Nicotine accelerates diabetes-induced retinal changes

Adam Boretsky, Praveena Gupta, Nima Tirgan, Rong Liu, Bernard F. Godley, Wenbo Zhang, Ronald Tilton, Massoud Motamedi

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Abstract Purpose: To investigate the effects of nicotine on retinal alterations in early-stage diabetes in an established rodent model. Materials and Methods: Sprague-Dawley rats were examined using a combination of confocal scanning laser ophthalmoscopy and spectral domain optical coherence tomography to determine changes in retinal structure in response to nicotine exposure, diabetes and the combined effects of nicotine and diabetes. Diabetes was induced by a single injection of 65 mg/kg streptozotocin and nicotine injections were administered subcutaneously daily. Retinal thickness in the superior, inferior, nasal and temporal quadrants were determined based on the spectral domain optical coherence tomography (SD-OCT) volume scans (20° × 20°) centered on the optic disc. Segmentation of discrete retinal layers was performed on a subset of SD-OCT cross-sections to further examine changes in each treatment group. Survival of neurons within the ganglion cell layer (GCL) was assessed by confocal morphometric imaging. Results: The control group did not experience any significant change throughout the study. The nicotine treatment group experienced an average decrease in total retinal thickness (TRT) of 9.4 μm with the majority of the loss localized within the outer nuclear layer (ONL) as determined by segmentation analysis (p < 0.05). The diabetic group exhibited a trend toward decreased TRT while segmentation analysis of the diabetic retinopathy (DR) group revealed significant thinning within the ONL (p < 0.05). The combination of nicotine and diabetes revealed a significant increase of 8.9 μm in the TRT (p < 0.05) accompanied by a decrease in the number of GCL neurons. Conclusions: We demonstrated significant temporal changes in retinal morphology in response to nicotine exposure, diabetes and with the combined effects of nicotine and diabetes. These findings may have implications in determining treatment strategies for diabetic patients using products containing nicotine, such as cigarettes, smokeless tobacco, electronic cigarettes or smoking cessation products.

Original languageEnglish
Pages (from-to)368-377
Number of pages10
JournalCurrent Eye Research
Volume40
Issue number4
DOIs
StatePublished - Apr 1 2015

Fingerprint

Nicotine
Optical Coherence Tomography
Ganglia
Tobacco Use Cessation Products
Smokeless Tobacco
Neurons
Ophthalmoscopy
Injections
Optic Disk
Diabetic Retinopathy
Streptozocin
Nose
Tobacco Products
Sprague Dawley Rats
Rodentia
Lasers
Therapeutics
Cell Count
Smoking
Control Groups

Keywords

  • Diabetes
  • Neurons
  • Nicotine
  • Retinal thickness
  • SD-OCT
  • SLO

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

Nicotine accelerates diabetes-induced retinal changes. / Boretsky, Adam; Gupta, Praveena; Tirgan, Nima; Liu, Rong; Godley, Bernard F.; Zhang, Wenbo; Tilton, Ronald; Motamedi, Massoud.

In: Current Eye Research, Vol. 40, No. 4, 01.04.2015, p. 368-377.

Research output: Contribution to journalArticle

Boretsky, Adam ; Gupta, Praveena ; Tirgan, Nima ; Liu, Rong ; Godley, Bernard F. ; Zhang, Wenbo ; Tilton, Ronald ; Motamedi, Massoud. / Nicotine accelerates diabetes-induced retinal changes. In: Current Eye Research. 2015 ; Vol. 40, No. 4. pp. 368-377.
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AU - Zhang, Wenbo

AU - Tilton, Ronald

AU - Motamedi, Massoud

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N2 - Abstract Purpose: To investigate the effects of nicotine on retinal alterations in early-stage diabetes in an established rodent model. Materials and Methods: Sprague-Dawley rats were examined using a combination of confocal scanning laser ophthalmoscopy and spectral domain optical coherence tomography to determine changes in retinal structure in response to nicotine exposure, diabetes and the combined effects of nicotine and diabetes. Diabetes was induced by a single injection of 65 mg/kg streptozotocin and nicotine injections were administered subcutaneously daily. Retinal thickness in the superior, inferior, nasal and temporal quadrants were determined based on the spectral domain optical coherence tomography (SD-OCT) volume scans (20° × 20°) centered on the optic disc. Segmentation of discrete retinal layers was performed on a subset of SD-OCT cross-sections to further examine changes in each treatment group. Survival of neurons within the ganglion cell layer (GCL) was assessed by confocal morphometric imaging. Results: The control group did not experience any significant change throughout the study. The nicotine treatment group experienced an average decrease in total retinal thickness (TRT) of 9.4 μm with the majority of the loss localized within the outer nuclear layer (ONL) as determined by segmentation analysis (p < 0.05). The diabetic group exhibited a trend toward decreased TRT while segmentation analysis of the diabetic retinopathy (DR) group revealed significant thinning within the ONL (p < 0.05). The combination of nicotine and diabetes revealed a significant increase of 8.9 μm in the TRT (p < 0.05) accompanied by a decrease in the number of GCL neurons. Conclusions: We demonstrated significant temporal changes in retinal morphology in response to nicotine exposure, diabetes and with the combined effects of nicotine and diabetes. These findings may have implications in determining treatment strategies for diabetic patients using products containing nicotine, such as cigarettes, smokeless tobacco, electronic cigarettes or smoking cessation products.

AB - Abstract Purpose: To investigate the effects of nicotine on retinal alterations in early-stage diabetes in an established rodent model. Materials and Methods: Sprague-Dawley rats were examined using a combination of confocal scanning laser ophthalmoscopy and spectral domain optical coherence tomography to determine changes in retinal structure in response to nicotine exposure, diabetes and the combined effects of nicotine and diabetes. Diabetes was induced by a single injection of 65 mg/kg streptozotocin and nicotine injections were administered subcutaneously daily. Retinal thickness in the superior, inferior, nasal and temporal quadrants were determined based on the spectral domain optical coherence tomography (SD-OCT) volume scans (20° × 20°) centered on the optic disc. Segmentation of discrete retinal layers was performed on a subset of SD-OCT cross-sections to further examine changes in each treatment group. Survival of neurons within the ganglion cell layer (GCL) was assessed by confocal morphometric imaging. Results: The control group did not experience any significant change throughout the study. The nicotine treatment group experienced an average decrease in total retinal thickness (TRT) of 9.4 μm with the majority of the loss localized within the outer nuclear layer (ONL) as determined by segmentation analysis (p < 0.05). The diabetic group exhibited a trend toward decreased TRT while segmentation analysis of the diabetic retinopathy (DR) group revealed significant thinning within the ONL (p < 0.05). The combination of nicotine and diabetes revealed a significant increase of 8.9 μm in the TRT (p < 0.05) accompanied by a decrease in the number of GCL neurons. Conclusions: We demonstrated significant temporal changes in retinal morphology in response to nicotine exposure, diabetes and with the combined effects of nicotine and diabetes. These findings may have implications in determining treatment strategies for diabetic patients using products containing nicotine, such as cigarettes, smokeless tobacco, electronic cigarettes or smoking cessation products.

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