Acute Hyperglycemia and Autonomic Function

Marfella, Raffaele; Nappo, Francesco; Marfella, M. A.; Giugliano, Dario

doi:10.2337/diacare.24.11.2016-b

Cited by 12 publications

(7 citation statements)

References 8 publications

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“…Finally, as possible pathogenetic mechanism and at the same time a common denominator of all the above interpretations, the increased production of free radicals evoked by high levels of glucose has been proposed. This view is supported by the study of Marfella et al [39], in which BRS reduction induced by acute hyperglycemia was prevented by administration of the antioxidant factor glutathione.…”

Section: Hemodynamic and Metabolic Parametersmentioning

confidence: 71%

Baroreflex Function: Determinants in Healthy Subjects and Disturbances in Diabetes, Obesity and Metabolic Syndrome

Skrapari¹,

Tentolouris²,

Katsilambros³

2006

CDR

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Arterial baroreceptors play an important role in the short-term regulation of arterial pressure, by reflex chronotropic effect on the heart and by reflex regulation of sympathetic outflow. Baroreflex sensitivity (BRS) represents an index of arterial baroreceptors function. Several methods of measuring BRS are available nowadays. Different factors influence BRS in the healthy population, including sex, age, blood pressure, heart rate, body fatness, arterial stiffness, blood glucose and insulin levels, as well as physical activity. Baroreceptors dysfunction is evident in diseases such as coronary artery disease, heart failure, arterial hypertension, diabetes mellitus and obesity. The underlying mechanism of BRS attenuation in diabetes or obesity is not yet well known; however, there is increasing evidence that it is at least partly related to autonomic nervous system dysfunction and particularly to sympathetic overactivity that accompanies these diseases. Blunted BRS provides prognostic information for cardiovascular diseases and possibly for diabetes, while its' prognostic information for obesity is not yet established. This review deals with the mechanisms affecting baroreflex function, the newer techniques of BRS estimation and the most recent insights of baroreflex function in the healthy population and in various diseases with emphasis on diabetes and obesity. In addition, the clinical implication of a reduced BRS in these disorders is discussed.

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Section: Hemodynamic and Metabolic Parametersmentioning

confidence: 71%

Baroreflex Function: Determinants in Healthy Subjects and Disturbances in Diabetes, Obesity and Metabolic Syndrome

Skrapari¹,

Tentolouris²,

Katsilambros³

2006

CDR

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“…One common feature of electrophysiological alterations caused by both hypoglycemia and hyperglycemia in the heart is prolongation of Q-T interval and the associated ventricular arrhythmias that are presumably responsible for sudden cardiac death in diabetic patients (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). However, the ionic mechanisms by which hyperglycemia and hypoglycemia prolong Q-T interval remained unclear, which is at least a part of the reasons why diabetic patients die of mainly cardiac complications.…”

mentioning

confidence: 99%

Impairment of Human Ether-à-Go-Go-related Gene (HERG) K+ Channel Function by Hypoglycemia and Hyperglycemia

Zhang

Han

Wang

et al. 2003

Journal of Biological Chemistry

113

104

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Hyperglycemia and hypoglycemia both can cause prolongation of the Q-T interval and ventricular arrhythmias. Here we studied modulation of human ether-à -gogo-related gene (HERG) K ؉ channel, the major molecular component of delayed rectifier K ؉ current responsible for cardiac repolarization, by glucose in HEK293 cells using whole-cell patch clamp techniques. We found that both hyperglycemia (extracellular glucose concentration Glucose, the primary end product of the digestion of glycogen, is essential for maintaining life activities in organisms. As a major source of metabolic fuel, degradation of glucose via glycolysis and subsequent oxidative phosphorylation generates high energy phosphates to power the biological processes in the cell. Yet, through an exquisitely complex network of control mechanisms, the rate of glucose metabolism is only as great as needed by the organisms. Moreover, glucose also has other regulatory effects on many cellular functions. Either inadequate or excessive glucose can be harmful to the living system. Therefore, the blood glucose level is dynamically controlled. However, under pathological conditions like diabetes, glucose cannot be efficiently utilized, and the blood glucose level rises. When the blood level of glucose is maintained higher than 7 mM, it is considered as hyperglycemia. Diabetes therapy, on the other hand, can lead to an overly low level of blood glucose, which is referred to as hypoglycemia when the level falls below 3 mM.Either hypoglycemia or hyperglycemia can have deleterious effects on the cells. One common feature of electrophysiological alterations caused by both hypoglycemia and hyperglycemia in the heart is prolongation of Q-T interval and the associated ventricular arrhythmias that are presumably responsible for sudden cardiac death in diabetic patients (1-10). However, the ionic mechanisms by which hyperglycemia and hypoglycemia prolong Q-T interval remained unclear, which is at least a part of the reasons why diabetic patients die of mainly cardiac complications.The human either-à -go-go-related gene (HERG) 1 encodes the rapid component of delayed rectifier K ϩ current in the heart, which is the major repolarizing current in the plateau voltage range of cardiac action potentials. HERG K ϩ channels are susceptible to genetic defects and environmental cues, with the consequence being depression of HERG function in most situations (9). Indeed, most of the cases of long Q-T syndrome are ascribed to dysfunction of HERG channels, particularly that induced by therapeutic drugs (13). It is conceivable that HERG alteration might also be involved in the Q-T prolongation induced by hyperglycemia and hypoglycemia. This thought prompted us to carry out a series of experiments to study the effects of glucose on HERG K ϩ channels and the potential mechanisms.

