scholarly journals Feeding Soy with Probiotic Attenuates Obesity-Related Metabolic Syndrome Traits in Obese Zucker Rats

2015 ◽  
Vol 06 (09) ◽  
pp. 780-789
Author(s):  
Lauren Mounts ◽  
Rajitha Sunkara ◽  
Louis Shackelford ◽  
Simon Ogutu ◽  
Lloyd T. Walker ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Zucker Rats ◽  
Obese Zucker Rats

scholarly journals Experimental rat models to study the metabolic syndrome

2009 ◽  
Vol 102 (9) ◽  
pp. 1246-1253 ◽  
Author(s):  
Amaya Aleixandre de Artiñano ◽  
Marta Miguel Castro
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Syndrome ◽  
Experimental Model ◽  
Insulin Dependent Diabetes Mellitus ◽  
Experimental Models ◽  
Zucker Rats ◽  
Dependent Diabetes Mellitus ◽  
The Metabolic Syndrome ◽  
Insulin Dependent ◽  
Obese Zucker Rats

Being the metabolic syndrome a multifactorial condition, it is difficult to find adequate experimental models to study this pathology. The obese Zucker rats, which are homozygous for the fa allele, present abnormalities similar to those seen in human metabolic syndrome and are a widely extended model of insulin resistance. The usefulness of these rats as a model of non-insulin-dependent diabetes mellitus is nevertheless questionable, and they neither can be considered a clear experimental model of hypertension. Some experimental models different from the obese Zucker rats have also been used to study the metabolic syndrome. Some derive from the spontaneously hypertensive rats (SHR). In this context, the most important are the obese SHR, usually named Koletsky rats. Hyperinsulinism, associated with either normal or slightly elevated levels of blood glucose, is present in these animals, but SHR/N-corpulent rats are a more appropriated model of non-insulin-dependent diabetes mellitus. The SHR/NDmc corpulent rats, a subline of SHR/N-corpulent rats, also exhibit metabolic and histopathologic characteristics associated with human metabolic disorders. A new animal model of the metabolic syndrome, stroke-prone–SHR (SHRSP) fatty rats, was obtained by introducing a segment of the mutant leptin receptor gene from the Zucker line heterozygous for the fa gene mutation into the genetic background of the SHRSP. Very recently, it has been developed as a non-obese rat model with hypertension, fatty liver and characteristics of the metabolic syndrome by transgenic overexpression of a sterol-regulatory element-binding protein in the SHR rats. The Wistar Ottawa Karlsburg W rats are also a new strain that develops a nearly complete metabolic syndrome. Moreover, a new experimental model of low-capacity runner rats has also been developed with elevated blood pressure levels together with the other hallmarks of the metabolic syndrome.

Metabolic syndrome increases endogenous carbon monoxide production to promote hypertension and endothelial dysfunction in obese Zucker rats

2006 ◽  
Vol 290 (3) ◽  
pp. R601-R608 ◽  
Author(s):  
Fruzsina K. Johnson ◽  
Robert A. Johnson ◽  
William Durante ◽  
Keith E. Jackson ◽  
Blake K. Stevenson ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Carbon Monoxide ◽  
Endothelial Dysfunction ◽  
Ldl Cholesterol ◽  
Oxidized Ldl ◽  
Zucker Rats ◽  
Protein Levels ◽  
Obese Zucker Rats ◽  
Oxide Synthase

Vascular heme oxygenase (HO) metabolizes heme to form carbon monoxide (CO). Increased heme-derived CO inhibits nitric oxide synthase and can contribute to hypertension via endothelial dysfunction in Dahl salt-sensitive rats. Obese Zucker rats (ZR) are models of metabolic syndrome. This study tests the hypothesis that endogenous CO formation is increased and contributes to hypertension and endothelial dysfunction in obese ZR. Awake obese ZR showed increased respiratory CO excretion, which was lowered by HO inhibitor administration [zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG) 25 μmol·kg−1·24 h−1 ip]. In awake obese ZR, chronically instrumented with femoral arterial catheters, blood pressure was elevated but was decreased by the HO inhibitor ZnDPBG. Body weight, blood glucose, glycated hemoglobin, plasma insulin, total and LDL cholesterol, oxidized LDL, and triglyceride levels were elevated in obese ZR, and, except for LDL cholesterol, were unchanged by HO inhibition. Total HO-1 protein levels were not different between lean and obese ZR aortas. In vitro experiments used isolated skeletal muscle arterioles with constant pressure and no flow, or constant midpoint, but altered endpoint pressures to establish graded levels of luminal flow. In obese ZR arterioles, responses to ACh and flow were attenuated. Acute in vitro pretreatment with an HO inhibitor, chromium mesoporphyrin, enhanced ACh and flow-induced dilation and abolished the differences between groups. Furthermore, exogenous CO prevented the restoration of flow-induced dilation by the HO inhibitor in obese ZR arterioles. These results suggest that HO-derived CO production is increased and promotes hypertension and arteriolar endothelial dysfunction in obese ZR with metabolic syndrome independent of affecting metabolic parameters.

