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Hyperinsulinemia/diabetes, hearing, and aging in the University of Wisconsin calorie restriction monkeys.

Identifieur interne : 000F02 ( Main/Exploration ); précédent : 000F01; suivant : 000F03

Hyperinsulinemia/diabetes, hearing, and aging in the University of Wisconsin calorie restriction monkeys.

Auteurs : Cynthia G. Fowler [États-Unis] ; Kirstin Beach Chiasson [États-Unis] ; Ricki J. Colman [États-Unis] ; Joseph W. Kemnitz [États-Unis] ; T Mark Beasley [États-Unis] ; Richard H. Weindruch [États-Unis]

Source :

RBID : pubmed:26163094

Descripteurs français

English descriptors

Abstract

The purpose of this study was to determine the effects of hyperinsulinemia/Type 2 diabetes mellitus (HI-T2DM) on hearing impairment using rhesus monkeys to obtain control over diet and lifestyle factors that confound human studies. The study is a retrospective evaluation of rhesus monkeys from the Wisconsin National Primate Research Center (WNPRC) study on caloric restriction and aging. The research questions were the following: 1. Is HI-T2DM related to hearing impairment? 2. If so, what is the site of lesion in the auditory system? and 3. What physiological factors affect the risk of hearing loss in HI-T2DM? Three groups of eight monkeys each were matched by sex and age; the caloric restricted (CR) monkeys had a reduced risk of diabetes, the normal control (NL) group had a normal risk, and the hyperinsulinemia/diabetes (HI-D) group had already developed HI-T2DM. Auditory testing included distortion product otoacoustic emissions (DPOAEs) with f2 frequencies from 2211 to 8837 Hz and auditory brainstem responses (ABRs) obtained with clicks and tone bursts (8, 16, and 32 kHz). DPOAEs had signal-to-noise ratios 8-17 dB larger in the NL group than in the HI-D and CR groups, signifying that cochlear function was best in the NL group. ABR thresholds were 5-8 dB better in the NL group than in the HI-D group, although no significant differences across the groups were evident for the thresholds, latencies, interwave intervals, or amplitudes. Correlations were significant for quadratic relations between body mass index (BMI) and DPOAE, with largest DPOAEs for animals in the middle of the BMI range. ABR thresholds elicited with 16 and 32 kHz signals were significantly correlated, positively with BMI and HbA1c, and negatively with KG (glucose tolerance), SI (insulin sensitivity index) and DI (disposition index). These findings suggest that the hearing loss associated with HI-T2DM is predominantly cochlear, and auditory structures underlying the higher frequencies are at risk with HI-T2DM. Loss of auditory function begins in the hyperinsulinemia, pre-diabetic state.

DOI: 10.1016/j.heares.2015.07.001
PubMed: 26163094
PubMed Central: PMC4581975


Affiliations:


