title: Low intensity exercise prevents disturbances in rat cardiac insulin signaling and endothelial nitric oxide synthase induced by high fructose diet.
abstract: Increase in fructose consumption together with decrease in physical activity contributes to the development of metabolic syndrome and consequently cardiovascular diseases. The current study examined the preventive role of exercise on defects in cardiac insulin signaling and function of endothelial nitric oxide synthase (eNOS) in fructose fed rats. Male Wistar rats were divided into control, sedentary fructose (received 10% fructose for 9 weeks) and exercise fructose (additionally exposed to low intensity exercise) groups. Concentration of triglycerides, glucose, insulin and visceral adipose tissue weight were determined to estimate metabolic syndrome development. Expression and/or phosphorylation of cardiac insulin receptor (IR), insulin receptor substrate 1 (IRS1), tyrosine-specific protein phosphatase 1B (PTP1B), Akt, extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) and eNOS were evaluated. Fructose overload increased visceral adipose tissue, insulin concentration and homeostasis model assessment index. Exercise managed to decrease visceral adiposity and insulin level and to increase insulin sensitivity. Fructose diet increased level of cardiac PTP1B and pIRS1 (Ser307), while levels of IR and ERK1/2, as well as pIRS1 (Tyr 632), pAkt (Ser473, Thr308) and pERK1/2 were decreased. These disturbances were accompanied by reduced phosphorylation of eNOS at Ser1177. Exercise managed to prevent most of the disturbances in insulin signaling caused by fructose diet (except phosphorylation of IRS1 at Tyr 632 and phosphorylation and protein expression of ERK1/2) and consequently restored function of eNOS. Low intensity exercise could be considered as efficient treatment of cardiac insulin resistance induced by fructose diet.
authors.affiliation: Laboratory for Molecular Biology and Endocrinology, Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001 Belgrade, Serbia.
authors.forename: Jelena
authors.initials: J
authors.lastname: Stanišić
authors.affiliation: Laboratory for Molecular Biology and Endocrinology, Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001 Belgrade, Serbia.
authors.forename: Goran
authors.initials: G
authors.lastname: Korićanac
authors.affiliation: Laboratory for Molecular Biology and Endocrinology, Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001 Belgrade, Serbia.
authors.forename: Tijana
authors.initials: T
authors.lastname: Ćulafić
authors.affiliation: Laboratory for Molecular Biology and Endocrinology, Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001 Belgrade, Serbia.
authors.forename: Snježana
authors.initials: S
authors.lastname: Romić
authors.affiliation: Laboratory for Molecular Biology and Endocrinology, Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001 Belgrade, Serbia.
authors.forename: Mojca
authors.initials: M
authors.lastname: Stojiljković
authors.affiliation: Laboratory for Molecular Biology and Endocrinology, Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001 Belgrade, Serbia.
authors.forename: Milan
authors.initials: M
authors.lastname: Kostić
authors.affiliation: Laboratory for Molecular Biology and Endocrinology, Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001 Belgrade, Serbia.
authors.forename: Marija
authors.initials: M
authors.lastname: Pantelić
authors.affiliation: Laboratory for Molecular Biology and Endocrinology, Vinča Institute of Nuclear Sciences, University of Belgrade, PO Box 522, 11001 Belgrade, Serbia. Electronic address: sradivojsa@vinca.rs.
authors.forename: Snežana
authors.initials: S
authors.lastname: Tepavčević
mesh_terms: D000818:Animals; D004032:Diet; D005247:Feeding Behavior / Q000187:drug effects; D005632:Fructose / Q000009:adverse effects*; D007328:Insulin / Q000378:metabolism* / Q000494:pharmacology; D055504:Insulin Receptor Substrate Proteins / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D010766:Phosphorylation / Q000187:drug effects; D010805:Physical Conditioning, Animal; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1 / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D017208:Rats, Wistar; D011972:Receptor, Insulin / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D005632:Fructose; D052250:Nitric Oxide Synthase Type III; D011972:Receptor, Insulin; D051057:Proto-Oncogene Proteins c-akt; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; C516610:Ptpn1 protein, rat
keywords: Endothelial nitric oxide synthase; Fructose; Heart; Insulin resistance; Insulin signaling pathway; Low intensity exercise