Effect of enriching the diet with menhaden oil or daily treatment with resolvin D1 on neuropathy in a mouse model of type 2 diabetes

Hanna Shevalye; Matthew S Yorek; Lawrence J Coppey; Amey Holmes; Matthew M Harper; Randy H Kardon; Mark A Yorek

doi:10.1152/jn.00224.2015

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Effect of enriching the diet with menhaden oil or daily treatment with resolvin D1 on neuropathy in a mouse model of type 2 diabetes

Journal article

Open access

Peer reviewed

Effect of enriching the diet with menhaden oil or daily treatment with resolvin D1 on neuropathy in a mouse model of type 2 diabetes

Hanna Shevalye, Matthew S Yorek, Lawrence J Coppey, Amey Holmes, Matthew M Harper, Randy H Kardon and Mark A Yorek

Journal of neurophysiology, Vol.114(1), pp.199-208

07/2015

DOI: 10.1152/jn.00224.2015

PMCID: PMC4507972

PMID: 25925322

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Abstract

The purpose of this study was to determine the effect of supplementing the diet of a mouse model of type 2 diabetes with menhaden (fish) oil or daily treatment with resolvin D1 on diabetic neuropathy. The end points evaluated included motor and sensory nerve conduction velocity, thermal sensitivity, innervation of sensory nerves in the cornea and skin, and the retinal ganglion cell complex thickness. Menhaden oil is a natural source for n-3 polyunsaturated fatty acids, which have been shown to have beneficial effects in other diseases. Resolvin D1 is a metabolite of docosahexaenoic acid and is known to have anti-inflammatory and neuroprotective properties. To model type 2 diabetes, mice were fed a high-fat diet for 8 wk followed by a low dosage of streptozotocin. After 8 wk of hyperglycemia, mice in experimental groups were treated for 6 wk with menhaden oil in the diet or daily injections of 1 ng/g body wt resolvin D1. Our findings show that menhaden oil or resolvin D1 did not improve elevated blood glucose, HbA1C, or glucose utilization. Untreated diabetic mice were thermal hypoalgesic, had reduced motor and sensory nerve conduction velocities, had decreased innervation of the cornea and skin, and had thinner retinal ganglion cell complex. These end points were significantly improved with menhaden oil or resolvin D1 treatment. Exogenously, resolvin D1 stimulated neurite outgrowth from primary cultures of dorsal root ganglion neurons from normal mice. These studies suggest that n-3 polyunsaturated fatty acids derived from fish oil could be an effective treatment for diabetic neuropathy.

Neurons - pathology

Diabetes Mellitus, Experimental - drug therapy

Neurites - physiology

Diabetes Mellitus, Experimental - diet therapy

Retinal Ganglion Cells - pathology

Hyperalgesia - diet therapy

Neuroprotective Agents - pharmacology

Diet, High-Fat

Neurons - physiology

Fish Oils - administration & dosage

Cornea - pathology

Diabetes Mellitus, Type 2

Neurons - drug effects

Neurites - drug effects

Skin - pathology

Diabetes Mellitus, Experimental - physiopathology

Diabetic Neuropathies - physiopathology

Anti-Inflammatory Agents - pharmacology

Mice, Inbred C57BL

Cells, Cultured

Ganglia, Spinal - physiology

Neural Conduction - physiology

Diabetic Neuropathies - drug therapy

Hot Temperature

Hyperalgesia - physiopathology

Docosahexaenoic Acids - pharmacology

Animals

Hyperalgesia - drug therapy

Diabetic Neuropathies - pathology

Diabetes Mellitus, Experimental - pathology

Skin - innervation

Cornea - innervation

Ganglia, Spinal - drug effects

Dietary Supplements

Diabetic Neuropathies - diet therapy

Details

Title: Subtitle: Effect of enriching the diet with menhaden oil or daily treatment with resolvin D1 on neuropathy in a mouse model of type 2 diabetes
Creators: Hanna Shevalye - Department of Internal Medicine, University of Iowa, Iowa City, Iowa
Matthew S Yorek - Department of Veterans Affairs Iowa City Health Care System, Iowa City, Iowa; Veterans Affairs Center for the Prevention and Treatment of Visual Loss, Iowa City, Iowa; and mark-yorek@uiowa.edu
Lawrence J Coppey - Department of Internal Medicine, University of Iowa, Iowa City, Iowa
Amey Holmes - Department of Veterans Affairs Iowa City Health Care System, Iowa City, Iowa
Matthew M Harper - Department of Veterans Affairs Iowa City Health Care System, Iowa City, Iowa; Department of Ophthalmology and Visual Sciences, University of Iowa, Iowa City, Iowa; Veterans Affairs Center for the Prevention and Treatment of Visual Loss, Iowa City, Iowa; and
Randy H Kardon - Department of Veterans Affairs Iowa City Health Care System, Iowa City, Iowa; Department of Ophthalmology and Visual Sciences, University of Iowa, Iowa City, Iowa; Veterans Affairs Center for the Prevention and Treatment of Visual Loss, Iowa City, Iowa; and
Mark A Yorek - Department of Veterans Affairs Iowa City Health Care System, Iowa City, Iowa; Department of Internal Medicine, University of Iowa, Iowa City, Iowa; Veterans Affairs Center for the Prevention and Treatment of Visual Loss, Iowa City, Iowa; and Fraternal Order of Eagles Diabetes Research Center, University of Iowa, Iowa City, Iowa
Resource Type: Journal article
Publication Details: Journal of neurophysiology, Vol.114(1), pp.199-208
DOI: 10.1152/jn.00224.2015
PMID: 25925322
PMCID: PMC4507972
NLM abbreviation: J Neurophysiol
ISSN: 1522-1598
eISSN: 1522-1598
Publisher: United States
Grant note: I01 RX000889 / RRD VA DK-081147 / NIDDK NIH HHS
Language: English
Date published: 07/2015
Academic Unit: Iowa Neuroscience Institute; Biology; Internal Medicine; Ophthalmology and Visual Sciences
Record Identifier: 9983980060602771

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