Obesity is a low-grade inflammatory disease and is associated with numerous comorbidities. The current study was aimed to evaluate the effects of vitamin D administrations on markers of inflammation and oxidative stress in adipose tissue of high-fat diet-induced obese rats. In the beginning of the study, 40 rats were divided into two groups: normal diet and high-fat diet (HFD) for 16 weeks; then, each group was subdivided into two groups including ND, ND + vitamin D, HFD, and HFD + vitamin D. Vitamin D supplementation was done for 5 weeks at 500 IU/kg dosage. Tumor necrosis factor (TNF)-α, interleukin (IL)-1β, monocyte chemoattractant protein (MCP)-1, transforming growth factor (TGF)-β and IL-6 concentrations and markers of oxidative stress including glutathione peroxidase (GPx), superoxide dismutase (SOD), malondialdehyde (MDA), and catalase (CAT) concentrations in adipose tissue of rats were determined using ELISA kits and spectrophotometry methods, respectively. Vitamin D treatment led to a significant reduction in adipose tissue TNF-α concentrations in both ND + vitamin D and HFD + vitamin D groups (P < 0.05). Adipose tissue MCP-1 concentration also reduced in HFD + vitamin D group compared with HFD group. Among markers of oxidative stress in adipose tissue, SOD and GPx concentrations significantly increased in adipose tissue of HFD + vitamin D treated group compared with other groups (P < 0.05). Reduced food intake and weight gain was also occurred after vitamin D treatment. Vitamin D improved adipose tissue oxidative stress and inflammatory parameters in obese rats. Vitamin D treatment was also associated with decreased food intake and decreased weight gain in animals under a high-fat diet. Further studies are needed to better clarify the underlying mechanisms.
BackgroundObesity is associated with numerous metabolic and inflammatory disorders. The current study was aimed to evaluate the effects of vitamin D administration on the markers of oxidative stress and inflammation in the cardiac tissue of high-fat diet induced obese rats.MethodsIn the beginning of the study, 40 male Wistar rats were divided into two groups: normal diet (ND) and high fat diet (HFD) for 16 weeks; then each group subdivided into two groups including: ND, ND + vitamin D, HFD and HFD + vitamin D. Vitamin D supplementation was done for 5 weeks at 500 IU/kg dosage. Tumor necrosis factor (TNF)-α concentration and markers of oxidative stress including glutathione peroxidase (GPx), superoxide dismutase (SOD), malondialdehyde (MDA) and catalase (CAT) concentrations in the cardiac tissue and serum concentrations of lipids in rats were determined using ELISA kits and spectrophotometry methods respectively.ResultsAccording to our results, GPx activity in ND and ND + vitamin D group was significantly higher compared with HFD group. Similarly, SOD activity was also significantly increased in ND + vitamin D group compared with ND and HFD groups. Moreover, vitamin D administration, significantly reduced catalase activity in ND + vitamin D and HFD + vitamin D groups (P < 0.05). TNF-α concentration in heart tissue in ND + vitamin D group significantly reduced compared with ND group. Cardiac tissue MDA concentration in baseline or after vitamin D administration did not changed significantly.ConclusionVitamin D improved cardiac oxidative stress and inflammatory markers in HFD induced obese rats. Further studies in human models are needed to further confirm the use of this nutrient in daily clinical practice.
Vitamin D reversed HFD-induced cognitive impairments by reduction of the NF-κB and elevation of BDNF concentrations and modulation of the BBB permeability in rats' hippocampus.
Vitamin D improved hippocampus oxidative stress and inflammatory markers in HFD-induced obese rats and improved cognitive performance. Further studies are needed to better clarify the underlying mechanisms.
BackgroundObesity induced brain inflammation is associated with cognitive disorders. We aimed to investigate the influence of vitamin D on hypothalamus and hippocampus inflammatory response in high-fat diet induced obese rats.MethodsIn the beginning of the study, 40 rats were divided into two groups: control diet and high fat diet (HFD) for 16 weeks; then each group subdivided into two groups including: N, ND + vitamin D, HFD and HFD + vitamin D. Vitamin D supplementation was done for 5 weeks at 500 IU/kg dosage. IL-6, IL-1β, NF-Kβ and acetylcholine (ACH) and brain derived neurotropic factor (BDNF) concentrations in hippocampus and hypothalamus homogenate samples were measured by commercial ELISA kits.ResultsVitamin D administration, reduced food intake and weight gain in studied groups (P < 0.001). Vitamin D reduced hippocampus acetylcholine concentrations in ND + vitamin D group (P < 0.001). High fat diet increased hippocampus IL-6 concentrations significantly (P < 0.05) compared with normal diet receiving groups. Vitamin D could not have significant effects on IL-6 concentrations. Vitamin D administrations reduced IL-1β, NF-Kβ and acetylcholine concentration and BDNF concentrations in ND + vitamin D compared with ND group. These reductions were not significant in HFD + vitamin D versus HFD group.ConclusionAccording to our results, vitamin D reduced food intake and weight gain and modulated the HFD induced inflammatory response in hippocampus and hypothalamus of high fat diet induced obesity. Therefore, this neurosteroid, can be suggested as a supplemental therapeutic tool in prevention of obesity related cognitive and neurodegenerative problems.
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