Aortic smooth muscle cell proliferation and endothelial nitric oxide synthase activity in fructose-fed rats

Miatello, Roberto; Risler, Norma; Castro, Claudia; González, Susana; Rüttler, Mariel; Cruzado, Montserrat

doi:10.1016/s0895-7061(01)02206-3

Cited by 47 publications

(50 citation statements)

References 33 publications

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“…7,21 Furthermore, hyperinsulinemia could activate the sympathetic nerve system, which in turn will elevate the BP. 26 These observations demonstrate that the existence of a functional sympathetic nervous system is required for the development of elevated BP and plasma insulin levels in fructose-fed rats. 27 Furthermore, in a clinical setting, derangements of the peripheral endothelial NO system have been related to the development of hypertension.…”

Section: Discussionmentioning

confidence: 73%

Caffeine Intake Improves Fructose-Induced Hypertension and Insulin Resistance by Enhancing Central Insulin Signaling

et al. 2014

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535I n humans, the intake of sugar-sweetened beverages is correlated with the prevalence of type 2 diabetes mellitus and obesity.1 High fructose intake is used as a well-established animal model for insulin resistance.2 Some studies have shown that chronic fructose intake in normal rats induces hypertension in association with insulin resistance.2,3 However, insulin infusion was found to stimulate local vasodilation by enhancing the action of nitric oxide (NO). 4 The effect of insulin on the baroreceptor reflex in nucleus tractus solitarii (NTS) is probably mediated by a change in sympathetic nervous activity. 4,5 Furthermore, sympathectomy can prevent the development of fructose-induced hypertension in rats. 6 Recent studies suggest that fructose consumption increases superoxide generation and attenuates baroreflex response. 7,8 Interestingly, inhibition of superoxide generation in NTS can reduce blood pressure (BP) in stroke-prone hypertensive rats. 9 The NTS is located in the dorsal medulla of the brain stem, which is the primary integrating center for cardiovascular regulation and other autonomic functions of the central nervous system. Furthermore, NO has important modulatory functions in the NTS, including the modulation of arterial BP and sympathetic nerve activity. 10 In previous experiments, we demonstrated that insulin microinjected into the NTS induces a depressor effect and initiates an interaction between insulin and phosphatidylinositol 3-kinase Abstract-Recent clinical studies found that fructose intake leads to insulin resistance and hypertension. Fructose consumption promotes protein fructosylation and formation of superoxide. In a previous study, we revealed that inhibition of superoxide production in the nucleus tractus solitarii (NTS) reduces blood pressure. Caffeine displays significant antioxidant ability in protecting membranes against oxidative damage and can lower the risk of insulin resistance. However, the mechanism through which caffeine improves fructose-induced insulin resistance is unclear. The aim of this study was to investigate whether caffeine consumption can abolish superoxide generation to enhance insulin signaling in the NTS, thereby reducing blood pressure in rats with fructose-induced hypertension. Treatment with caffeine for 4 weeks decreased blood pressure, serum fasting glucose, insulin, homeostatic model assessment-insulin resistance, and triglyceride levels and increased the serum direct high-density lipoprotein level in fructose-fed rats but not in control rats. Caffeine treatment resulted in the recovery of fructose-induced decrease in nitric oxide production in the NTS. Immunoblotting and immunofluorescence analyses further showed that caffeine reduced the fructoseinduced phosphorylation of insulin receptor substrate 1 (IRS1 S307) and reversed Akt S473 and neuronal nitric oxide synthase phosphorylation. Similarly, caffeine was able to improve insulin sensitivity and decrease insulin levels in the NTS evoked by fructose. Caffeine intake also reduced the production o...

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Section: Discussionmentioning

confidence: 73%

Caffeine Intake Improves Fructose-Induced Hypertension and Insulin Resistance by Enhancing Central Insulin Signaling

et al. 2014

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“…It has been reported previously that reduced eNOS function may underscore cardiac and smooth muscle atherogenesis in fructose-induced insulin resistance and metabolic syndrome [37]. Recent evidence from our laboratory revealed that gene delivery of eNOS into cardiomyocytes directly improved cardiac contractile function through a phosphatidylinositol-3-kinase-dependent mechanism [35].…”

Section: Discussionmentioning

confidence: 82%

Cardiac overexpression of catalase rescues cardiac contractile dysfunction induced by insulin resistance: role of oxidative stress, protein carbonyl formation and insulin sensitivity

