Arginine and aerobic training prevent endothelial and metabolic alterations in rats at high risk for the development of the metabolic syndrome – CORRIGENDUM

Medeiros, Renata Jurema; Gaique, Thaiane Gadioli; Bento-Bernardes, Thais; Kindlovits, Raquel; Gomes, Tamiris Carolini; Motta, Nadia Alice Vieira; Brito, Fernanda; Fernandes-Santos, Caroline; Oliveira, Karen Brajão de; Nóbrega, Antônio Cláudio Lucas da

doi:10.1017/s0007114517002616

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“…Furthermore, fructose consumption is increasing worldwide. Fructose is positively associated with systemic metabolic disturbances, which leads to impaired cardiac function, cardiomyocyte morphology and molecular signalling (Medeiros et al, 2017). Due to the impairment of insulin signalling and the insulin receptor β-subunit (IRβ)-phosphoinositide 3-kinase (PI3K)-AKT pathway that is promoted by ingestion of fructose, hyperinsulinaemia is often present (Gugliucci, 2017;McMullen et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Molecular mechanisms underlying fructose‐induced cardiovascular disease: exercise, metabolic pathways and microRNAs

Kindlovits

Bertoldi

Rocha

et al. 2021

Experimental Physiology

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During the onset of cardiovascular disease (CVD), disturbances in myocardial vascularization, cell proliferation and protein expression are observed. Aerobic training prevents CVD, but the underlying mechanisms behind left ventricle (LV) hypertrophy are not fully elucidated. The aim of this study was to investigate the mechanisms by which aerobic training protects the heart from LV hypertrophy during the onset of fructose-induced cardiometabolic disease. Male Wistar rats were allocated to four groups (n = 8/group): control sedentary (C), control training (CT), fructose sedentary (F) and fructose training (FT). The C and CT groups received drinking water, and the F and FT groups received D-fructose (10% in water). After 2 weeks, the CT and FT rats were assigned to a treadmill training protocol at moderate intensity for 8 weeks (60 min/day, 4 days/week). After 10 weeks, LV morphological remodelling, cardiomyocyte apoptosis, microRNAs and the insulin signalling pathway were investigated. The F group had systemic cardiometabolic alterations, which were normalised by aerobic training. The LV weight increased in the FT group, myocardium vascularisation decreased in the F group, and the cardiomyocyte area increased in the CT, F and FT groups. Regarding protein expression, total insulin receptor β-subunit (IRβ) decreased in the F group; phospho (p)-IRβ and phosphoinositide 3-kinase (PI3K) increased in the FT group; total-AKT and p-AKT increased in all of the groups; p-p70S6 kinase (p70S6K) protein was higher in the CT group; and p-extracellular signal-regulated kinase (ERK) increased in the CT and FT groups. MiR-126, miR-195 and cardiomyocyte apoptosis did not differ among the groups. Aerobic training activates p-p70S6K and p-ERK, and during the onset of a CVD, it can activate the IRβ-PI3K-AKT pathway.

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Section: Introductionmentioning

confidence: 99%

“…High fructose consumption also increases serum TAG (Medeiros et al, 2017) and endothelin-1 (ET-1) in humans (Tran et al, 2009), which further aggravates the cardiometabolic risk.…”

Section: Introductionmentioning

confidence: 99%