Glucose acts in the CNS to regulate gastric motility during hypoglycemia

Shi, Mingyi; Jones, Allison R.; Niedringhaus, Mark; Pearson, Rebecca; Biehl, Ann M.; Ferreira, Manuel; Sahibzada, Niaz; Verbalis, Joseph G.; Gillis, Richard A.

doi:10.1152/ajpregu.00179.2003

Cited by 28 publications

(36 citation statements)

References 37 publications

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“…72). To test whether the gastroinhibition is mediated by withdrawal of cholinergic tone, peripheral muscarinic receptors are maximally activated via intravenous administration of the nonselective cholinergic muscarinic agonist bethanecol (30,42,58,59). Under these conditions, if DVC microinjection of CCK-8s no longer induces gastroinhibition, this implies that the pathway used is "overcome" by the maximal receptor activation induced by bethanecol.…”

Section: Resultsmentioning

confidence: 99%

Effects of brain stem cholecystokinin-8s on gastric tone and esophageal-gastric reflex

Holmes¹,

Tong²,

Travagli³

2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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Holmes GM, Tong M, Travagli RA. Effects of brain stem cholecystokinin-8s on gastric tone and esophageal-gastric reflex. Am J Physiol Gastrointest Liver Physiol 296: G621-G631, 2009. First published January 8, 2009 doi:10.1152/ajpgi.90567.2008.-The actions of cholecystokinin (CCK) on gastrointestinal functions occur mainly via paracrine effects on peripheral sensory vagal fibers, which engage vago-vagal brain stem circuits to convey effector responses back to the gastrointestinal tract. Recent evidence suggests, however, that CCK also affects brain stem structures directly. Many electrophysiological studies, including our own, have shown that brain stem vagal circuits are excited by sulfated CCK (CCK-8s) directly, and we have further demonstrated that CCK-8s induces a remarkable degree of plasticity in GABAergic brain stem synapses. In the present study, we used fasted, anesthetized Sprague-Dawley rats to investigate the effects of brain stem administration of CCK-8s on gastric tone before and after activation of the esophageal-gastric reflex. CCK-8s microinjected in the dorsal vagal complex (DVC) or applied on the floor of the fourth ventricle induced an immediate and transient decrease in gastric tone. Upon recovery of gastric tone to baseline values, the gastric relaxation induced by esophageal distension was attenuated or even reversed. The effects of CCK-8s were antagonized by vagotomy or fourth ventricular, but not intravenous, administration of the CCK-A antagonist lorglumide, suggesting a central, not peripheral, site of action. The gastric relaxation induced by DVC microinjection of CCK-8s was unaffected by pretreatment with systemic bethanecol but was completely blocked by N G -nitro-L-arginine methyl ester, suggesting a nitrergic mechanism of action. These data suggest that 1) brain stem application of CCK-8s induces a vagally mediated gastric relaxation; 2) the CCK-8s-induced gastric relaxation is mediated via activation of nonadrenergic, noncholinergic pathways; and 3) CCK-8s reverses the esophageal-gastric reflex transiently.vago-vagal reflexes; gastric reflexes ESOPHAGEAL DISTENSION has long been recognized to elicit a robust and reflexive gastric relaxation (21). Early models of gastrointestinal vago-vagal reflexes presented a framework to explain many of the features of the brain stem circuits devoted to gastric reflex control, whereby stimulation of sensory vagal afferent fibers activates second-order neurons of the nucleus tractus solitarii (NTS). Subsequently, these second-order neurons modulate the output of preganglionic neurons in the dorsal motor nucleus of the vagus (DMV) that, in turn, control gastric functions to complete the vago-vagal loop (reviewed in Ref. 72).The esophageal-gastric reflex (or receptive relaxation) decreases gastric tone and allows swallowed food to be transported to the stomach with a minimal increase in intragastric pressure. Neurophysiological studies by Jean first showed the association of neurons of the caudal brain stem with esophageal function (reviewed in Re...

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Section: Resultsmentioning

confidence: 99%

Effects of brain stem cholecystokinin-8s on gastric tone and esophageal-gastric reflex

Holmes¹,

Tong²,

Travagli³

2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Experimental evidence suggests the actions of glucose to alter gastric function involve vagovagal reflexes (18,41). These reflexes consist of three components, the first of which is a sensory limb comprising chemo-and mechanosensory elements linked to vagal afferent fibers (49).…”

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confidence: 99%

d-Glucose modulates synaptic transmission from the central terminals of vagal afferent fibers

