scholarly journals Shexiang Baoxin Pill Corrects Metabolic Disorders in a Rat Model of Metabolic Syndrome by Targeting Mitochondria

2018 ◽  
Vol 9 ◽  
Author(s):  
Dan Wei ◽  
Ningning Zheng ◽  
Lanyan Zheng ◽  
Leting Wang ◽  
Liang Song ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Rat Model ◽  
Metabolic Disorders ◽  
Shexiang Baoxin Pill

Abstract 278: The Glucocorticoid Receptor Antagonist RU486 Ameliorates Cold Stress-induced Exacerbation of Cardiac and Adipose Tissue Pathology and Metabolic Disorders in a Rat Model of Metabolic Syndrome

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Kai Nagasawa ◽  
Natsumi Matsuura ◽  
Yuji Minagawa ◽  
Shogo Ito ◽  
Yusuke Sano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Cold Stress ◽  
Rat Model ◽  
Metabolic Disorders ◽  
Glucose And Lipid Metabolism ◽  
Obese Rats ◽  
Antagonist Ru486

Introduction: Chronic stress, when combined with hyperphagia, can affect adiposity and metabolism. However, few studies have reported the effects of cold stress on cardiovascular and metabolic disorders in metabolic syndrome (MetS). We investigated the effects of chronic cold stress and glucocorticoid receptor (GR) blockade on cardiac and adipose tissue pathology and gene expression and on glucose and lipid metabolism in a rat model of MetS. Methods and Results: We used DahlS.Z-Leprfa/Leprfa (DS/obese) rats which are derived from a cross between Dahl salt-sensitive and Zucker rats and represent a new animal model of MetS. DS/obese rats were exposed to cold stress (ice-cold water, 1 cm depth, 2 h/day) for 4 weeks beginning at 9 weeks of age with or without the GR antagonist RU486 (2 mg/kg/day, sc). Age-matched homozygous lean (DahlS.Z-Lepr+/Lepr+, or DS/lean) littermates of DS/obese rats served as controls. Chronic cold stress exacerbated hypertension as well as left ventricular (LV) hypertrophy, fibrosis and diastolic dysfunction, in a manner sensitive to RU486. Cold stress and RU486 did not affect body weight or visceral and subcutaneous fat mass. In contrast, cold stress further increased superoxide production and NADPH oxidase activity in the heart as well as macrophage infiltration and the expression of proinflammatory genes in LV and visceral fat tissue. RU486 treatment inhibited these changes in gene expression, as well as cardiac oxidative stress and inflammation and adipose tissue inflammation. Cold stress further up-regulated cardiac renin-angiotensin-aldosterone system gene expression as well as the expression of GR and 11β-hydroxysteroid dehydrogenase type 1 genes in LV and visceral adipose tissue, and all of these effects were attenuated by RU486. In addition, RU486 ameliorated the stress-induced deterioration of dyslipidemia (elevations in low-density lipoprotein cholesterol, triglycerides, and free fatty acid) as well as that of glucose intolerance and insulin resistance. Conclusions: The present results indicate that GRs may be involved in cold stress-induced exacerbation of cardiac and adipose tissue pathology as well as that of glucose and lipid metabolism in a rat model of MetS.

Myocardial Ischemic-reperfusion Injury in a Rat Model of Metabolic Syndrome

Obesity ◽  
2008 ◽  
Vol 16 (10) ◽  
pp. 2253-2258 ◽  
Author(s):  
Mahmood S. Mozaffari ◽  
Stephen W. Schaffer
Keyword(s):  
Metabolic Syndrome ◽  
Reperfusion Injury ◽  
Rat Model ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion

scholarly journals Emerging roles of C1Q tumor necrosis factor-related proteins in metabolic diseases

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Manjunath Ramanjaneya ◽  
Jayakumar Jerobin ◽  
Ilham Bettahi ◽  
Kodappully Sivaraman Siveen ◽  
Abdul-Badi Abou-Samra
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Metabolic Disorders ◽  
Pharmacological Intervention ◽  
Alcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Related Proteins ◽  
Necrosis Factor

AbstractObesity and insulin resistance are key elements of the metabolic syndrome, which includes type 2 diabetes (T2D), dyslipidemia, systemic inflammation, hypertension, elevated risk for cardiovascular diseases, non-alcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS). C1Q Tumor necrosis factor-related proteins (CTRPs) have recently emerged as important regulators of metabolism as a core component in the interrelationship between insulin resistance, adiposity and inflammation. To date 15 CTRP members have been identified and most of the CTRPs are dysregulated in obesity, T2D, coronary artery disease and NAFLD. Pharmacological intervention and lifestyle modification alter expression of CTRPs in circulation and in metabolically active tissues. CTRPs enhance metabolism mainly through activation of AMPK/AKT dependent pathways and possess insulin sensitizing properties. Thus dysregulated expression of CTRPs in metabolic disorders could contribute to the pathogenesis of the disease. For these reasons CTRPs appear to be promising targets for early detection, prevention and treatment of metabolic disorders. This review article aims at exploring the role of CTRPs in metabolic syndrome.

scholarly journals SP074SERINE PROTEASE INHIBITION ATTENUATES SALT-SENSITIVE HYPERTENSION AND KIDNEY INJURY IN A RAT MODEL OF METABOLIC SYNDROME