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“…SA reverses hyperglycemia, hyperinsulinemia, and hyperleptinemia in WD-induced obese mice [ 28 , 29 , 30 , 31 ]. The present study demonstrated that SA treatment decreased plasma insulin, glucose, and leptin levels in obese WT mice as well as in obese TRPV1 −/− mice.…”

Section: Discussionmentioning

confidence: 99%

Ablation of TRPV1 Abolishes Salicylate-Induced Sympathetic Activity Suppression and Exacerbates Salicylate-Induced Renal Dysfunction in Diet-Induced Obesity

Zhong

Wang

2021

Cells

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Sodium salicylate (SA), a cyclooxygenase inhibitor, has been shown to increase insulin sensitivity and to suppress inflammation in obese patients and animal models. Transient receptor potential vanilloid 1 (TRPV1) is a nonselective cation channel expressed in afferent nerve fibers. Cyclooxygenase-derived prostaglandins are involved in the activation and sensitization of TRPV1. This study tested whether the metabolic and renal effects of SA were mediated by the TRPV1 channel. Wild-type (WT) and TRPV1−/− mice were fed a Western diet (WD) for 4 months and received SA infusion (120mg/kg/day) or vehicle for the last 4 weeks of WD feeding. SA treatment significantly increased blood pressure in WD-fed TRPV1−/− mice (p < 0.05) but not in WD-fed WT mice. Similarly, SA impaired renal blood flow in TRPV1−/− mice (p < 0.05) but not in WT mice. SA improved insulin and glucose tolerance in both WT and TRPV1−/− mice on WD (all p < 0.05). In addition, SA reduced renal p65 and urinary prostaglandin E2, prostaglandin F1α, and interleukin-6 in both WT and TRPV1−/− mice (all p < 0.05). SA decreased urine noradrenaline levels, increased afferent renal nerve activity, and improved baroreflex sensitivity in WT mice (all p < 0.05) but not in TRPV1−/− mice. Importantly, SA increased serum creatinine and urine kidney injury molecule-1 levels and decreased the glomerular filtration rate in obese WT mice (all p < 0.05), and these detrimental effects were significantly exacerbated in obese TRPV1−/− mice (all p < 0.05). Lastly, SA treatment increased urine albumin levels in TRPV1−/− mice (p < 0.05) but not in WT mice. Taken together, SA-elicited metabolic benefits and anti-inflammatory effects are independent of TRPV1, while SA-induced sympathetic suppression is dependent on TRPV1 channels. SA-induced renal dysfunction is dependent on intact TRPV1 channels. These findings suggest that SA needs to be cautiously used in patients with obesity or diabetes, as SA-induced renal dysfunction may be exacerbated due to impaired TRPV1 in obese and diabetic patients.

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Acute Hyperglycemia and Autonomic Function

Cited by 12 publications

References 8 publications

Baroreflex Function: Determinants in Healthy Subjects and Disturbances in Diabetes, Obesity and Metabolic Syndrome

Baroreflex Function: Determinants in Healthy Subjects and Disturbances in Diabetes, Obesity and Metabolic Syndrome

Impairment of Human Ether-à-Go-Go-related Gene (HERG) K+ Channel Function by Hypoglycemia and Hyperglycemia

Ablation of TRPV1 Abolishes Salicylate-Induced Sympathetic Activity Suppression and Exacerbates Salicylate-Induced Renal Dysfunction in Diet-Induced Obesity

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