Review of a causal role of fructose-containing sugars in myocardial susceptibility to ischemia/reperfusion injury

Maarman, Gerald J.; Mendham, Amy E.; Lamont, Kim; George, Cindy

doi:10.1016/j.nutres.2017.03.003

Cited by 9 publications

(6 citation statements)

References 107 publications

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“…A high-fructose diet can increase tissue oxidative stress (7), which promotes inflammation and increases risk for insulin resistance (8) and cardiovascular disease (26). Because it has also been shown that leptin can attenuate the response to an inflammatory challenge (48), whether leptin resistance in LS rats was associated with a change in inflammatory status was tested, but no significant levels of proinflammatory cytokines were found in serum from LS or HS rats.…”

Section: R606 Leptin Resistance In Sucrose-drinking Ratsmentioning

confidence: 99%

Source of dietary sucrose influences development of leptin resistance in male and female rats

Harris

2018

American Journal of Physiology-Regulatory, Integrative and Comp

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Male rats offered 30% sucrose solution in addition to chow develop leptin resistance without an increase in energy intake or body fat. This study tested whether the leptin resistance was dependent on the physical form of the sucrose. Sprague-Dawley rats were offered a sucrose-free (NS) diet, a 66.6% of energy as sucrose (HS) diet, or the NS diet + 30% sucrose solution (LS). Sucrose intake of LS rats equaled that of HS rats, but total carbohydrate intake exceeded that of HS rats. After 33 days, male and female LS rats were resistant to the inhibitory effect of peripherally administered leptin on food intake. LS rats drank small, frequent meals of sucrose during light and dark periods, whereas HS rats consumed more meals during the dark than the light period and remained responsive to leptin. Diet did not affect daily energy intake or insulin sensitivity. There was a small increase in body fat in the female rats. Leptin sensitivity was restored within 5 days of withdrawal from sucrose in male LS rats. This rapid reversal suggested that leptin resistance was associated with the metabolic impact of drinking sucrose. An experiment was carried out to test whether activity of the hexosamine biosynthetic pathway and glycation of leptin signaling proteins were increased in LS rats, but the results were equivocal. A final experiment determined that female LS rats were leptin-resistant within 18 days of access to sucrose solution and that the small, but significant, increase in body fat was associated with increased adipocyte glucose utilization and insulin responsiveness, which may have been secondary to adipocyte leptin resistance.

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Section: R606 Leptin Resistance In Sucrose-drinking Ratsmentioning

confidence: 99%

Source of dietary sucrose influences development of leptin resistance in male and female rats

Harris

2018

American Journal of Physiology-Regulatory, Integrative and Comp

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“…In late 2014, the United Nations (UN) declared that type 2 diabetes mellitus (DM), obesity and metabolic syndrome had outpaced infectious diseases as the main global threat to human health [1]. The World Health Organization (WHO) highlighted high fructose consumption, mainly in the form of sweetened beverages, as a risk factor for several metabolic diseases [2]. DM is a systemic disease that affects many organs, including the eye, and leads to high healthcare costs.…”

Section: Introductionmentioning

confidence: 99%

Dapagliflozin Prevents NOX- and SGLT2-Dependent Oxidative Stress in Lens Cells Exposed to Fructose-Induced Diabetes Mellitus

Chen

et al. 2019

IJMS

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Purpose: Cataracts in patients with diabetes mellitus (DM) are a major cause of blindness in developed and developing countries. This study aims to examine whether the generation of reactive oxygen species (ROS) via the increased expression of glucose transporters (GLUTs) and the receptor for advanced glycation end products (RAGE) influences the cataract development in DM. Methods: Lens epithelial cells (LECs) were isolated during cataract surgery from patients without DM or with DM, but without diabetic retinopathy. In a rat model, fructose (10% fructose, 8 or 12 weeks) with or without dapagliflozin (1.2 mg/day, 2 weeks) treatment did induce DM, as verified by blood pressure and serum parameter measurements. Immunofluorescence stainings and immunoblottings were used to quantify the protein levels. Endogenous O2˙¯ production in the LECs was determined in vivo with dihydroethidium stainings. Results: We investigated that GLUT levels in LECs differed significantly, thus leading to the direct enhancement of RAGE-associated superoxide generation in DM patients with cataracts. Superoxide production was significantly higher in LECs from rats with fructose-induced type 2 DM, whereas treatment with the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin prevented this effect in fructose-fed rats. Protein expression levels of the sodium/glucose cotransporter 2 (SGLT2), GLUT1, GLUT5, the nicotinamide adenine dinucleotide phosphate reduced form (NADPH) oxidase subunit p67-phox, NOX2/4 and RAGE were upregulated in fructose-fed animals, whereas dapagliflozin treatment reversed these effects. Conclusions: In rats with fructose-induced DM, dapagliflozin downregulates RAGE-induced NADPH oxidase expression in LECs via the inactivation of GLUTs and a reduction in ROS generation. These novel findings suggest that the SGLT2 inhibitor dapagliflozin may be a candidate for the pharmacological prevention of cataracts in patients with DM.

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“…Moreover, epidemiological studies show that incidence of this disorder has dramatically increased to epidemic proportions [ 6 , 7 , 8 , 9 ]. Numerous factors have contributed to this phenomenon, principally caused by sedentary lifestyle-related factors such as over-nutrition, lack of exercise and particularly obesity [ 10 , 11 , 12 ]. Efforts to develop countermeasures to onset and pathogenesis of T2DM, have focused particularly on physiological energy utilization mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Long Term Osmotic Mini Pump Treatment with Alpha-MSH Improves Myocardial Function in Zucker Diabetic Fatty Rats

et al. 2017

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The present investigation evaluates the cardiovascular effects of the anorexigenic mediator alpha-melanocyte stimulating hormone (MSH), in a rat model of type 2 diabetes. Osmotic mini pumps delivering MSH or vehicle, for 6 weeks, were surgically implanted in Zucker Diabetic Fatty (ZDF) rats. Serum parameters, blood pressure, and weight gain were monitored along with oral glucose tolerance (OGTT). Echocardiography was conducted and, following sacrifice, the effects of treatment on ischemia/reperfusion cardiac injury were assessed using the isolated working heart method. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity was measured to evaluate levels of oxidative stress, and force measurements were performed on isolated cardiomyocytes to determine calcium sensitivity, active tension and myofilament co-operation. Vascular status was also evaluated on isolated arterioles using a contractile force measurement setup. The echocardiographic parameters ejection fraction (EF), fractional shortening (FS), isovolumetric relaxation time (IVRT), mitral annular plane systolic excursion (MAPSE), and Tei-index were significantly better in the MSH-treated group compared to ZDF controls. Isolated working heart aortic and coronary flow was increased in treated rats, and higher Hill coefficient indicated better myofilament co-operation in the MSH-treated group. We conclude that MSH improves global heart functions in ZDF rats, but these effects are not related to the vascular status.

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Review of a causal role of fructose-containing sugars in myocardial susceptibility to ischemia/reperfusion injury

Cited by 9 publications

References 107 publications

Source of dietary sucrose influences development of leptin resistance in male and female rats

Source of dietary sucrose influences development of leptin resistance in male and female rats

Dapagliflozin Prevents NOX- and SGLT2-Dependent Oxidative Stress in Lens Cells Exposed to Fructose-Induced Diabetes Mellitus

Long Term Osmotic Mini Pump Treatment with Alpha-MSH Improves Myocardial Function in Zucker Diabetic Fatty Rats

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