Alterations in Antioxidant Defence Systems and Metal Profiles in Liver of Rats with Metabolic Syndrome Induced with High-Sucrose Diet

The underlying mechanisms for the detrimental consequences of a high-fructose diet in animal models are not clear. However, the possibility exists that fructose feeding facilitates oxidative damage. Thus, the aim of the present study was to assess, in weaning rats, the effect of a high-sucrose diet v. starch diet for 2 weeks on oxidative stress variables. Plasma lipid levels were measured and lipid peroxidation was evaluated by urine and plasma thiobarbituric acid-reactive substances (TBARS). The susceptibilities of several tissues to peroxidation were determined in tissue homogenates after in vitro lipid peroxidation. Antioxidant defence variables were evaluated by measuring plasma and heart vitamin E levels, and heart superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities. Higher plasma triacylglycerol (P<0·01) and TBARS (P<0·01) levels were found in rats fed the sucrose diet as compared with the starch-fed group, whereas plasma α-tocopherol levels were significantly decreased in the sucrose-fed group compared with the starch-fed group (P<0·01). Higher urine TBARS (P<0·01) were found in the sucrose-fed group compared with the starch-fed group, suggesting increased production of these substances from lipid peroxidation in vivo. Higher susceptibility to peroxidation in heart, thymus and pancreas was also found in the sucrose-fed group v. the starch-fed group. No statistical differences were observed for liver TBARS level between the two groups. Heart SOD activity was significantly decreased (P<0·001) in the sucrose-fed group compared with the starch-fed group, whereas heart vitamin E level and GPX activity were not different between the groups. However, the in vitro generation of superoxide radical in heart homogenate, measured by electron spin resonance detection and spin trapping, was not increased in the sucrose-fed group compared with starch-fed rats. Altogether, the results indicate that a short-term consumption of a high-sucrose diet negatively affects the balance of free radical production and antioxidant defence in rats, leading to increased lipid susceptibility to peroxidation.

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The N- and L-Type Calcium Channel Blocker Cilnidipine Suppresses Renal Injury in Dahl Rats Fed a High-Sucrose Diet, an Experimental Model of Metabolic Syndrome

Nephron Physiology ◽

10.1159/000085713 ◽

2005 ◽

Vol 101 (1) ◽

pp. p1-p13 ◽

Cited By ~ 38

Author(s):

Tomoyuki Konda ◽

Azusa Enomoto ◽

Junko Matsushita ◽

Akira Takahara ◽

Toshiki Moriyama

Keyword(s):

Metabolic Syndrome ◽

Calcium Channel ◽

Experimental Model ◽

Calcium Channel Blocker ◽

Renal Injury ◽

Channel Blocker ◽

Sucrose Diet ◽

High Sucrose Diet ◽

High Sucrose

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Changes in Insulin Secretion, KATP and Ba Currents in Rat Pancreatic Beta Cells from Rats with Metabolic Syndrome, Induced by a High Sucrose Diet

Biophysical Journal ◽

10.1016/j.bpj.2010.12.750 ◽

2011 ◽

Vol 100 (3) ◽

pp. 100a

Author(s):

Myrian Velasco ◽

Carlos Larque ◽

Marcia Hiriart

Keyword(s):

Metabolic Syndrome ◽

Insulin Secretion ◽

Beta Cells ◽

Pancreatic Beta Cells ◽

Sucrose Diet ◽

High Sucrose Diet ◽

High Sucrose

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Metabolic Syndrome in the Rat: Females are Protected Against the Pro-Oxidant Effect of a High Sucrose Diet

Experimental Biology and Medicine ◽

10.1177/153537020222700918 ◽

2002 ◽

Vol 227 (9) ◽

pp. 837-842 ◽

Cited By ~ 38

Author(s):