Wan¹,

Browning²

2008

American Journal of Physiology-Gastrointestinal and Liver Physi

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Wan S, Browning KN. D-Glucose modulates synaptic transmission from the central terminals of vagal afferent fibers. Am J Physiol Gastrointest Liver Physiol 294: G757-G763, 2008. First published January 17, 2008 doi:10.1152/ajpgi.00576.2007.-Experimental evidence suggests that glucose modulates gastric functions via vagally mediated effects. It is unclear whether glucose affects only peripheral vagal nerve activity or whether glucose also modulates vagal circuitry at the level of the brain stem. This study used whole cell patch-clamp recordings from neurons of the nucleus of the tractus solitarius (NTS) to assess whether acute variations in glucose modulates vagal brain stem neurocircuitry. Increasing D-glucose concentration induced a postsynaptic response in 40% of neurons; neither the response type (inward vs. outward current) nor response magnitude was altered in the presence of tetrodotoxin suggesting direct effects on the NTS neuronal membrane. In contrast, reducing D-glucose concentration induced a postsynaptic response (inward or outward current) in 54% of NTS neurons; tetrodotoxin abolished these responses, suggesting indirect sites of action. The frequency, but not amplitude, of spontaneous and miniature excitatory postsynaptic currents (EPSCs) was correlated with D-glucose concentration in 79% of neurons tested (n ϭ 48). Prior surgical afferent rhizotomy abolished the ability of D-glucose to modulate spontaneous EPSC frequency, suggesting presynaptic actions at vagal afferent nerve terminals to modulate glutamatergic synaptic transmission. In experiments in which EPSCs were evoked via electrical stimulation of the tractus solitarius, EPSC amplitude correlated with D-glucose concentration. These effects were not mimicked by L-glucose, suggesting the involvement of glucose metabolism, not uptake, in the nerve terminal. These data suggest that the synaptic connections between vagal afferent nerve terminals and NTS neurons are a strong candidate for consideration as one of the sites where glucose-evoked changes in vagovagal reflexes occurs. brain stem; electrophysiology; vagus DELAYED GASTRIC EMPTYING, or gastroparesis (diabetic gastropathy) in its extreme state, is reported in ϳ35-50% of patients with Type 1 or Type 2 diabetes (17,25,44,52) and is associated with early satiety, nausea, vomiting, and abdominal pain. Autonomic nerve dysfunction(s) undoubtedly contribute to the development of this syndrome (52), but reports that physiological hyperglycemia delays gastric emptying have led to the understanding that poor glycemic control per se may be responsible for at least some of these symptoms (25,26,37,38,45). Acute changes in blood glucose concentration, even within the physiological range, have profound effects on gastrointestinal functions, including gastric emptying. In healthy subjects, gastric emptying of both solids and liquids is slower at a blood glucose concentration of 8 mM than at 4 mM, and profound hyperglycemia (15 mM) causes a clear relaxation of the proximal stomach (29, 37). Hypoglycemia,...

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“…BDL rats) treated under KX anesthesia had less gastric mucosal damage from ethanol stimulus. While the specific process by which KX anesthetics affect GBF is unknown, previous studies demonstrate that glucose levels are improved under treatment with KX anesthetics via α2-adrenoreceptor activation [19] and in turn the glucose acts to impair vagal activity in the stomach [20] . Therefore, it suggests that the increase of glucose serves to increase the pressure of GBF.…”

Section: Discussionmentioning

confidence: 99%

“…Physiological changes in the blood glucose concentration have been reported to modulate gastrointestinal motor function [21,22] , particularly stomach motor function [20] . For example, hyperglycemia has been documented to exert an inhibitory effect on gastric function under a number of experimental conditions and in a wide range of species.…”

Section: Discussionmentioning

confidence: 99%

“…In terms of mechanism, it has been proposed by several investigators that glucose acts to impair vagal activity to the stomach [23][24][25] . In addition, there are some studies showing that systemically administered glucose produces a decrease in efferent activity of the gastric vagus nerve [20,26,27] . Moreover, it has been proposed that glucose acts in the hepatic portal area to inhibit hepatic afferent nerve traffic to the brain which results in a reflex reduction in efferent activity of the gastric vagus nerve [26,28] .…”

Section: Discussionmentioning

confidence: 99%

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Effect of anesthetics on gastric damage using two models of portal hypertension

Câmara

Moi²,

Ferraz³

et al. 2010

WJGPT

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AIM:To investigate the effect of sodium pentobarbitone (SP) or ketamine/xylazine (KX) anesthetics on acute gastric injury. METHODS:Portal hypertension was induced by bile duct ligation (BDL) or portal vein stenosis (PVS). Ethanol (EtOH)-induced gastric damage was assessed using ex vivo gastric chamber experiments. Gastric blood flow (GBF) was also measured by laser doppler flowmetry. RESULTS:EtOH-induced gastric damage was reduced in BDL rats under KX anesthesia in comparison to those under SP anesthesia. GBF dysfunction in fasted BDL rats was partially restored under KX anesthesia. In contrast, in fasted PVS rats, EtOH-induced gastric damage was increased under KX anesthesia while GBF was reduced. CONCLUSION:The use of KX anesthesia in experimental procedures involving cirrhotic rats (but not those with pure portal hypertension) is preferable to SP anesthesia. Câmara PRS, Moi GP, Ferraz JGP, Zeitune JMR. Effect of anes thetics on gastric damage using two models of portal hyperten sion.

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Glucose acts in the CNS to regulate gastric motility during hypoglycemia

Cited by 28 publications

References 37 publications

Effects of brain stem cholecystokinin-8s on gastric tone and esophageal-gastric reflex

Effects of brain stem cholecystokinin-8s on gastric tone and esophageal-gastric reflex

d-Glucose modulates synaptic transmission from the central terminals of vagal afferent fibers

Effect of anesthetics on gastric damage using two models of portal hypertension

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