Low-intensity exercise in the prevention of cardiac insulin resistance-related inflammation and disturbances in NOS and MMP-9 regulation in fructose-fed ovariectomized rats

Exercise is important nonpharmacological treatment for improvement of insulin sensitivity in menopause. However, its effect on menopausal cardiac insulin resistance is needing further research. We investigated protective effects of low-intensity exercise on cardiac insulin signaling, inflammation, r...

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Published in:Applied physiology, nutrition, and metabolism nutrition, and metabolism, 2019-11, Vol.44 (11), p.1219-1229
Main Authors: Stanisic, Jelena, Koricanac, Goran, Kostic, Milan, Stojiljkovic, Mojca, Culafic, Tijana, Romic, Snjezana, Tepavcevic, Snezana
Format: Article
Language:English
Subjects:
Animals
cardiac insulin signaling
Diabetes therapy
Endothelium
exercice de faible intensité
Exercise
Female
Fructose
Fructose - adverse effects
Heart - physiopathology
Homeostasis
Inflammation
Inflammation - prevention & control
Insulin Resistance
low-intensity exercise
Matrix Metalloproteinase 9 - metabolism
matrix metalloproteinase type 9
Menopause
métalloprotéinase matricielle 9
Nitric oxide
nitric oxide synthase
Nitric Oxide Synthase Type II - metabolism
Nitric Oxide Synthase Type III - metabolism
Ovariectomy
oxyde nitrique synthase
Phosphatase
Phosphatases
Phosphorylation
Physical Conditioning, Animal
Prevention
Protein Tyrosine Phosphatase, Non-Receptor Type 1 - metabolism
Rats
Rats, Wistar
RNA
Rodents
Signal Transduction
signalisation de l’insuline cardiaque
Suppressor of Cytokine Signaling 3 Protein - metabolism
Transcription Factor RelA - metabolism
Tumor Necrosis Factor-alpha - metabolism
Tumor necrosis factor-TNF
Type 2 diabetes
Tyrosine
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Summary:Exercise is important nonpharmacological treatment for improvement of insulin sensitivity in menopause. However, its effect on menopausal cardiac insulin resistance is needing further research. We investigated protective effects of low-intensity exercise on cardiac insulin signaling, inflammation, regulation of nitric oxide synthase (NOS) and matrix metalloproteinase 9 (MMP-9) in ovariectomized (OVX) Wistar rats, submitted to 10% fructose solution for 9 weeks. OVX rats were divided into control, sedentary fructose, and exercise fructose groups. Measurements of physical and biochemical characteristics were carried out to evaluate metabolic syndrome development. Messenger RNA and protein levels and phosphorylation of cardiac insulin signaling molecules, endothelial and inducible NOS (eNOS and iNOS), p65 subunit of nuclear factor κB (NFκB), tumor necrosis factor α (TNF-α), suppressor of cytokine signaling 3 (SOCS3), and MMP-9 were analyzed. Fructose increased insulin level, homeostasis model assessment (HOMA) index, and visceral adipose tissue weight, while low-intensity exercise prevented insulin level and HOMA index increase. Fructose also decreased cardiac pAkt (Ser473), peNOS (Ser1177) and increased insulin receptor substrate 1 (IRS1) phosphorylation at Ser307, pNFκB (Ser276) and NFκB and MMP-9 content, without any effect on iNOS, protein-tyrosine phosphatase 1B, TNF-α, and SOCS3. Exercise prevented changes in pIRS1 (Ser307), pAkt (Ser473), peNOS (Ser1177), pNFκB (Ser276), and NFκB expression. In addition, exercise increased pIRS1 (Tyr632), pAkt (Thr308), and eNOS expression. Low-intensity exercise prevented cardiac insulin signaling disarrangement in fructose-fed OVX rats and therefore eNOS dysfunction, as well as pro-inflammatory signaling activation, without effect on tissue remodeling, suggesting physical training as a way to reduce cardiovascular risk.
ISSN:1715-5312
1715-5320
DOI:10.1139/apnm-2018-0785