Pregnancy Is Enough to Provoke Deleterious Effects in Descendants of Fructose-Fed Mothers and Their Fetuses

The role of fructose in the global obesity and metabolic syndrome epidemic is widely recognized. However, its consumption is allowed during pregnancy. We have previously demonstrated that maternal fructose intake in rats induces detrimental effects in fetuses. However, these effects only appeared in adult descendants after a re-exposure to fructose. Pregnancy is a physiological state that leads to profound changes in metabolism and hormone response. Therefore, we wanted to establish if pregnancy in the progeny of fructose-fed mothers was also able to provoke an unhealthy situation. Pregnant rats from fructose-fed mothers (10% w/v) subjected (FF) or not (FC) to a fructose supplementation were studied and compared to pregnant control rats (CC). An OGTT was performed on the 20th day of gestation, and they were sacrificed on the 21st day. Plasma and tissues from mothers and fetuses were analyzed. Although FF mothers showed higher AUC insulin values after OGTT in comparison to FC and CC rats, ISI was lower and leptinemia was higher in FC and FF rats than in the CC group. Accordingly, lipid accretion was observed both in liver and placenta in the FC and FF groups. Interestingly, fetuses from FC and FF mothers also showed the same profile observed in their mothers on lipid accumulation, leptinemia, and ISI. Moreover, hepatic lipid peroxidation was even more augmented in fetuses from FC dams than those of FF mothers. Maternal fructose intake produces in female progeny changes that alter their own pregnancy, leading to deleterious effects in their fetuses.

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Changes in lipid peroxidation during pregnancy and after delivery in rats: effect of pinealectomy

Reproduction ◽

10.1530/reprod/119.1.143 ◽

2000 ◽

pp. 143-149 ◽

Cited By ~ 9

Author(s):

RM Sainz ◽

RJ Reiter ◽

JC Mayo ◽

J Cabrera ◽

DX Tan ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Oxidative Damage ◽

Energy Demand ◽

Physiological State ◽

High Energy ◽

Free Radical Scavengers ◽

Radical Scavengers ◽

Oxygen Requirement ◽

Pregnant Rats

Pregnancy is a physiological state accompanied by a high energy demand of many bodily functions and an increased oxygen requirement. Because of the increased intake and utilization of oxygen, increased levels of oxidative stress would be expected. In the present study, the degree of lipid peroxidation was examined in different tissues from non-pregnant and pregnant rats after the delivery of their young. Melatonin and other indole metabolites are known to be direct free radical scavengers and indirect antioxidants. Thus the effect of pinealectomy at 1 month before pregnancy on the accumulation of lipid damage was investigated in non-pregnant and pregnant rats after the delivery of their young. Malonaldehyde and 4-hydroxyalkenal concentrations were measured in the lung, uterus, liver, brain, kidney, thymus and spleen from intact and pinealectomized pregnant rats soon after birth of their young and at 14 and 21 days after delivery. The same parameters were also evaluated in intact and pinealectomized non-pregnant rats. Shortly after delivery, lipid oxidative damage was increased in lung, uterus, brain, kidney and thymus of the mothers. No differences were detected in liver and spleen. Pinealectomy enhanced this effect in the uterus and lung. It is concluded that during pregnancy high levels of oxidative stress induce an increase in oxidative damage to lipids, which in some cases is inhibited by the antioxidative actions of pineal indoles.

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Acetaldehyde-mediated hepatic lipid peroxidation: Role of superoxide and ferritin

Biochemical and Biophysical Research Communications ◽

10.1016/0006-291x(87)90348-2 ◽

1987 ◽

Vol 143 (3) ◽

pp. 984-990 ◽

Cited By ~ 32

Author(s):

S. Shaw ◽

E. Jayatilleke

Keyword(s):

Lipid Peroxidation ◽

Hepatic Lipid ◽

Hepatic Lipid Peroxidation

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The dynamics of indicators of peroxide metabolism in patients with cicatricial skin deformations in combination with metabolic syndrome in complex use of physiotherapeutic treatment methods and drinking mineral waters

Fizioterapevt (Physiotherapist) ◽

10.33920/med-14-2104-06 ◽

2021 ◽

pp. 45-55

Author(s):