scholarly journals Metabolic syndrome impairs reactivity and wall mechanics of cerebral resistance arteries in obese Zucker rats

2015 ◽  
Vol 309 (11) ◽  
pp. H1846-H1859 ◽  
Author(s):  
Steven D. Brooks ◽  
Evan DeVallance ◽  
Alexandre C. d'Audiffret ◽  
Stephanie J. Frisbee ◽  
Lawrence E. Tabone ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Vascular Reactivity ◽  
Ex Vivo ◽  
Cerebral Hypoperfusion ◽  
Zucker Rats ◽  
North American Population ◽  
Functional Changes ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Obese Zucker Rats

The metabolic syndrome (MetS) is highly prevalent in the North American population and is associated with increased risk for development of cerebrovascular disease. This study determined the structural and functional changes in the middle cerebral arteries (MCA) during the progression of MetS and the effects of chronic pharmacological interventions on mitigating vascular alterations in obese Zucker rats (OZR), a translationally relevant model of MetS. The reactivity and wall mechanics of ex vivo pressurized MCA from lean Zucker rats (LZR) and OZR were determined at 7–8, 12–13, and 16–17 wk of age under control conditions and following chronic treatment with pharmacological agents targeting specific systemic pathologies. With increasing age, control OZR demonstrated reduced nitric oxide bioavailability, impaired dilator (acetylcholine) reactivity, elevated myogenic properties, structural narrowing, and wall stiffening compared with LZR. Antihypertensive therapy (e.g., captopril or hydralazine) starting at 7–8 wk of age blunted the progression of arterial stiffening compared with OZR controls, while treatments that reduced inflammation and oxidative stress (e.g., atorvastatin, rosiglitazone, and captopril) improved NO bioavailability and vascular reactivity compared with OZR controls and had mixed effects on structural remodeling. These data identify specific functional and structural cerebral adaptations that limit cerebrovascular blood flow in MetS patients, contributing to increased risk of cognitive decline, cerebral hypoperfusion, and ischemic stroke; however, these pathological adaptations could potentially be blunted if treated early in the progression of MetS.

Tesaglitazar, a dual PPARα/γ agonist, ameliorates glucose and lipid intolerance in obese Zucker rats

2005 ◽  
Vol 289 (4) ◽  
pp. R938-R946 ◽  
Author(s):  
Nicholas D. Oakes ◽  
Pia Thalén ◽  
Therese Hultstrand ◽  
Severina Jacinto ◽  
Germán Camejo ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Glucose Tolerance ◽  
Zucker Rats ◽  
Oral Glucose ◽  
Therapeutic Effects ◽  
The Metabolic Syndrome ◽  
Increased Risk ◽  
Mass Load ◽  
Obese Zucker Rats

