Exercise training decreases proinflammatory profile in Zucker diabetic (type 2) fatty rats

Lemos, E. Teixeira de; Reis, Flávio; Baptista, Sofia; Pinto, Rui; Sepodes, Bruno; Vala, Helena; Rocha‐Pereira, Petronila; Correia-da-Silva, Georgina; Teixeira, Natércia; Santos-Silva, Alice; Carvalho, Lina; Teixeira, Frederico; Das, Undurti N.

doi:10.1016/j.nut.2008.08.014

Cited by 90 publications

(77 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The observed alterations in platelet turnover might contribute to explain the fact that ZD showed increased platelet number and size compared with ZC as immature platelets are larger in size. Interleukin-6 likely contributes to enhance megakaryopoiesis in ZD, as increased interleukin-6 levels have been previously observed in these animals [40][41][42] (in line with that observed in obese and patients with diabetes mellitus), and interleukin-6 has been proven to increase platelet count by inducing hepatic synthesis of thrombopoietin, the main regulator of megakaryopoiesis. 8,43,44 Moreover, ZD platelets also showed an increased activation in response to thrombin, which together with their increased size reflects a hyperreactive state, as large platelets are more reactive and aggregable because of the fact that they contain denser granules, secrete more serotonin and β-thromboglobulin, and produce more thromboxane A2.…”

Section: Discussionsupporting

confidence: 77%

Platelets Derived From the Bone Marrow of Diabetic Animals Show Dysregulated Endoplasmic Reticulum Stress Proteins That Contribute to Increased Thrombosis

Vera

Vilahur

Ferrer-Lorente

et al. 2012

ATVB

View full text Add to dashboard Cite

Objective-Patients with diabetes mellitus have an increased risk of suffering atherothrombotic syndromes and are prone to clustering cardiovascular risk factors. However, despite their dysregulated glucose metabolism, intensive glycemic control has proven insufficient to reduce thrombotic complications. Therefore, we aimed to elucidate the determinants of thrombosis in a model of type 2 diabetes mellitus with cardiovascular risk factors clustering. Methods and Results-Intravital microscopy was used to analyze thrombosis in vivo in Zucker diabetic fatty rats (ZD) and lean normoglycemic controls. Bone marrow (BM) transplants were performed to test the contribution of each compartment (blood or vessel wall) to thrombogenicity. ZD showed significantly increased thrombosis compared with lean normoglycemic controls. BM transplants demonstrated the key contribution of the hematopoietic compartment to increased thrombogenicity. Indeed, lean normoglycemic controls transplanted with ZD-BM showed increased thrombosis with normal glucose levels, whereas ZD transplanted with lean normoglycemic controls-BM showed reduced thrombosis despite presenting hyperglycemia. Significant alterations in megakaryopoiesis and platelet-endoplasmic reticulum stress proteins, protein disulfide isomerase and 78-kDa glucose-regulated protein, were detected in ZD, and increased tissue factor procoagulant activity was detected in plasma and whole blood of ZD. Conclusion-Our

show abstract

Section: Discussionsupporting

confidence: 77%

Platelets Derived From the Bone Marrow of Diabetic Animals Show Dysregulated Endoplasmic Reticulum Stress Proteins That Contribute to Increased Thrombosis

Vera

Vilahur

Ferrer-Lorente

et al. 2012

ATVB

View full text Add to dashboard Cite

show abstract

“…The training was initiated from 5 minutes on the first day to reach to 60mindaily during 12 days. 26 Swimming exercise carried out in a rectangular tank (100 ×60 ×80cm) with water maintained at 34-36°C. After swimming, animals were dried and kept in a warm place, and then returned to their cages.…”

Section: Swim Training Protocolmentioning

confidence: 99%

Swim Training Improves HOMA-IR in Type 2 Diabetes Induced by High Fat Diet and Low Dose of Streptozotocin in Male Rats

Ghiasi¹,

Soufi²,

Somi³

et al. 2015

Adv Pharm Bull

View full text Add to dashboard Cite

“…Obesity is also associated with a 'low grade of inflammation', a term that includes an atypical increase in the systemic concentration of TNF-␣ , IL-6, IL-1 ␤ and C-reactive protein (CRP) [1] . Both IL-6 and TNF-␣ are the main inflammatory mol-Manso /Ortega Neuroimmunomodulation 2011;18:123-130 124 ecules associated with obesity-related inflammation, and they are involved in MS-associated metabolic disorders [2][3][4][5] . IL-6 enhances systemic levels of CRP [1,6] , a good inflammatory marker, which is usually increased in individuals and animals suffering from MS.…”

Section: Introductionmentioning

confidence: 99%

Habitual Physical Exercise Improves Macrophage IL-6 and TNF-α Deregulated Release in the Obese Zucker Rat Model of the Metabolic Syndrome

Martín-Cordero

Garcı́a

Hinchado

et al. 2010

Neuroimmunomodulation

View full text Add to dashboard Cite

Objectives: The first objective was to evaluate whether the metabolic syndrome (MS) involves deregulation of TNF-α and IL-6 release by non-infiltrated peritoneal macrophages, using obese Zucker rats as the experimental model of MS and lean Zucker rats as a reference for healthy control values. The second purpose was to evaluate in the obese rats the effects of habitual exercise and of a bout of acute exercise on the observed MS-associated deregulation in the release of TNF-α and IL-6 by peritoneal macrophages. Methods: The habitual exercise consisted of treadmill running: 5 days/week for 14 weeks and 35 cm/s for 35 min in the last month. The acute exercise consisted of a single session of 25–35 min at 35 cm/s. The constitutive or lipopolysaccharide (LPS)-induced release of TNF-α and IL-6 by cultured (24 h, 5% CO₂, 100% relative humidity) peritoneal macrophages was determined by ELISA. Results: Macrophages from the obese rats released more IL-6 than those from the lean healthy rats, both spontaneously and after LPS stimulation. However, both spontaneous and LPS-induced release of TNF-α was lower in the obese rats. This deregulated balance in the release of IL-6 and TNF-α in the obese rats was clearly improved following adherence to the program of habitual exercise, reflected by a decrease in the spontaneous release of IL-6 together with a better regulation between the spontaneous and LPS-induced release of TNF-α, approaching the behavior of the lean healthy rats. In addition, an acute bout of exercise decreased the spontaneous release of IL-6 and increased the spontaneous release of TNF-α in the sedentary, but not in the exercise-adapted obese rats. Conclusion: MS involves a deregulation of TNF-α and IL-6 release by non-infiltrated peritoneal macrophages, which is improved by habitual physical activity.

show abstract

Exercise training decreases proinflammatory profile in Zucker diabetic (type 2) fatty rats

Cited by 90 publications

References 52 publications

Platelets Derived From the Bone Marrow of Diabetic Animals Show Dysregulated Endoplasmic Reticulum Stress Proteins That Contribute to Increased Thrombosis

Platelets Derived From the Bone Marrow of Diabetic Animals Show Dysregulated Endoplasmic Reticulum Stress Proteins That Contribute to Increased Thrombosis

Swim Training Improves HOMA-IR in Type 2 Diabetes Induced by High Fat Diet and Low Dose of Streptozotocin in Male Rats

Habitual Physical Exercise Improves Macrophage IL-6 and TNF-α Deregulated Release in the Obese Zucker Rat Model of the Metabolic Syndrome

Contact Info

Product

Resources

About