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Bioelectronic modulation of carotid sinus nerve activity in the rat: a potential therapeutic approach for type 2 diabetes

Aims/hypothesis A new class of treatments termed bioelectronic medicines are now emerging that aim to target individual nerve fibres or specific brain circuits in pathological conditions to repair lost function and reinstate a healthy balance. Carotid sinus nerve (CSN) denervation has been shown to... Full description

Journal Title: Diabetologia 2018, Vol.61 (3), p.700-710
Main Author: Sacramento, Joana F
Other Authors: Chew, Daniel J , Melo, Bernardete F , Donegá, Matteo , Dopson, Wesley , Guarino, Maria P , Robinson, Alison , Prieto-Lloret, Jesus , Patel, Sonal , Holinski, Bradley J , Ramnarain, Nishan , Pikov, Victor , Famm, Kristoffer , Conde, Silvia V
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: Berlin/Heidelberg: Springer Berlin Heidelberg
ID: ISSN: 0012-186X
Link: https://www.ncbi.nlm.nih.gov/pubmed/29332196
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recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6448966
title: Bioelectronic modulation of carotid sinus nerve activity in the rat: a potential therapeutic approach for type 2 diabetes
format: Article
creator:
  • Sacramento, Joana F
  • Chew, Daniel J
  • Melo, Bernardete F
  • Donegá, Matteo
  • Dopson, Wesley
  • Guarino, Maria P
  • Robinson, Alison
  • Prieto-Lloret, Jesus
  • Patel, Sonal
  • Holinski, Bradley J
  • Ramnarain, Nishan
  • Pikov, Victor
  • Famm, Kristoffer
  • Conde, Silvia V
subjects:
  • Animal models
  • Animals
  • Article
  • Blood Glucose - metabolism
  • C-Peptide - blood
  • Carotid body
  • Carotid sinus
  • Carotid Sinus - innervation
  • Carotid sinus nerve
  • Chemoreception
  • Corticosterone - blood
  • Denervation
  • Dextrose
  • Diabetes
  • Diabetes mellitus
  • Diabetes mellitus (non-insulin dependent)
  • Diabetes Mellitus, Type 2 - blood
  • Diabetes Mellitus, Type 2 - physiopathology
  • Drinking water
  • Electromyography
  • Glucose
  • Glucose tolerance
  • Glucose tolerance tests
  • Health aspects
  • Heart diseases
  • Homeostasis
  • Human Physiology
  • Hypoxia
  • Insulin
  • Insulin - blood
  • Insulin resistance
  • Insulin Resistance - physiology
  • Interfaces
  • Internal Medicine
  • Intolerance
  • KHFAC modulation
  • Male
  • Medicine
  • Medicine & Public Health
  • Metabolic Diseases
  • Metabolism
  • Neuromodulation
  • Nitric Oxide - blood
  • Plethysmography
  • Rats
  • Rodents
  • Sinus
  • Sucrose
  • Surgery
  • Type 2 diabetes
ispartof: Diabetologia, 2018, Vol.61 (3), p.700-710
description: Aims/hypothesis A new class of treatments termed bioelectronic medicines are now emerging that aim to target individual nerve fibres or specific brain circuits in pathological conditions to repair lost function and reinstate a healthy balance. Carotid sinus nerve (CSN) denervation has been shown to improve glucose homeostasis in insulin-resistant and glucose-intolerant rats; however, these positive effects from surgery appear to diminish over time and are heavily caveated by the severe adverse effects associated with permanent loss of chemosensory function. Herein we characterise the ability of a novel bioelectronic application, classified as kilohertz frequency alternating current (KHFAC) modulation, to suppress neural signals within the CSN of rodents. Methods Rats were fed either a chow or high-fat/high-sucrose (HFHSu) diet (60% lipid-rich diet plus 35% sucrose drinking water) over 14 weeks. Neural interfaces were bilaterally implanted in the CSNs and attached to an external pulse generator. The rats were then randomised to KHFAC or sham modulation groups. KHFAC modulation variables were defined acutely by respiratory and cardiac responses to hypoxia (10% O 2  + 90% N 2 ). Insulin sensitivity was evaluated periodically through an ITT and glucose tolerance by an OGTT. Results KHFAC modulation of the CSN, applied over 9 weeks, restored insulin sensitivity (constant of the insulin tolerance test [K ITT ] HFHSu sham, 2.56 ± 0.41% glucose/min; K ITT HFHSu KHFAC, 5.01 ± 0.52% glucose/min) and glucose tolerance (AUC HFHSu sham, 1278 ± 20.36 mmol/l × min; AUC HFHSu KHFAC, 1054.15 ± 62.64 mmol/l × min) in rat models of type 2 diabetes. Upon cessation of KHFAC, insulin resistance and glucose intolerance returned to normal values within 5 weeks. Conclusions/interpretation KHFAC modulation of the CSN improves metabolic control in rat models of type 2 diabetes. These positive outcomes have significant translational potential as a novel therapeutic modality for the purpose of treating metabolic diseases in humans.