Insulin resistance, impaired glucose tolerance, high circulating levels of free fatty acids (FFA), and postprandial hyperlipidemia are associated with the metabolic syndrome, which has been linked to increased risk of cardiovascular disease. We studied the metabolic responses to an oral glucose/triglyceride (TG) (1.7/2.0 g/kg lean body mass) load in three groups of conscious 7-h fasted Zucker rats: lean healthy controls, obese insulin-resistant/dyslipidemic controls, and obese rats treated with the dual peroxisome proliferator-activated receptor α/γ agonist, tesaglitazar, 3 μmol·kg−1·day−1 for 4 wk. Untreated obese Zucker rats displayed marked insulin resistance, as well as glucose and lipid intolerance in response to the glucose/TG load. The 2-h postload area under the curve values were greater for glucose (+19%), insulin (+849%), FFA (+53%), and TG (+413%) compared with untreated lean controls. Treatment with tesaglitazar lowered fasting plasma glucose, improved glucose tolerance, substantially reduced fasting and postload insulin levels, and markedly lowered fasting TG and improved lipid tolerance. Fasting FFA were not affected, but postprandial FFA suppression was restored to levels seen in lean controls. Mechanisms of tesaglitazar-induced lowering of plasma TG were studied separately using the Triton WR1339 method. In anesthetized, 5-h fasted, obese Zucker rats, tesaglitazar reduced hepatic TG secretion by 47%, increased plasma TG clearance by 490%, and reduced very low-density lipoprotein (VLDL) apolipoprotein CIII content by 86%, compared with obese controls. In conclusion, the glucose/lipid tolerance test in obese Zucker rats appears to be a useful model of the metabolic syndrome that can be used to evaluate therapeutic effects on impaired postprandial glucose and lipid metabolism. The present work demonstrates that tesaglitazar ameliorates these abnormalities and enhances insulin sensitivity in this animal model.

scholarly journals Distinct temporal phases of microvascular rarefaction in skeletal muscle of obese Zucker rats

2014 ◽  
Vol 307 (12) ◽  
pp. H1714-H1728 ◽  
Author(s):  
Jefferson C. Frisbee ◽  
Adam G. Goodwill ◽  
Stephanie J. Frisbee ◽  
Joshua T. Butcher ◽  
Robert W. Brock ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Metabolic Syndrome ◽  
Leukocyte Adhesion ◽  
Oxidant Stress ◽  
Therapeutic Interventions ◽  
Zucker Rats ◽  
Tnf Α ◽  
Obese Zucker Rats ◽  
No Bioavailability ◽  
Microvascular Rarefaction

Evolution of metabolic syndrome is associated with a progressive reduction in skeletal muscle microvessel density, known as rarefaction. Although contributing to impairments to mass transport and exchange, the temporal development of rarefaction and the contributing mechanisms that lead to microvessel loss are both unclear and critical areas for investigation. Although previous work suggests that rarefaction severity in obese Zucker rats (OZR) is predicted by the chronic loss of vascular nitric oxide (NO) bioavailability, we have determined that this hides a biphasic development of rarefaction, with both early and late components. Although the total extent of rarefaction was well predicted by the loss in NO bioavailability, the early pulse of rarefaction developed before a loss of NO bioavailability and was associated with altered venular function (increased leukocyte adhesion/rolling), and early elevation in oxidant stress, TNF-α levels, and the vascular production of thromboxane A2 (TxA2). Chronic inhibition of TNF-α blunted the severity of rarefaction and also reduced vascular oxidant stress and TxA2 production. Chronic blockade of the actions of TxA2 also blunted rarefaction, but did not impact oxidant stress or inflammation, suggesting that TxA2 is a downstream outcome of elevated reactive oxygen species and inflammation. If chronic blockade of TxA2 is terminated, microvascular rarefaction in OZR skeletal muscle resumes, but at a reduced rate despite low NO bioavailability. These results suggest that therapeutic interventions against inflammation and TxA2 under conditions where metabolic syndrome severity is moderate or mild may prevent the development of a condition of accelerated microvessel loss with metabolic syndrome.

The Effect of Anthocyanin-Rich Purple Vegetable Diets on Metabolic Syndrome in Obese Zucker Rats

2017 ◽  
Vol 20 (12) ◽  
pp. 1240-1249 ◽  
Author(s):  
Hala M. Ayoub ◽  
Mary Ruth McDonald ◽  
James Alan Sullivan ◽  
Rong Tsao ◽  
Mathew Platt ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Zucker Rats ◽  
Obese Zucker Rats

scholarly journals Altered wall mechanics of conduit arteries of obese Zucker rats with progression of metabolic syndrome (867.8)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Paul Chantler ◽  
Sara Fournier ◽  
Evan DeVallance ◽  
Joshua Butcher ◽  
Jefferson Frisbee
Keyword(s):  
Metabolic Syndrome ◽  
Zucker Rats ◽  
Obese Zucker Rats

Altered arachidonic acid metabolism impairs functional vasodilation in metabolic syndrome

