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Related Concept Videos

Diabetic Retinopathy01:27

Diabetic Retinopathy

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DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...
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Drugs Acting on Autonomic Ganglia: Stimulants01:23

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Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating...
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Diabetic Neuropathy01:22

Diabetic Neuropathy

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DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
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Diabetic Nephropathy01:28

Diabetic Nephropathy

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Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration...
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Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

68
Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular...
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Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

23
PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
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Related Experiment Video

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Retinal Pathophysiological Evaluation in a Rat Model
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Nicotine accelerates diabetes-induced retinal changes.

Adam Boretsky1, Praveena Gupta, Nima Tirgan

  • 1Center for Biomedical Engineering .

Current Eye Research
|June 10, 2014
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Summary

Nicotine and diabetes significantly alter retinal thickness and neuron survival. Combined use shows increased retinal thickness but reduced ganglion cell neurons, impacting diabetic retinopathy progression.

Keywords:
DiabetesSD-OCTSLOneuronsnicotineretinal thickness

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Area of Science:

  • Ophthalmology
  • Diabetology
  • Toxicology

Background:

  • Diabetic retinopathy is a leading cause of blindness.
  • Nicotine exposure from various sources may affect ocular health.

Purpose of the Study:

  • To investigate the impact of nicotine on retinal changes in early-stage diabetes using a rodent model.
  • To analyze structural retinal alterations induced by nicotine, diabetes, and their combination.

Main Methods:

  • Utilized Sprague-Dawley rats with streptozotocin-induced diabetes and daily nicotine administration.
  • Employed confocal scanning laser ophthalmoscopy and spectral domain optical coherence tomography (SD-OCT) for retinal analysis.
  • Assessed total retinal thickness, layer-specific changes via segmentation, and ganglion cell layer (GCL) neuron survival.

Main Results:

  • Nicotine alone decreased total retinal thickness, primarily in the outer nuclear layer (ONL).
  • Diabetes showed a trend toward decreased retinal thickness, with significant ONL thinning.
  • Combined nicotine and diabetes increased total retinal thickness but significantly reduced GCL neuron survival.

Conclusions:

  • Nicotine and diabetes induce distinct and combined temporal changes in retinal morphology.
  • Findings suggest potential implications for managing diabetic patients using nicotine-containing products.
  • Further research is warranted to understand the clinical impact on diabetic retinopathy treatment strategies.