Abstract P282: Time Restricted Feeding In Mice On A Chronic High Fat Diet Leads To Reduced Aortic Damage And Oxidative Stress

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Claudia Edell ◽  
Paramita Pati ◽  
Carmen De Miguel ◽  
Jackson Colson ◽  
Gwendolyn Davis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Food Intake ◽  
High Fat Diet ◽  
Oxidative Stress Marker ◽  
Active Period ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Significant Difference ◽  
Ad Libitum ◽  
And Oxidative Stress

Diet-induced obesity is associated with an increased risk of developing cardiovascular disease (CVD) . Aortic damage and stiffness are critical risk factors for CVD progression, especially with chronic high fat diet (HFD). Mice fed HFD ad libitum have increased food intake during the inactive period. We previously showed that HFD leads to significantly reduced blood pressure (BP) dipping and that time restricted food availability to the active period (TRF) in the final 2 weeks of HFD restores BP dipping. Thus, we hypothesized that TRF will reduce aortic damage and stiffness in chronic HFD mice. Utilizing this same mouse model of ad libitum chronic HFD (20 weeks 45% fat diet, male C57Bl6/J mice) compared to normal fat diet (NFD, 10% fat) and TRF intervention (food during lights off active period only from weeks 18-20), we determined aortic fibrosis and stiffness. By histological staining and quantitative analysis of the fibrosis area, HFD+TRF mice had significantly reduced fibrosis compared to HFD mice (% fibrosis per area, NFD: 143, NFD+TRF: 132, HFD: 175, HFD+TRF: 105, 2-way ANOVA, TRF effect: p=0.02). Aortic stiffness was measured by pulse wave velocity (PWV, Vevo 3100). We found that HFD fed mice have a significant increase in PWV compared to NFD group with no significant difference in the HFD+TRF and NFD+TRF groups compared to the NFD group (PWV m/sec, NFD: 1.60, NFD+TRF: 1.5, HFD: 2.30, HFD+TRF: 1.70, 2-way ANOVA, diet effect: p=0.02). We further analyzed plasma sE-selectin (endothelial-specific damage marker) and 8-isoprostane (oxidative stress marker) in HFD and HFD+TRF mice. Plasma from HFD+TRF mice showed significantly reduced sE-selectin and 8-isoprostane compared to HFD mice (sE-selectin ng/ml, HFD: 3.50, HFD+TRF: 1.85, p=0.027; 8-isoprostane ng/ml, HFD: 159.1, HFD+TRF: 59.6, p=0.008). Thus, TRF in chronic HFD mice leads to reduced endothelial injury and oxidative stress that is correlated with reduced aortic fibrosis and stiffness compared to ad libitum HFD mice. This study highlights that restricting the time of food intake in a model of diet-induced obesity minimizes CVD risk by reducing aortic damage and oxidative stress.

scholarly journals Countering adipose tissue dysfunction could underlie the superiority of telmisartan in the treatment of obesity-related hypertension

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Yahya M. Naguib ◽  
Rehab M. Samaka ◽  
Mohamed S. Rizk ◽  
Omnia Ameen ◽  
Shaimaa M. Motawea
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
High Fat Diet ◽  
Serum Lipids ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Adipose Tissue Dysfunction ◽  
Visceral Adipose ◽  
And Oxidative Stress

Abstract Background The prevalence of hypertension and obesity has increased significantly in recent decades. Hypertension and obesity often coexist, and both are associated with increased cardiovascular mortality. Obese hypertensive patients usually require special anti-hypertensive treatment strategy due to the increased risk of treatment resistance. Molecules that can target both obesity and hypertension underlying pathologies should get more attention. Herein, we evaluated the therapeutic effects of telmisartan, with special interest in visceral adipose tissue dysfunction, in obesity-related hypertension rat model. Methods Thirty male Wistar rats weighing 150–200 g were equally divided into: 1—Control group (fed normal laboratory diet for 24 weeks), 2—Diet-induced obesity group (DIO, fed high fat diet for 24 weeks), and 3—Diet-induced obesity treated with telmisartan group (DIO + Tel, fed high fat diet and received telmisartan for 24 weeks). At the end of the study, anthropometrical parameters were evaluated. Systolic blood pressure and heart rate were measured. Blood samples were collected for the measurement of serum lipids, adipokines, cardiac, renal, inflammatory, and oxidative stress biomarkers. Kidneys were removed and used for histopathological studies, and visceral adipose tissue was utilized for histopathological, immunohistochemical and RT-PCR studies. Results High fat diet resulted in obesity-related changes in anthropometrical parameters, elevation of blood pressure, increase in heart rate, higher serum levels of cardiac, inflammatory and kidney function biomarkers, with altered serum lipids, adipokines and oxidative stress markers. Morphological changes (H&E and PAS-stained sections) were noticed in kidneys and visceral adipose tissue. Immunohistochemistry and RT-PCR studies confirmed adipose tissue dysfunction and over-expression of inflammatory and oxidative stress proteins. Telmisartan countered obesity-induced alterations in cardiovascular, renal, and adipose tissue functions. Conclusion Adipose tissue dysfunction could be the core pathophysiology of obesity-related hypertension. Besides its anti-hypertensive effect, telmisartan had profound actions on visceral adipose tissue structure and function. Attention should be given to polymodal molecules targeting adipose tissue-related disorders.