language: eng
source:
identifier: ISSN: 0012-186X
fulltext: no_fulltext
issn:
  • 0012-186X
  • 1432-0428
url: Link


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titleBioelectronic modulation of carotid sinus nerve activity in the rat: a potential therapeutic approach for type 2 diabetes
creatorSacramento, Joana F ; Chew, Daniel J ; Melo, Bernardete F ; Donegá, Matteo ; Dopson, Wesley ; Guarino, Maria P ; Robinson, Alison ; Prieto-Lloret, Jesus ; Patel, Sonal ; Holinski, Bradley J ; Ramnarain, Nishan ; Pikov, Victor ; Famm, Kristoffer ; Conde, Silvia V
creatorcontribSacramento, Joana F ; Chew, Daniel J ; Melo, Bernardete F ; Donegá, Matteo ; Dopson, Wesley ; Guarino, Maria P ; Robinson, Alison ; Prieto-Lloret, Jesus ; Patel, Sonal ; Holinski, Bradley J ; Ramnarain, Nishan ; Pikov, Victor ; Famm, Kristoffer ; Conde, Silvia V
descriptionAims/hypothesis A new class of treatments termed bioelectronic medicines are now emerging that aim to target individual nerve fibres or specific brain circuits in pathological conditions to repair lost function and reinstate a healthy balance. Carotid sinus nerve (CSN) denervation has been shown to improve glucose homeostasis in insulin-resistant and glucose-intolerant rats; however, these positive effects from surgery appear to diminish over time and are heavily caveated by the severe adverse effects associated with permanent loss of chemosensory function. Herein we characterise the ability of a novel bioelectronic application, classified as kilohertz frequency alternating current (KHFAC) modulation, to suppress neural signals within the CSN of rodents. Methods Rats were fed either a chow or high-fat/high-sucrose (HFHSu) diet (60% lipid-rich diet plus 35% sucrose drinking water) over 14 weeks. Neural interfaces were bilaterally implanted in the CSNs and attached to an external pulse generator. The rats were then randomised to KHFAC or sham modulation groups. KHFAC modulation variables were defined acutely by respiratory and cardiac responses to hypoxia (10% O 2  + 90% N 2 ). Insulin sensitivity was evaluated periodically through an ITT and glucose tolerance by an OGTT. Results KHFAC modulation of the CSN, applied over 9 weeks, restored insulin sensitivity (constant of the insulin tolerance test [K ITT ] HFHSu sham, 2.56 ± 0.41% glucose/min; K ITT HFHSu KHFAC, 5.01 ± 0.52% glucose/min) and glucose tolerance (AUC HFHSu sham, 1278 ± 20.36 mmol/l × min; AUC HFHSu KHFAC, 1054.15 ± 62.64 mmol/l × min) in rat models of type 2 diabetes. Upon cessation of KHFAC, insulin resistance and glucose intolerance returned to normal values within 5 weeks. Conclusions/interpretation KHFAC modulation of the CSN improves metabolic control in rat models of type 2 diabetes. These positive outcomes have significant translational potential as a novel therapeutic modality for the purpose of treating metabolic diseases in humans.
