Hepatic electrical stimulation reduces blood glucose in diabetic rats

Chen, J.; Pasricha, Pankaj J.; Yin, Jie; Lin, Li; Chen, J. D. Z.

doi:10.1111/j.1365-2982.2010.01556.x

Cited by 13 publications

(5 citation statements)

References 39 publications

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“…In contrast, oral sCT, by following the endogenous physiological pathway and thereby resulting in higher drug concentrations in the splanchnic circulation could cause pronounced exposure to receptors and nerves located in the pancreatic and portal area. In support of this hypothesis, stimulation of hepatic vagal afferents resulting in hypothalamic mediated insulin secretion has been demonstrated to improve hyperglycaemia in ZDF rats (Chen et al ., 2010). Additionally, in preliminary experiments, the CT receptor was localized by immunohistochemistry as being dispersed throughout the pancreas islet including beta cells (unpublished data).…”

Section: Discussionmentioning

confidence: 99%

Oral salmon calcitonin attenuates hyperglycaemia and preserves pancreatic beta‐cell area and function in Zucker diabetic fatty rats

Feigh

Andreassen

Neutzsky-Wulff

et al. 2012

British J Pharmacology

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BACKGROUND AND PURPOSE Oral salmon calcitonin (sCT), a dual‐action amylin and calcitonin receptor agonist, improved glucose homeostasis in diet‐induced obese rats. Here, we have evaluated the anti‐diabetic efficacy of oral sCT using parameters of glycaemic control and beta‐cell morphology in male Zucker diabetic fatty (ZDF) rats, a model of type 2 diabetes. EXPERIMENTAL APPROACH Male ZDF rats were treated with oral sCT (0.5, 1.0 or 2 mg·kg−1) or oral vehicle twice daily from age 8 to 18 weeks. Zucker lean rats served as control group. Fasting and non‐fasted blood glucose, glycosylated haemoglobin (HbA1c) and levels of pancreas and incretin hormones were determined. Oral glucose tolerance test and i.p. glucose tolerance test were compared, and beta‐cell area and function were evaluated. KEY RESULTS Oral sCT treatment dose‐dependently attenuated fasting and non‐fasted hyperglycaemia during the intervention period. At the end of the study period, oral sCT treatment by dose decreased diabetic hyperglycaemia by ∼9 mM and reduced HbA1c levels by 1.7%. Furthermore, a pronounced reduction in glucose excursions was dose‐dependently observed for oral sCT treatment during oral glucose tolerance test. In addition, oral sCT treatment sustained hyperinsulinaemia and attenuated hyperglucagonaemia and hypersecretion of total glucagon‐like peptide‐1 predominantly in the basal state. Lastly, oral sCT treatment dose‐dependently improved pancreatic beta‐cell function and beta‐cell area at study end. CONCLUSIONS AND IMPLICATIONS Oral sCT attenuated diabetic hyperglycaemia in male ZDF rats by improving postprandial glycaemic control, exerting an insulinotropic and glucagonostatic action in the basal state and by preserving pancreatic beta‐cell function and beta‐cell area.

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Section: Discussionmentioning

confidence: 99%

Oral salmon calcitonin attenuates hyperglycaemia and preserves pancreatic beta‐cell area and function in Zucker diabetic fatty rats

Feigh

Andreassen

Neutzsky-Wulff

et al. 2012

British J Pharmacology

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“…That is, application of a 4-mA, 300-μsec, and 70-msec stimulus, which corresponds to electrical stimulation parameters used in gastric stimulation for the reduction of nausea, results in a significant increase in circulating glucose (explained by a likely attenuation in whole body glucose uptake because of the observed decrease in insulin associated with the stimulus). However, application of a 4-mA, 300-μsec, and 25-msec stimulus, results in a decrease in glucose with an associated increase in circulating insulin (Chen et al 2010). While in both instances there is a clear direct effect on hepatic tissues by the electrical stimulus resulting in local changes in glycogenesis and glycogenolysis, it is also clear that the stimulation of the present hepatic vagus nerve alters the secretion of insulin by the pancreas (Rozman et al 2002;Rozman and Bunc 2004).…”

Section: Some Additional Comparisons Of Hepatic Ultrasound To Implant...mentioning

confidence: 99%

Noninvasive Neuromodulation of Peripheral Nerve Pathways Using Ultrasound and Its Current Therapeutic Implications

Puleo

Cotero

2019

Cold Spring Harb Perspect Med

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“…Intriguingly, a previous study demonstrated that hepatic electrical stimulation decreased fasting and fed blood glucose in normal and diabetic rats, a result that may be mediated by the release of glucagon-like peptide-1 (GLP-1) (33). Moreover, another previous study demonstrated that SGES using optically appropriate parameters improved vagotomy-induced impairment in gastric accommodation resulting from vagotomy (34).…”

Section: Discussionmentioning

confidence: 99%

Gastric electrical stimulation improves enteric neuronal survival

Wang

Song

et al. 2017

International Journal of Molecular Medicine

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Research and clinical experience with vagotomy have confirmed that damage to the central nervous system severely affects physiological movement in the gastrointestinal system. The aim of this study was to investigate the effects of synchronized dual-pulse gastric electrical stimulation (SGES) on the apoptosis of enteric neurons and the possible pathways involved in these effects in vagotomized rats. For this purpose, Male Sprague-Dawley (SD) rats were randomized into a control group, an early subdiaphragmatic vagotomized group (ESDV group), an early subdiaphragmatic vagotomized group with short-term SGES (ESDV + SSGES group), a terminal subdiaphragmatic vagotomized group (TSDV group) and a terminal subdiaphragmatic vagotomized group with long-term SGES (TSDV + LSGES group). The expression levels of connexin 43 (Cx43), glial cell line-derived neurotrophic factor (GDNF), p-Akt, pan-Akt and PGP9.5 were assessed by RT-qPCR, western blot analysis and immunofluorescence staining. Apoptosis was determined by terminal-deoxynucleoitidyl transferase-mediated nick-end labeling (TUNEL) assay. We found that Cx43 expression was decreased in the ESDV and TSDV groups, but was significantly upregulated in the SSGES and LSGES groups. In addition, the GDNF and PGP9.5 expression levels were significantly decreased in the ESDV group compared with the control and TSDV groups and were upregulated in both the SSGES and LSGES groups. The LSGES group exhibited a clear increase in p-Akt expression compared with the TSDV group. Fewer TUNEL-positive cells were observed in the SSGES and LSGES groups than in the ESDV and TSDV groups. More TUNEL-positive cells were found in the stomach of rats subjected to subdiaphragmatic vagotomy. On the whole, our data indicate that SGES improved enteric neuronal survival, possibly through GDNF and the phosphatidylinositol 3-kinase (PI3K)/Akt pathways.

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Hepatic electrical stimulation reduces blood glucose in diabetic rats

Abstract: Hepatic electrical stimulation is capable of reducing both fasting and fed blood glucose in normal, and type 1 and type 2 diabetic rats and the effect may be partially mediated via an increase in GLP-1 release.

Cited by 13 publications

References 39 publications

Oral salmon calcitonin attenuates hyperglycaemia and preserves pancreatic beta‐cell area and function in Zucker diabetic fatty rats

Oral salmon calcitonin attenuates hyperglycaemia and preserves pancreatic beta‐cell area and function in Zucker diabetic fatty rats

Noninvasive Neuromodulation of Peripheral Nerve Pathways Using Ultrasound and Its Current Therapeutic Implications

Gastric electrical stimulation improves enteric neuronal survival

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