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Intranasal Insulin Ameliorates Experimental Diabetic Neuropathy

2009· article· en· 71 citations· W2099512544 on OpenAlex· 10.2337/db08-1287

Why is this work in the frame?

A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

Canadian affiliationAn author listed a Canadian institution. This is the only route the usual frame has.
Canadian funderA Canadian agency funded it. The work may carry no Canadian affiliation at all.

Post-publication record

Nature
Retraction
Reason
Duplication of/in Image;Investigation by Journal/Publisher;Manipulation of Images;
Date
5/1/2014 0:00
Flagged by OpenAlex?
Yes

Source: Retraction Watch, joined by DOI. OpenAlex records retraction as is_retracted, a boolean over a state space with at least four values, so it cannot express an expression of concern, a correction or a reinstatement — it reports them as false, which reads as “fine”.

Abstract

OBJECTIVE: We hypothesized that intranasal insulin (I-I) delivery targets the nervous system while avoiding potential adverse systemic effects when compared with subcutaneous insulin (S-I) for experimental streptozotocin-induced diabetic peripheral neuropathy (DPN). RESEARCH DESIGN AND METHODS: I-I or S-I at 0.87 IU daily or placebo were delivered in separate cohorts of diabetic and nondiabetic CD1 mice during 8 months of diabetes. Radiolabeled insulin detection was used to compare delivery and biodistribution for I-I and S-I. Biweekly behavioral testing and monthly electrophysiological and quantitative studies assessed progression of DPN. At and before end point, morphometric analysis of DRG, peripheral nerve, distal epidermal innervation, and specific molecular markers were evaluated. RESULTS: Radiolabeled I-I resulted in more rapid and concentrated delivery to the spinal cord and DRG with less systemic insulin exposure. When compared with S-I or intranasal placebo, I-I reduced overall mouse mortality and sensory loss while improving neuropathic pain and electrophysiological/morphological abnormalities in diabetic mice. I-I restored mRNA and protein levels of phosphoinositide 3-kinase/Akt, cyclic AMP response element-binding protein, and glycogen synthase kinase 3beta to near normal levels within diabetic DRGs. CONCLUSIONS: I-I slows the progression of experimental DPN in streptozotocin mice, avoids adverse effects associated with S-I treatment, and prolongs lifespan when compared with S-I. I-I may be a promising approach for the treatment of DPN.

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The record

Venue
Diabetes
Topic
Pain Mechanisms and Treatments
Field
Medicine
Canadian institutions
Hotchkiss Brain InstituteUniversity of Calgary
Funders
Alberta Heritage Foundation for Medical ResearchFondation pour la Recherche MédicaleCanadian Diabetes Association
Keywords
MedicineNasal administrationInsulinDiabetic neuropathyDiabetes mellitusInternal medicineEndocrinologyPharmacology
Has abstract in OpenAlex
yes