2006 ◽  
Vol 290 (1) ◽  
pp. R134-R138 ◽  
Author(s):  
Lusha Xiang ◽  
Jay S. Naik ◽  
Benjamin L. Hodnett ◽  
Robert L. Hester
Keyword(s):  
Metabolic Syndrome ◽  
Arachidonic Acid ◽  
Sodium Nitroprusside ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Zucker Rats ◽  
Thromboxane Receptor ◽  
Obese Zucker Rats ◽  
Prostacyclin Analog ◽  
Arteriolar Diameter

These studies tested the hypothesis that in obese Zucker rats (OZRs), a model of metabolic syndrome, the impaired functional vasodilation is due to increased thromboxane receptor (TP)-mediated vasoconstriction and/or decreased prostacyclin-induced vasodilation. Spinotrapezius arcade arterioles from 12-wk-old lean (LZR) and OZR were chosen for microcirculatory observation. Arteriolar diameter (5 LZR and 6 OZR) was measured after 2 min of muscle stimulation in the absence or presence of 1 μM SQ-29548 (TP antagonist). Additionally, arteriolar diameter (6 for each group) was measured after application of iloprost (prostacyclin analog; 0.28, 2.8, and 28 μM), arachidonic acid (10 μM), and sodium nitroprusside (0.1, 1, and 10 μM) in the absence or presence of 1 μM SQ-29548. A 10 μM concentration of adenosine was used to induce a maximal dilation. Basal diameters were not different between LZRs and OZRs. Functional hyperemia and arachidonic acid-mediated vasodilations were significantly attenuated in OZR compared with LZR, and treatment with 1 μM SQ-29548 significantly enhanced the dilations in OZRs, although it had no effect in LZRs. Vasodilatory responses to iloprost and sodium nitroprusside (1 and 10 μM) were significantly reduced in OZR. Adenosine-mediated vasodilation was not different between groups. These results suggest that the impaired functional dilation in the OZR is due to an increased TP-mediated vasoconstriction and a decreased PGI2-induced vasodilation.

scholarly journals Cardiovascular Changes Related to Metabolic Syndrome: Evidence in Obese Zucker Rats

2020 ◽  
Vol 21 (6) ◽  
pp. 2035 ◽  
Author(s):  
Ilenia Martinelli ◽  
Daniele Tomassoni ◽  
Michele Moruzzi ◽  
Proshanta Roy ◽  
Carlo Cifani ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Heart Tissue ◽  
Cellular Adhesion ◽  
Oxidative Status ◽  
Zucker Rats ◽  
Cellular Adhesion Molecules ◽  
Tissue Changes ◽  
Obese Zucker Rats ◽  
Factor Α ◽  
Cell Adhesion Molecule 1

Metabolic syndrome (MetS) is a predictor of cardiovascular diseases, commonly associated with oxidative stress and inflammation. However, the pathogenic mechanisms are not yet fully elucidated. The aim of the study is to evaluate the oxidative status and inflammation in the heart of obese Zucker rats (OZRs) and lean Zucker rats (LZRs) at different ages. Morphological and morphometric analyses were performed in the heart. To study the oxidative status, the malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), protein oxidation, and antioxidant enzymes were measured in plasma and heart. To elucidate the inflammatory markers involved, immunohistochemistry and Western blot were performed for cellular adhesion molecules and proinflammatory cytokines. OZRs were characterized by hypertension, hyperlipidemia, hyperglycemia, and insulin resistance. The obesity increased MDA and decreased the activities of superoxide dismutase (SOD) in plasma as well as in the heart, associated with cardiomyocytes hypertrophy. OxyBlot in plasma and in heart showed an increase of oxidativestate proteins in OZRs. Vascular cell adhesion molecule-1, interleukin-6, and tumor necrosis factor-α expressions in OZRs were higher than those of LZRs. However, these processes did not induce apoptosis or necrosis of cardiomyocytes. Thus, MetS induces the lipid peroxidation and decreased antioxidant defense that leads to heart tissue changes and coronary inflammation.

Impaired in vivo venous constriction in conscious obese Zucker rats with metabolic syndrome

2006 ◽  
Vol 373 (6) ◽  
pp. 451-456 ◽  
Author(s):  
Dongzhe Song ◽  
Simon R. Hutchings ◽  
Catherine C. Y. Pang
Keyword(s):  
Metabolic Syndrome ◽  
Zucker Rats ◽  
Obese Zucker Rats
Sign in / Sign up

Export Citation Format

Share Document