Jérôme Busserolles ◽

Andrzej Mazur ◽

Elyett Gueux ◽

Edmond Rock ◽

Yves Rayssiguier

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Lipid Peroxidation ◽

Heart Tissue ◽

Female Rats ◽

Hormonal Status ◽

Sucrose Diet ◽

High Sucrose Diet ◽

Oxidant Effect ◽

High Sucrose

Metabolic syndrome is more prevalent in men than in women. In an experimental dietary model of metabolic syndrome, the high-fructose–fed rat, oxidative stress has been observed in males. Given that estradiol has been documented to exert an antioxidant effect, we investigated whether female rats were better protected than males against the adverse effects of a high-sucrose diet, and we studied the influence of hormonal status in female rats. Males and females were first fed a sucrose-based or starch-based diet for 2 weeks. In the males, the plasma triglyceride (TG)-raising effect of sucrose was accompanied by significantly lowered plasma α-tocopherol and a significantly lowered α-tocopherol/TG ratio (30%), suggesting that vitamin E depletion may predispose lipoproteins to subsequent oxidative stress. In males, after exposure of heart tissue homogenate to iron-induced lipid peroxidation, thiobarbituric reactive substances were significantly higher in the sucrose-fed than in the starch-fed rats. In contrast, in sucrose-fed females, neither a decrease in vitamin E/TG ratio nor an increased susceptibility of heart tissue to peroxidation was observed, despite both a significantly decreased heart superoxide dismutase activity (14%) and a significant 3-fold increase in plasma nitric oxide concentration compared with starch-fed females. The influence of hormonal status in female rats was then assessed using intact, ovariectomized, or estradlol-supplemented ovariectomized female rats fed the sucrose or starch diet for 2 weeks. After exposure of heart tissue to iron-induced lipid peroxidation, higher susceptibility to peroxidation was found only in ovariectomized females fed the sucrose diet compared with the starch group and not in intact females or ovariectomized females supplemented with estradiol. Thus, estrogens, by their effects on antioxidant capacity, might explain the sexual difference in the pro-oxidant effect of sucrose diet resulting in metabolic syndrome in rats.

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A Model of Metabolic Syndrome and Related Diseases with Intestinal Endotoxemia in Rats Fed a High Fat and High Sucrose Diet

PLoS ONE ◽

10.1371/journal.pone.0115148 ◽

2014 ◽

Vol 9 (12) ◽

pp. e115148 ◽

Cited By ~ 40

Author(s):

Xin Zhou ◽

Dewu Han ◽

Ruiling Xu ◽

Suhong Li ◽

Huiwen Wu ◽

...

Keyword(s):

Metabolic Syndrome ◽

High Fat ◽

Sucrose Diet ◽

High Sucrose Diet ◽

High Sucrose

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Effect of Beilschmedia obscura on the prevention of high fat/high sucrose diet induced metabolic syndrome on male Albino Wistar rats

Metabolism Open ◽

10.1016/j.metop.2021.100156 ◽

2021 ◽

pp. 100156

Author(s):

Florine Essouman Mbappe ◽

Ferdinand Lanvin Edoun Ebouel ◽

Fils Armand Ella ◽

Bruno Dupon Ambamba Akamba ◽

Jules Kamga Nanhah ◽

...

Keyword(s):

Metabolic Syndrome ◽

Wistar Rats ◽

High Fat ◽

Sucrose Diet ◽

High Sucrose Diet ◽

High Sucrose

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SHR-Zbtb16 Minimal Congenic Strain Reveals Nutrigenetic Interaction Between Zbtb16 and High-Sucrose Diet

Physiological Research ◽

10.33549/physiolres.934423 ◽

2020 ◽

pp. 521-527

Author(s):

E ŠKOLNÍKOVÁ ◽

L ŠEDOVÁ ◽

F LIŠKA ◽

O ŠEDA

Keyword(s):

Metabolic Syndrome ◽

Congenic Strain ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Metabolic Effects ◽

Standard Diet ◽

Low Density ◽

Sucrose Diet ◽

High Sucrose Diet ◽

High Sucrose

Both prenatal and postnatal excessive consumption of dietary sucrose or fructose was shown to be detrimental to health and contributing to pathogenesis of metabolic syndrome. Our knowledge of genetic determinants of individual sensitivity to sucrose-driven metabolic effects is limited. In this study, we have tested the hypothesis that a variation of metabolic syndrome-related gene, Zbtb16 (Zinc Finger and BTB Domain Containing 16 will affect the reaction to high-sucrose diet (HSD) content in “matched” nutritional exposition settings, i.e. maternal HSD with re-exposition to HSD in adulthood vs. standard diet. We compared metabolic profiles of adult males of spontaneously hypertensive rats (SHR) and a single-gene, minimal congenic strain SHR-Zbtb16 fed either standard diet or exposed to HSD prenatally throughout gestation and nursing and again at the age of 6 months for the period of 14 days. HSD exposition led to increased adiposity in both strains and decrease of glucose tolerance and cholesterol (Ch) concentrations in majority of low-density lipoprotein (LDL) particle classes and in very large and large high-density lipoprotein (HDL) in SHR-Zbtb16 male offspring. There was a similar pattern of HSD-induced increase of triacylglycerols in chylomicrons and very low-density lipoprotein (VLDL) of both strains, though the increase of (triacylglycerol) TAG content was clearly more pronounced in SHR. We observed significant STRAIN*DIET interactions for the smallest LDL particles as their TAG content decreased in SHR-Zbtb16 and did not change in SHR in response to HSD. In summary, we provide evidence of nutrigenetic interaction between Zbtb16 and HSD in context of pathogenesis of metabolic syndrome.

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