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languageeng
publisherBerlin/Heidelberg: Springer Berlin Heidelberg
subjectAnimal models ; Animals ; Article ; Blood Glucose - metabolism ; C-Peptide - blood ; Carotid body ; Carotid sinus ; Carotid Sinus - innervation ; Carotid sinus nerve ; Chemoreception ; Corticosterone - blood ; Denervation ; Dextrose ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - physiopathology ; Drinking water ; Electromyography ; Glucose ; Glucose tolerance ; Glucose tolerance tests ; Health aspects ; Heart diseases ; Homeostasis ; Human Physiology ; Hypoxia ; Insulin ; Insulin - blood ; Insulin resistance ; Insulin Resistance - physiology ; Interfaces ; Internal Medicine ; Intolerance ; KHFAC modulation ; Male ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Metabolism ; Neuromodulation ; Nitric Oxide - blood ; Plethysmography ; Rats ; Rodents ; Sinus ; Sucrose ; Surgery ; Type 2 diabetes
ispartofDiabetologia, 2018, Vol.61 (3), p.700-710
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7Prieto-Lloret, Jesus
8Patel, Sonal
9Holinski, Bradley J
10Ramnarain, Nishan
11Pikov, Victor
12Famm, Kristoffer
13Conde, Silvia V
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descriptionAims/hypothesis A new class of treatments termed bioelectronic medicines are now emerging that aim to target individual nerve fibres or specific brain circuits in pathological conditions to repair lost function and reinstate a healthy balance. Carotid sinus nerve (CSN) denervation has been shown to improve glucose homeostasis in insulin-resistant and glucose-intolerant rats; however, these positive effects from surgery appear to diminish over time and are heavily caveated by the severe adverse effects associated with permanent loss of chemosensory function. Herein we characterise the ability of a novel bioelectronic application, classified as kilohertz frequency alternating current (KHFAC) modulation, to suppress neural signals within the CSN of rodents. Methods Rats were fed either a chow or high-fat/high-sucrose (HFHSu) diet (60% lipid-rich diet plus 35% sucrose drinking water) over 14 weeks. Neural interfaces were bilaterally implanted in the CSNs and attached to an external pulse generator. The rats were then randomised to KHFAC or sham modulation groups. KHFAC modulation variables were defined acutely by respiratory and cardiac responses to hypoxia (10% O 2  + 90% N 2 ). Insulin sensitivity was evaluated periodically through an ITT and glucose tolerance by an OGTT. Results KHFAC modulation of the CSN, applied over 9 weeks, restored insulin sensitivity (constant of the insulin tolerance test [K ITT ] HFHSu sham, 2.56 ± 0.41% glucose/min; K ITT HFHSu KHFAC, 5.01 ± 0.52% glucose/min) and glucose tolerance (AUC HFHSu sham, 1278 ± 20.36 mmol/l × min; AUC HFHSu KHFAC, 1054.15 ± 62.64 mmol/l × min) in rat models of type 2 diabetes. Upon cessation of KHFAC, insulin resistance and glucose intolerance returned to normal values within 5 weeks. Conclusions/interpretation KHFAC modulation of the CSN improves metabolic control in rat models of type 2 diabetes. These positive outcomes have significant translational potential as a novel therapeutic modality for the purpose of treating metabolic diseases in humans.
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titleBioelectronic modulation of carotid sinus nerve activity in the rat: a potential therapeutic approach for type 2 diabetes
authorSacramento, Joana F ; Chew, Daniel J ; Melo, Bernardete F ; Donegá, Matteo ; Dopson, Wesley ; Guarino, Maria P ; Robinson, Alison ; Prieto-Lloret, Jesus ; Patel, Sonal ; Holinski, Bradley J ; Ramnarain, Nishan ; Pikov, Victor ; Famm, Kristoffer ; Conde, Silvia V
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21Glucose tolerance
22Glucose tolerance tests
23Health aspects
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25Homeostasis
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48Surgery
49Type 2 diabetes
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abstractAims/hypothesis A new class of treatments termed bioelectronic medicines are now emerging that aim to target individual nerve fibres or specific brain circuits in pathological conditions to repair lost function and reinstate a healthy balance. Carotid sinus nerve (CSN) denervation has been shown to improve glucose homeostasis in insulin-resistant and glucose-intolerant rats; however, these positive effects from surgery appear to diminish over time and are heavily caveated by the severe adverse effects associated with permanent loss of chemosensory function. Herein we characterise the ability of a novel bioelectronic application, classified as kilohertz frequency alternating current (KHFAC) modulation, to suppress neural signals within the CSN of rodents. Methods Rats were fed either a chow or high-fat/high-sucrose (HFHSu) diet (60% lipid-rich diet plus 35% sucrose drinking water) over 14 weeks. Neural interfaces were bilaterally implanted in the CSNs and attached to an external pulse generator. The rats were then randomised to KHFAC or sham modulation groups. KHFAC modulation variables were defined acutely by respiratory and cardiac responses to hypoxia (10% O 2  + 90% N 2 ). Insulin sensitivity was evaluated periodically through an ITT and glucose tolerance by an OGTT. Results KHFAC modulation of the CSN, applied over 9 weeks, restored insulin sensitivity (constant of the insulin tolerance test [K ITT ] HFHSu sham, 2.56 ± 0.41% glucose/min; K ITT HFHSu KHFAC, 5.01 ± 0.52% glucose/min) and glucose tolerance (AUC HFHSu sham, 1278 ± 20.36 mmol/l × min; AUC HFHSu KHFAC, 1054.15 ± 62.64 mmol/l × min) in rat models of type 2 diabetes. Upon cessation of KHFAC, insulin resistance and glucose intolerance returned to normal values within 5 weeks. Conclusions/interpretation KHFAC modulation of the CSN improves metabolic control in rat models of type 2 diabetes. These positive outcomes have significant translational potential as a novel therapeutic modality for the purpose of treating metabolic diseases in humans.
copBerlin/Heidelberg
pubSpringer Berlin Heidelberg
pmid29332196
doi10.1007/s00125-017-4533-7
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