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Le document en format XML

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<term>Aging (MeSH)</term>
<term>Animals (MeSH)</term>
<term>Auditory Threshold (physiology)</term>
<term>Blood Glucose (analysis)</term>
<term>Body Mass Index (MeSH)</term>
<term>Caloric Restriction (MeSH)</term>
<term>Cochlea (physiology)</term>
<term>Diabetes Complications (MeSH)</term>
<term>Diabetes Mellitus, Type 2 (complications)</term>
<term>Diabetes Mellitus, Type 2 (physiopathology)</term>
<term>Evoked Potentials, Auditory, Brain Stem (physiology)</term>
<term>Female (MeSH)</term>
<term>Hearing (MeSH)</term>
<term>Hearing Loss (complications)</term>
<term>Hyperinsulinism (complications)</term>
<term>Hyperinsulinism (physiopathology)</term>
<term>Life Style (MeSH)</term>
<term>Macaca mulatta (MeSH)</term>
<term>Male (MeSH)</term>
<term>Models, Animal (MeSH)</term>
<term>Otoacoustic Emissions, Spontaneous (physiology)</term>
<term>Prediabetic State (complications)</term>
<term>Reproducibility of Results (MeSH)</term>
<term>Retrospective Studies (MeSH)</term>
<term>Risk Factors (MeSH)</term>
<term>Signal-To-Noise Ratio (MeSH)</term>
</keywords>
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<term>Animaux (MeSH)</term>
<term>Cochlée (physiologie)</term>
<term>Complications du diabète (MeSH)</term>
<term>Diabète de type 2 (complications)</term>
<term>Diabète de type 2 (physiopathologie)</term>
<term>Facteurs de risque (MeSH)</term>
<term>Femelle (MeSH)</term>
<term>Glycémie (analyse)</term>
<term>Hyperinsulinisme (complications)</term>
<term>Hyperinsulinisme (physiopathologie)</term>
<term>Indice de masse corporelle (MeSH)</term>
<term>Macaca mulatta (MeSH)</term>
<term>Mode de vie (MeSH)</term>
<term>Modèles animaux (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Ouïe (MeSH)</term>
<term>Perte d'audition (complications)</term>
<term>Potentiels évoqués auditifs du tronc cérébral (physiologie)</term>
<term>Rapport signal-bruit (MeSH)</term>
<term>Reproductibilité des résultats (MeSH)</term>
<term>Restriction calorique (MeSH)</term>
<term>Seuil auditif (physiologie)</term>
<term>Vieillissement (MeSH)</term>
<term>Émissions otoacoustiques spontanées (physiologie)</term>
<term>État prédiabétique (complications)</term>
<term>Études rétrospectives (MeSH)</term>
</keywords>
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<term>Blood Glucose</term>
</keywords>
<keywords scheme="MESH" qualifier="analyse" xml:lang="fr">
<term>Glycémie</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en">
<term>Diabetes Mellitus, Type 2</term>
<term>Hearing Loss</term>
<term>Hyperinsulinism</term>
<term>Prediabetic State</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr">
<term>Cochlée</term>
<term>Potentiels évoqués auditifs du tronc cérébral</term>
<term>Seuil auditif</term>
<term>Émissions otoacoustiques spontanées</term>
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<term>Auditory Threshold</term>
<term>Cochlea</term>
<term>Evoked Potentials, Auditory, Brain Stem</term>
<term>Otoacoustic Emissions, Spontaneous</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr">
<term>Diabète de type 2</term>
<term>Hyperinsulinisme</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en">
<term>Diabetes Mellitus, Type 2</term>
<term>Hyperinsulinism</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Aging</term>
<term>Animals</term>
<term>Body Mass Index</term>
<term>Caloric Restriction</term>
<term>Diabetes Complications</term>
<term>Female</term>
<term>Hearing</term>
<term>Life Style</term>
<term>Macaca mulatta</term>
<term>Male</term>
<term>Models, Animal</term>
<term>Reproducibility of Results</term>
<term>Retrospective Studies</term>
<term>Risk Factors</term>
<term>Signal-To-Noise Ratio</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="fr">
<term>Animaux</term>
<term>Complications du diabète</term>
<term>Diabète de type 2</term>
<term>Facteurs de risque</term>
<term>Femelle</term>
<term>Hyperinsulinisme</term>
<term>Indice de masse corporelle</term>
<term>Macaca mulatta</term>
<term>Mode de vie</term>
<term>Modèles animaux</term>
<term>Mâle</term>
<term>Ouïe</term>
<term>Perte d'audition</term>
<term>Rapport signal-bruit</term>
<term>Reproductibilité des résultats</term>
<term>Restriction calorique</term>
<term>Vieillissement</term>
<term>État prédiabétique</term>
<term>Études rétrospectives</term>
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<front>
<div type="abstract" xml:lang="en">The purpose of this study was to determine the effects of hyperinsulinemia/Type 2 diabetes mellitus (HI-T2DM) on hearing impairment using rhesus monkeys to obtain control over diet and lifestyle factors that confound human studies. The study is a retrospective evaluation of rhesus monkeys from the Wisconsin National Primate Research Center (WNPRC) study on caloric restriction and aging. The research questions were the following: 1. Is HI-T2DM related to hearing impairment? 