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Published on: December 2, 2016
Effects of Melatonin Supplementation on the Aortic Wall in a Diet-Induced Obesity Rat Model
Dariya Chivchibashi-Pavlova1, George S Stoyanov2,3, Kameliya Bratoeva1
1Physiology and Pathophysiology, Medical University of Varna, Varna, BGR.
Insights
Melatonin supplementation prevented diet-induced aortic wall thickening and endothelial dysfunction in rats. This antioxidant may protect against cardiovascular disease risk factors associated with obesity.
Area of Science:
- Cardiovascular research
- Endocrinology
- Vascular biology
Background:
- Cardiovascular disease (CVD) remains a leading global cause of mortality.
- Arterial wall thickness and abdominal obesity are key indicators of CVD risk.
- Obesity-induced oxidative stress and inflammation contribute to vascular pathologies.
Purpose of the Study:
- To investigate the vasoprotective effects of melatonin.
- To assess melatonin's impact on aortic wall thickness in a diet-induced obesity rat model.
- To evaluate the association between abdominal obesity and aortic intima-media thickness.
Main Methods:
- Male Wistar rats were fed a high-fructose diet (HFD) for 12 weeks.
- Groups included control, HFD, HFD with melatonin, and control with melatonin.
- Aortic wall thickness and functional properties (Kernogan's index) were analyzed morphometrically.
Main Results:
- HFD significantly increased body weight, aortic wall thickness, and Kernogan's index.
- Morphometric analysis revealed detrimental changes in the vessel wall of HFD rats.
- Melatonin supplementation effectively prevented these HFD-induced adverse effects.
Conclusions:
- High-fructose diet induced pathomorphological and morphometric changes in the abdominal aorta, indicative of endothelial dysfunction.
- Melatonin administration demonstrated significant vasoprotective effects.
- Melatonin supplementation regressed vascular wall remodeling and restored aortic functional capacity.
Abstract:
Background Cardiovascular disease (CVD) is still the leading cause of death globally. Alterations in the arterial wall architecture predict CVD morbidity and mortality and are associated with other CVD risk factors. Aortic wall thickness is closely linked to short- and long-term CVD morbidity and mortality, even without pronounced atherosclerotic changes. Obesity increases the risk of a broad spectrum of pathologies with vascular manifestation, which are often pathogenically associated with chronic oxidative stress and inflammatory response. Hence, as an antioxidant and anti-inflammatory agent, the pineal gland hormone melatonin is expected to have vasoprotective effects. This study evaluated the effects of melatonin supplementation on aortic wall thickness by assessing the cross-sectional associations of abdominal obesity with aortic intima-media thickness in a diet-induced obesity rat model. Methodology The model comprised of male Wistar rats that were on a high-fructose diet (HFD) (20% glucose-fructose corn syrup) for 12 weeks; the rats were divided into four groups (n = 8): control, HFD, HFD and melatonin supplementation (per os - 4 mg/kg/24h), and control and melatonin supplementation. All rats received a standard rodent diet and tap water. Zoometric measurements and the Lee index were calculated. Morphometric analysis of the abdominal aorta was performed by staining with hematoxylin-eosin and measuring the thickness of the abdominal aortic wall. For this, we used the Aperio Image Scope software. To evaluate the functional properties of the abdominal aorta, the modified Kernogan's index (KI) was employed. Results The results showed significantly elevated body weight (Lee index), KI, and wall thickness of the aorta abdominalis with morphometric changes in the vessel wall in HFD rats compared to the control group. Melatonin supplementation prevented these changes. Conclusions The administration of HFD to Wistar rats led to pathomorphological and morphometric changes in their abdominal aorta, which constitute the main diagnostic criteria of endothelial dysfunction. Melatonin supplementation regressed vascular wall remodeling and restored its functional capacity.
