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

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.

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Yahya M. Naguib ◽  
Rehab M. Samaka ◽  
Mohamed S. Rizk ◽  
Omnia Ameen ◽  
Shaimaa M. Motawea

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.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Shoumen Lasker ◽  
Md Mizanur Rahman ◽  
Faisal Parvez ◽  
Mushfera Zamila ◽  
Pintu Miah ◽  
...  

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.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1669-1669
Author(s):  
Ya Pei ◽  
Hye Won Kang

Abstract Objectives Under obesity state, adipose tissue derived inflammatory mediators circulate all over the body and induce low-grade chronic inflammation, which is the main cause for the development of metabolic diseases. Moreover, inflammation-induced reactive oxygen species (ROS) cause oxidative stress, a process in damaging cellular structure and functions. Recently, microRNAs (miRNAs) were found to potentially regulate inflammation and its associated diseases. Brown adipose tissue (BAT) protects against obesity through thermogenic activity to increase energy expenditure. However, high levels of inflammation, ROS generation and aberrant level of miRNAs result in the dysfunction of BAT. Previously, quercetin showed anti-obesity effect through BAT activation. Thus, the purpose of this study was sought to investigate the effect of quercetin on high fat diet (HFD)-induced inflammation and oxidative stress in BAT. Methods C57BL/6 male mice were fed with a HFD or HFD supplemented with 1% quercetin (HFDQ) for 16 weeks. Total RNA was isolated from BAT to measure the expression of target mRNAs such as tumor necrosis factor alpha (TNFa), interleukin (IL) 1b, IL6, inducible nitric oxide synthase (iNOS), cyclooxygenase (COX) 2, NADPH oxidase (NOX) 2, nuclear factor E2-related factor (NRF) 2, superoxide dismutase (SOD) 2, SOD3, and catalase that are involved in regulation of inflammation and oxidative stress, and microRNA (miRNA)-155, a master regulator of inflammation, using a quantitative PCR. Results BAT of HFDQ-fed mice exhibited decreased expression of COX2, TNFa, IL1b, IL6, and iNOS compared to that of HFD-induced obese mice. NOX2 gene encoding an enzyme that generates ROS was also decreased in BAT of HFDQ-fed mice. The genes such as SOD2, SOD3, NRF2, and catalase that are involved in regulation of antioxidant enzymes were significantly increased. As the cognate gene of TNFa, miRNA-155 levels were downregulated. Conclusions Quercetin ameliorates HFD-induced inflammation and oxidative stress in BAT by regulating miRNA-155. Intake of quercetin may improve obese conditions by regulating BAT function through anti-inflammatory and antioxidant effects. Funding Sources This work was supported by USDA.


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