2016 ◽  
Vol 31 (suppl_1) ◽  
pp. i110-i110
Author(s):  
Yutaka Kakizoe ◽  
Teruhiko Mizumoto ◽  
Terumasa Nakagawa ◽  
Manabu Hayata ◽  
Yuichiro Izumi ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Rat Model ◽  
Kidney Injury ◽  
Protease Inhibition ◽  
Salt Sensitive Hypertension

scholarly journals Insulin resistance in penile arteries from a rat model of metabolic syndrome

2010 ◽  
Vol 161 (2) ◽  
pp. 350-364 ◽  
Author(s):  
Cristina Contreras ◽  
Ana Sánchez ◽  
Pilar Martínez ◽  
Rafaela Raposo ◽  
Belén Climent ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Rat Model ◽  
Penile Arteries

Vitamin D3 potentiates the nephroprotective effects of vildagliptin‐metformin combination in a rat model of metabolic syndrome

2021 ◽  
Author(s):  
Nehal S. Wahba ◽  
Rasha H. Abdel‐Ghany ◽  
Salah A. Ghareib ◽  
Mohamed Abdel‐Aal ◽  
Amira E. Alsemeh ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Vitamin D3 ◽  
Rat Model

Abstract P033: Relationship Between Adiponectin Level and Metabolic Syndrome after Weight Loss in Patients with Abdominal Obesity

Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Aelita Berezina ◽  
Olga Belyaeva ◽  
Olga Berkovich ◽  
Elena Baranova ◽  
Tatyina Karonova
Keyword(s):  
Metabolic Syndrome ◽  
Weight Loss ◽  
Abdominal Obesity ◽  
Metabolic Disorders ◽  
Intervention Program ◽  
Adiponectin Level ◽  
The Metabolic Syndrome ◽  
Outpatient Intervention ◽  
Before And After ◽  
The Relationship

Objective: to investigate the relationship between adiponectin level and metabolic syndrome (MS) after weight loss in patients with abdominal obesity (AO). Method: A 3-year randomized lifestyle intervention trial performed in 153 patients with AO, age 43,2±0,8 yrs, BMI 32,1±1,9 kg/m 2 . 74 patients keep hypocaloric diet (gr.1), 79 patients keep diet and performed aerobic exercise (gr.2). Adiponectin concentration, body mass (BM), waist circumference (WC), body fat (BF), BMI, the levels of BP, glucose, insulin, HOMA-IR, TC, HDL-C, LDL-C, TG, CRP were measured before and after a 3-years outpatient intervention program. Results. 100% patients with AO had some metabolic disorders and 38% had MS before the treatment. The adiponectin levels and others parameters didn’t differ between the groups before intervention (p>0,05). In 3 years 53 (71,6%) and 58 (73,4%) patients from 1 and 2 groups reduced weight. The rate of improving BM, BMI, BF, WC, HDL-C, TG and insulin was grater in patients gr.2 (p<0,05). The favorable dynamics of MS (MS didn’t appeared at the end of study or didn’t registered in patients who had it before) didn’t differ between the groups 1 and 2 (81,1% and 91,4%, p>0,05). The increasing of adiponectin level occurred more often in patients gr.2, than gr.1 (93,1% and 58,5%, p=0,001, respectively). Adiponectin level increased only in patients gr.2 (18,0±1,1mcg/ml and 23,8±1,3 mcg/ml, p= [[Unable to Display Character: &#1088;]]=0,0001), didn’t changed in gr.1 (p>0,05). It was established that in patients with combination of weight loss and increasing of adiponectin level favorable dynamics of MS occurred more often than in patients who lost weight without increasing of adiponectin level (91,7% and 69,2%, p=0,0001). In patients with favorable dynamics of MS increasing of adiponectin level had met more often, than in patients with unfavorable dynamics of MS (MS continued or appeared) (88,6% and 11,4%, p=0,0001). Increasing of adiponectin level associated with positive dynamics of the MS - OR=9,1 (4,0-20,6). Conclusion. Combination of weight loss and increasing of adiponectin level associated with favorable dynamics of the metabolic syndrome.

scholarly journals Targeting Mitochondria as Therapeutic Strategy for Metabolic Disorders

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Daniela Sorriento ◽  
Antonietta Valeria Pascale ◽  
Rosa Finelli ◽  
Anna Lisa Carillo ◽  
Roberto Annunziata ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Mitochondrial Dysfunction ◽  
Small Molecules ◽  
Metabolic Disorders ◽  
Therapeutic Strategy ◽  
Cell Metabolism ◽  
Therapeutic Interventions ◽  
Mtdna Mutations ◽  
Pathological Conditions ◽  
Mitochondria Targeting

Mitochondria are critical regulator of cell metabolism; thus, mitochondrial dysfunction is associated with many metabolic disorders. Defects in oxidative phosphorylation, ROS production, or mtDNA mutations are the main causes of mitochondrial dysfunction in many pathological conditions such as IR/diabetes, metabolic syndrome, cardiovascular diseases, and cancer. Thus, targeting mitochondria has been proposed as therapeutic approach for these conditions, leading to the development of small molecules to be tested in the clinical scenario. Here we discuss therapeutic interventions to treat mitochondrial dysfunction associated with two major metabolic disorders, metabolic syndrome, and cancer. Finally, novel mechanisms of regulation of mitochondrial function are discussed, which open new scenarios for mitochondria targeting.

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