2. If so, what is the site of lesion in the auditory system? and 3. What physiological factors affect the risk of hearing loss in HI-T2DM? Three groups of eight monkeys each were matched by sex and age; the caloric restricted (CR) monkeys had a reduced risk of diabetes, the normal control (NL) group had a normal risk, and the hyperinsulinemia/diabetes (HI-D) group had already developed HI-T2DM. Auditory testing included distortion product otoacoustic emissions (DPOAEs) with f2 frequencies from 2211 to 8837 Hz and auditory brainstem responses (ABRs) obtained with clicks and tone bursts (8, 16, and 32 kHz). DPOAEs had signal-to-noise ratios 8-17 dB larger in the NL group than in the HI-D and CR groups, signifying that cochlear function was best in the NL group. ABR thresholds were 5-8 dB better in the NL group than in the HI-D group, although no significant differences across the groups were evident for the thresholds, latencies, interwave intervals, or amplitudes. Correlations were significant for quadratic relations between body mass index (BMI) and DPOAE, with largest DPOAEs for animals in the middle of the BMI range. ABR thresholds elicited with 16 and 32 kHz signals were significantly correlated, positively with BMI and HbA1c, and negatively with KG (glucose tolerance), SI (insulin sensitivity index) and DI (disposition index). These findings suggest that the hearing loss associated with HI-T2DM is predominantly cochlear, and auditory structures underlying the higher frequencies are at risk with HI-T2DM. Loss of auditory function begins in the hyperinsulinemia, pre-diabetic state. </div>
</front>
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<Month>07</Month>
<Day>12</Day>
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<Abstract>
<AbstractText>The purpose of this study was to determine the effects of hyperinsulinemia/Type 2 diabetes mellitus (HI-T2DM) on hearing impairment using rhesus monkeys to obtain control over diet and lifestyle factors that confound human studies. The study is a retrospective evaluation of rhesus monkeys from the Wisconsin National Primate Research Center (WNPRC) study on caloric restriction and aging. The research questions were the following: 1. Is HI-T2DM related to hearing impairment? 2. If so, what is the site of lesion in the auditory system? and 3. What physiological factors affect the risk of hearing loss in HI-T2DM? Three groups of eight monkeys each were matched by sex and age; the caloric restricted (CR) monkeys had a reduced risk of diabetes, the normal control (NL) group had a normal risk, and the hyperinsulinemia/diabetes (HI-D) group had already developed HI-T2DM. Auditory testing included distortion product otoacoustic emissions (DPOAEs) with f2 frequencies from 2211 to 8837 Hz and auditory brainstem responses (ABRs) obtained with clicks and tone bursts (8, 16, and 32 kHz). DPOAEs had signal-to-noise ratios 8-17 dB larger in the NL group than in the HI-D and CR groups, signifying that cochlear function was best in the NL group. ABR thresholds were 5-8 dB better in the NL group than in the HI-D group, although no significant differences across the groups were evident for the thresholds, latencies, interwave intervals, or amplitudes. Correlations were significant for quadratic relations between body mass index (BMI) and DPOAE, with largest DPOAEs for animals in the middle of the BMI range. ABR thresholds elicited with 16 and 32 kHz signals were significantly correlated, positively with BMI and HbA1c, and negatively with KG (glucose tolerance), SI (insulin sensitivity index) and DI (disposition index). These findings suggest that the hearing loss associated with HI-T2DM is predominantly cochlear, and auditory structures underlying the higher frequencies are at risk with HI-T2DM. Loss of auditory function begins in the hyperinsulinemia, pre-diabetic state. </AbstractText>
<CopyrightInformation>Copyright © 2015 Elsevier B.V. All rights reserved.</CopyrightInformation>
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<LastName>Fowler</LastName>
<ForeName>Cynthia G</ForeName>
<Initials>CG</Initials>
<AffiliationInfo>
<Affiliation>Department of Communication Sciences and Disorders, University of Wisconsin-Madison, 1975 Willow Drive Madison, Madison, WI 53706, USA. Electronic address: cgfowler@wisc.edu.</Affiliation>
</AffiliationInfo>
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<LastName>Chiasson</LastName>
<ForeName>Kirstin Beach</ForeName>
<Initials>KB</Initials>
<AffiliationInfo>
<Affiliation>Cascade Ear, Nose, Throat, and Facial Plastic Surgery, Klamath Falls, OR, USA.</Affiliation>
</AffiliationInfo>
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<ForeName>Ricki J</ForeName>
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<AffiliationInfo>
<Affiliation>Wisconsin National Primate Research Center, University of Wisconsin-Madison, 1220 Capitol Court, Madison, WI 53715-1299, USA. Electronic address: rcolman@primate.wisc.edu.</Affiliation>
</AffiliationInfo>
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<ForeName>Joseph W</ForeName>
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<Affiliation>Wisconsin National Primate Research Center, University of Wisconsin-Madison, 1220 Capitol Court, Madison, WI 53715-1299, USA; Department of Cell and Regenerative Biology, University of Wisconsin-Madison, 1220 Capitol Court, Madison, WI 53715-1299, USA. Electronic address: kemnitz@primate.wisc.edu.</Affiliation>
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<Initials>TM</Initials>
<AffiliationInfo>
<Affiliation>Department of Biostatistics, School of Public Health, Ryals Public Health Bldg., University of Alabama at Birmingham, Birmingham, AL 35294, USA. Electronic address: mbeasley@ms.soph.uab.edu.</Affiliation>
</AffiliationInfo>
</Author>
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<Affiliation>Department of Medicine, University of Wisconsin-Madison, Room B72 Veterans Admin Hospital, William S. Middleton Memorial Veterans Hospital, 2500 Overlook Terrace, Madison, WI 53705-2286, USA. Electronic address: rhweindr@wisc.edu.</Affiliation>
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