients with IBD, there is evidence for a sympatho‐vagal imbalance, functional enteric neuronal depletion and hyporeactivity of the hypothalamic‐pituitary‐adrenal axis. Direct or transcutaneous vagal neuromodulation up‐regulates the cholinergic anti‐inflammatory pathway in pre‐clinical and clinical models with down‐regulation of systemic and local intestinal inflammation. This is supported by two small studies in Crohn's disease although remains to be investigated in ulcerative colitis. Conclusions Modulating the cholinergic anti‐inflammatory pathway influences inflammation both systemically and at a local intestinal level. It represents a potentially underutilised anti‐inflammatory therapeutic strategy. Given the likely pathogenic role of the autonomic nervous system in patients with IBD, vagal neuromodulation, an apparently safe and successful means of increasing vagal tone, warrants further clinical exploration.

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Section: Evidence Of Autonomic Dysfunction In Ibd and Proposed Mechanmentioning

confidence: 99%

Review article: the role of the autonomic nervous system in the pathogenesis and therapy of IBD

Mogilevski

Burgell

Aziz

et al. 2019

Aliment Pharmacol Ther

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“…The impact of CAN on patients with DM can be devastating, with CAN shown to be associated with increased mortality, CVD, chronic kidney disease (CKD), and morbidity of DM 6–8. The aim of this manuscript is to review the latest developments related to the epidemiology, pathogenesis, diagnosis, consequences, and treatment of CAN in patients with DM.…”

Section: Introductionmentioning

confidence: 99%

Cardiac autonomic neuropathy in patients with diabetes mellitus: current perspectives

Fisher

Tahrani

2017

DMSO

113

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Cardiac autonomic neuropathy (CAN) is a common and often-underdiagnosed complication of diabetes mellitus (DM). CAN is associated with increased mortality, cardiovascular disease, chronic kidney disease, and morbidity in patients with DM, but despite these significant consequences CAN often remains undiagnosed for a prolonged period. This is commonly due to the disease being asymptomatic until the later stages, as well as a lack of easily available screening strategies. In this article, we review the latest developments in the epidemiology, pathogenesis, diagnosis, consequences, and treatments of CAN in patients with DM.

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“…Compelling evidence on the importance of inflammation in the pathogenesis of DNP has been accumulated over the last decades [4]. However, there is no effective therapy for inflammation or for DNP.…”

Section: Discussionmentioning

confidence: 99%

“…Diabetic neuropathy (DNP), such as cardiac autonomic neuropathy (CAN), is a relatively common and often devastating complication of T2DM. Autonomic innervation regulates heart rate and overall cardiac output [3,4]. There is sympathetic neuroaxonal dystrophy in T2DM [5].…”

Section: Introductionmentioning

confidence: 99%

LncRNA NONRATT021972 siRNA attenuates P2X7 receptor expression and inflammatory cytokine production induced by combined high glucose and free fatty acids in PC12 cells

Liu

et al. 2016

Purinergic Signalling

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Diabetic neuropathy (DNP) is a frequent chronic complication of diabetes mellitus with potentially lifethreatening outcomes. High glucose and elevated free fatty acids (FFAs) have been recently recognized as major causes of nervous system damage in diabetes. Our previous study has indicated extracellular stimuli, such as high glucose and/or FFA stress, may activate the p38 mitogen-activated protein kinase (MAPK) signaling pathway and induce a p38 MAPK-dependent sensitization of the P2X7 receptor and release of inflammatory factors in PC12 cells, while the mechanisms underlying remain to be elucidated. Long noncoding RNAs (lncRNAs) play important roles in diverse biological processes, including activation of a series of pathway signalings. Here, we showed combined high D-glucose and FFAs ( H G H F ) i n d u c e d a n i n c r e m e n t o f l n c R N A -NONRATT021972 (NONCODE ID, nc021972) in PC12 cells. Nc021972 small interference RNA (siRNA) alleviated HGHF-induced activation of p38 MAPK, expression of the P2X7 receptor, and [Ca 2+ ] i increment upon P2X7 receptor activation. Further experiments showed that there existed a crosstalk between nc021972 and the p38 MAPK signaling pathway. Inhibition of p38 MAPK signaling decreased nc021972-induced expression of the P2X7 receptor and [Ca 2+ ] i increment upon P2X7 receptor activation. Also, nc021972 siRNA inhibited HGHF-induced PC12 release of TNF-α and IL-6 and rescued decreased cell viability mediated by the P2X7 receptor. Therefore, inhibition of nc021972 may serve as a novel therapeutic strategy for diabetes complicated with nervous inflammatory diseases.

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Diabetic autonomic neuropathy

Cited by 112 publications

References 214 publications

Review article: the role of the autonomic nervous system in the pathogenesis and therapy of IBD

Review article: the role of the autonomic nervous system in the pathogenesis and therapy of IBD

Cardiac autonomic neuropathy in patients with diabetes mellitus: current perspectives

LncRNA NONRATT021972 siRNA attenuates P2X7 receptor expression and inflammatory cytokine production induced by combined high glucose and free fatty acids in PC12 cells

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