et al. 2006

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Aims/hypothesis: Insulin resistance leads to oxidative stress and cardiac dysfunction. This study examined the impact of catalase on insulin-resistanceinduced cardiac dysfunction, oxidative damage and insulin sensitivity. Methods: Insulin resistance was initiated in FVB and catalase-transgenic mice by 12 weeks of sucrose feeding. Contractile and intracellular Ca 2+ properties were evaluated in cardiomyocytes including peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR 90 ), half-width duration (HWD), maximal velocity of shortening/relengthening (±dL/dt), fura-fluorescence intensity change (ΔFFI) and intracellular Ca 2+ clearance rate (τ). Reactive oxygen species (ROS) and protein damage were evaluated with dichlorodihydrofluorescein and protein carbonyl formation. Results: Sucrose-fed mice displayed hyperinsulinaemia, impaired glucose tolerance and normal body weight. Myocytes from FVB sucrose-fed mice exhibited depressed PS and ±dL/dt, prolonged TR 90 and τ, and reduced ΔFFI associated with normal TPS and HWD compared with those from starch-fed control mice. ROS and protein carbonyl formation were elevated in FVB sucrose-fed mice. Insulin sensitivity was reduced, evidenced by impaired insulin-stimulated 2-deoxy-D-[ 3 H] glucose uptake. Western blot analysis indicated that sucrose feeding: (1) inhibited insulin-stimulated phosphorylation of insulin receptor and Akt; (2) enhanced proteintyrosine phosphatase 1B (PTP1B) expression; and (3) suppressed endothelial nitric oxide synthase (eNOS) and Na + -Ca 2+ exchanger expression without affecting peroxisome proliferator-activated receptor γ (PPARγ), sarco(endo)plasmic reticulum Ca 2+ -ATPase isozyme 2a and phospholamban. Catalase ablated insulin-resistanceinduced mechanical dysfunction, ROS production and protein damage, and reduced eNOS, but not insulin insensitivity. Catalase itself decreased resting FFI and enhanced expression of PTP1B and PPARγ. Conclusions/ interpretation: These data indicate that catalase rescues insulin-resistance-induced cardiac dysfunction related to ROS production and protein oxidation but probably does not improve insulin sensitivity.

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“…Actions of ANG II in this model are associated with the development of hypertension, suppression of adiponectin secretion (26), increase of adipocyte size (9), and generation of oxidative stress (32). In addition, blockade of ANG II abolished the increased VSMC proliferation, restored eNOS activity (19), and improved the insulin sensitivity (11). Since hyperuricemia is associated with activation of RAS (18,21), it is tempting to speculate that increased synthesis of ANG II in this model could be secondary to the rise of plasma uric acid.…”

Section: Discussionmentioning

confidence: 89%

Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats

Sánchez‐Lozada

Tapia

Jiménez

et al. 2007

American Journal of Physiology-Renal Physiology

298

205

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Sá nchez-Lozada LG, Tapia E, Jiménez A, Bautista P, Cristó bal M, Nepomuceno T, Soto V, Á vila-Casado C, Nakagawa T, Johnson RJ, Herrera-Acosta J, Franco M. Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats. Am J Physiol Renal Physiol 292: F423-F429, 2007. First published August 29, 2006; doi:10.1152/ajprenal.00124.2006.-Fructose intake has been recently linked to the epidemic of metabolic syndrome and, in turn, the metabolic syndrome has been epidemiologically linked with renal progression. The renal hemodynamic effects of fructose intake are unknown, as well as the effects of different routes of administration. Metabolic syndrome was induced in rats over 8 wk by either a high-fructose diet (60%, F60, n ϭ 7) or by adding fructose to drinking water (10%, F10, n ϭ 7). Body weight and food and fluid intake of each rat were measured weekly during the follow-up. At baseline and at the end of wk 8, systolic blood pressure, plasma uric acid, and triglycerides were measured. At the end of week 8 glomerular hemodynamics was evaluated by micropuncture techniques. Wall thickening in outer cortical and juxtamedullary afferent arterioles was assessed by immunohistochemistry and computer image analysis. Fructose administration either in diet or drinking water induced hypertension, hyperuricemia, and hypertriglyceridemia; however, there was a progressive increment in these parameters with higher fructose intake (CϽF10ϽF60). In addition, the F60 rats developed kidney hypertrophy, glomerular hypertension, cortical vasoconstriction, and arteriolopathy of preglomerular vessels. In conclusion, fructoseinduced metabolic syndrome is associated with renal disturbances characterized by renal hypertrophy, arteriolopathy, glomerular hypertension, and cortical vasoconstriction. These changes are best observed in rats administered high doses (60% diet) of fructose. uric acid; obesity METABOLIC SYNDROME IS A PATHOPHYSIOLOGICAL entity characterized by insulin resistance, hyperinsulinemia, dyslipidemia, hypertension, and obesity (27). The risk for developing diabetes type 2, cardiovascular disease, and renal disease is increased with increasing manifestations of the various components of the syndrome within any individual.The macronutrient content of the diet has been linked to the metabolic syndrome. Recently, consumption of dietary fructose has been suggested to be one of the environmental factors contributing to the development of obesity and the accompanying abnormalities of the metabolic syndrome (7). In fact, a well-known experimental model of metabolic syndrome is induced by high consumption of fructose; this model induces hypertension, hypertriglyceridemia, hyperinsulinemia, and insulin resistance in rats (12). Fructose consumption is able to produce these effects because fructose is more lipogenic than glucose and usually causes greater elevations of triglycerides (10), which, in turn, increases intramyocellular triglyceride content in the skeletal muscle, causing...

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Aortic smooth muscle cell proliferation and endothelial nitric oxide synthase activity in fructose-fed rats

Cited by 47 publications

References 33 publications

Caffeine Intake Improves Fructose-Induced Hypertension and Insulin Resistance by Enhancing Central Insulin Signaling

Caffeine Intake Improves Fructose-Induced Hypertension and Insulin Resistance by Enhancing Central Insulin Signaling

Cardiac overexpression of catalase rescues cardiac contractile dysfunction induced by insulin resistance: role of oxidative stress, protein carbonyl formation and insulin sensitivity

Fructose-induced metabolic syndrome is associated with glomerular hypertension and renal microvascular damage in rats

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