scholarly journals High-fat diet-induced metabolic syndrome and oxidative stress in obese rats are ameliorated by yogurt supplementation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Shoumen Lasker ◽  
Md Mizanur Rahman ◽  
Faisal Parvez ◽  
Mushfera Zamila ◽  
Pintu Miah ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
High Fat Diet ◽  
Alternative Therapy ◽  
High Fat ◽  
Stress Markers ◽  
Diet Induced Obesity ◽  
Obese Rats ◽  
Male Wistar Rats ◽  
And Oxidative Stress

AbstractThe main objective of this experiment was to determine the effects of yogurt supplementation on fat deposition, oxidative stress, inflammation and fibrosis in the liver of rats with high-fat (HF) diet-induced obesity. Male Wistar rats were used in this study and were separated into the following four different groups: the control, control + yogurt, high fat and high fat+ yogurt groups. The high fat groups received a HF diet for eight weeks. A 5% yogurt (w/w) supplement was also provided to rats fed the HF diet. Yogurt supplementation prevented glucose intolerance and normalized liver-specific enzyme activities in the HF diet-fed rats. Yogurt supplementation also significantly reduced the levels of oxidative stress markers in the plasma and liver of HF diet-fed rats. Moreover, inflammatory cell infiltration, collagen deposition and fibrosis in the liver of HF diet-fed rats were also prevented by yogurt supplementation. Furthermore, yogurt supplementation normalized the intestinal lining and brush border in HF diet-fed rats. This study suggests that yogurt supplementation potentially represents an alternative therapy for the prevention of metabolic syndrome in HF diet-fed rats.

scholarly journals Prenatal influences on leptin sensitivity and susceptibility to diet-induced obesity

2006 ◽  
Vol 189 (2) ◽  
pp. 355-363 ◽  
Author(s):  
Stefan O Krechowec ◽  
Mark Vickers ◽  
Arieh Gertler ◽  
Bernhard H Breier
Keyword(s):  
Food Intake ◽  
High Fat Diet ◽  
Adult Life ◽  
Female Offspring ◽  
Leptin Resistance ◽  
Reduce Food Intake ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Leptin Sensitivity ◽  
Ad Libitum

Obesity and type 2 diabetes are world wide health issues and their incidence is rapidly increasing. Currently the biological factors responsible for the development of obesity are only partially understood. Recent research has shown that maternal nutrition during pregnancy may have long-term metabolic consequences in offspring. In the present study we investigated interactions between prenatal and postnatal nutrition on leptin sensitivity and obesity development. Wistar rats were time-mated and randomly assigned to either ad-libitum (AD) or to 30% of ad-libitum (UN) food intake throughout pregnancy. After weaning, female offspring were fed standard chow, a high-fat diet or a calorie restricted diet. Female offspring of UN dams were growth retarded at birth and showed increased susceptibility to diet-induced obesity on a high-fat diet. At 142 ± 5 days of age, leptin sensitivity was measured as a response to 14 days of leptin treatment (2.5 μg/g/day, s.c.). In UN offspring fed chow, leptin treatment failed to reduce food intake and weight loss was diminished. This leptin resistance observed in UN offspring was independent of diet-induced obesity and was associated with fasting hyperinsulinemia and hypertriglyceridemia. Our study suggests that prenatal nutrition can shape future susceptibility to obesity through alterations in leptin sensitivity and changes in energy metabolism during adult life.

scholarly journals Calorie Restriction with a High-Fat Diet Effectively Attenuated Inflammatory Response and Oxidative Stress-Related Markers in Obese Tissues of the High Diet Fed Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Seungae Park ◽  
Na-Young Park ◽  
Giuseppe Valacchi ◽  
Yunsook Lim
Keyword(s):  
Oxidative Stress ◽  
Adipose Tissue ◽  
Systemic Inflammation ◽  
Calorie Restriction ◽  
High Fat Diet ◽  
Heme Oxygenase 1 ◽  
High Fat ◽  
Expression Levels ◽  
Diet Induced Obesity ◽  
And Oxidative Stress

Obesity characterized by increased mass of adipose tissue leads to systemic inflammation. Calorie restriction (CR) improves parameters associated with immune response and antioxidant defense. We hypothesized that CR with a high fat diet (HFCR) regulates local and systemic inflammation and oxidative stress damage in a high fat diet induced obesity (HF group). We investigated effect of HFCR on inflammation and oxidative stress-related markers in liver and adipose tissues as well as adipokines in plasma. HFCR lowered liver triglyceride levels, total cholesterol levels, and the plasma leptin/adiponectin ratio to normal levels and improved glucose tolerance. HFCR also improved fatty liver and normalized adipocyte size and morphology. HFCR reduced lipid peroxidation and decreased the expression levels of inducible nitric oxide synthetase, cyclooxygenase-2, NF-E2-related factor, and heme oxygenase-1 in the liver. Moreover, HFCR suppressed the expression levels of C- reactive protein and manganese superoxide dismutase in the adipose tissue in the HF group. These results suggest that HFCR may have beneficial effects on inflammation and oxidative stress as well as lipid profiles in the HF diet induced obesity. Moreover, HFCR may be a good way to increase compliance in obese patients and to prevent obesity induced complications without changes in dietary pattern.

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