K.V. Kazatseva ◽

S.N. Nagornev ◽

V.K. Frolkov ◽

E.V. Gusakova

Keyword(s):

Metabolic Syndrome ◽

Lipid Peroxidation ◽

Antioxidant Enzymes ◽

Mineral Water ◽

Effective Means ◽

Mineral Waters ◽

Combined Use ◽

Pathogenetic Therapy ◽

Peroxidation Processes

The article analyzes the role of lipid peroxidation processes in the pathogenesis of cicatricial skin changes, including in patients with metabolic syndrome. Baseline indices of LPO processes and antioxidant enzymes in patients with metabolic syndrome indicate the development of oxidative stress and accumulation of cytotoxic carbonyl products. The course use of a combination of fermenkol phonophoresis, fractional photothermolysis and mineral water «Essentuki №17» in patients with cicatricial changes in the skin and metabolic syndrome is accompanied by a decrease in the severity of insulin resistance and lipid peroxidation processes. The use of a complex of physiotherapeutic factors and drinking mineral water contributes to an increase in the coefficient of antioxidant protection by 54%. The revealed dynamics of the assessed parameters is realized due to the elimination of molecular inhibitors of antioxidant enzymes in conditions of an increase in the receptor sensitivity of tissues to insulin and a decrease in the level of glycemia. The manifestation of antioxidant activity in the combined use of physiotherapeutic methods and mineral waters for drinking purposes allows this technology to be considered as an effective means of pathogenetic therapy of cicatricial deformities of the skin in combination with metabolic syndrome.

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The role of aldehyde oxidase in ethanol-induced hepatic lipid peroxidation in the rat

Biochemical Journal ◽

10.1042/bj2680579 ◽

1990 ◽

Vol 268 (3) ◽

pp. 579-583 ◽

Cited By ~ 85

Author(s):

S Shaw ◽

E Jayatilleke

Keyword(s):

Lipid Peroxidation ◽

Free Radicals ◽

Liver Injury ◽

Xanthine Oxidase ◽

Aldehyde Oxidase ◽

Ethanol Metabolism ◽

Dependent Manner ◽

Hepatic Lipid ◽

Hepatic Lipid Peroxidation

Hepatic lipid peroxidation has been implicated in the pathogenesis of alcohol-induced liver injury, but the mechanism(s) by which ethanol metabolism or resultant free radicals initiate lipid peroxidation is not fully defined. The role of the molybdenum-containing enzymes aldehyde oxidase and xanthine oxidase in the generation of such free radicals was investigated by measuring alkane production (lipoperoxidation products) in isolated rat hepatocytes during ethanol metabolism. Inhibition of aldehyde oxidase and xanthine oxidase (by feeding tungstate at 100 mg/day per kg) decreased alkane production (80-95%), whereas allopurinol (20 mg/kg by mouth), a marked inhibitor of xanthine oxidase, inhibited alkane production by only 35-50%. Addition of acetaldehyde (0-100 microM) (in the presence of 50 microM-4-methylpyrazole) increased alkane production in a dose-dependent manner (Km of aldehyde oxidase for acetaldehyde 1 mM); menadione, an inhibitor of aldehyde oxidase, virtually inhibited alkane production. Desferrioxamine (5-10 microM) completely abolished alkane production induced by both ethanol and acetaldehyde, indicating the importance of catalytic iron. Thus free radicals generated during the metabolism of acetaldehyde by aldehyde oxidase may be a fundamental mechanism in the initiation of alcohol-induced liver injury.

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Copper-Fructose Interactions: A Novel Mechanism in the Pathogenesis of NAFLD

Nutrients ◽

10.3390/nu10111815 ◽

2018 ◽

Vol 10 (11) ◽

pp. 1815 ◽

Cited By ~ 5

Author(s):

Ming Song ◽

Miriam Vos ◽

Craig McClain

Keyword(s):

Metabolic Syndrome ◽

Causal Effect ◽

Critical Role ◽

Metabolic Effects ◽

Nonalcoholic Fatty Liver ◽

Copper Status ◽

Fructose Intake ◽

The Metabolic Syndrome ◽

High Fructose

Compelling epidemiologic data support the critical role of dietary fructose in the epidemic of obesity, metabolic syndrome and nonalcoholic fatty liver disease (NAFLD). The metabolic effects of fructose on the development of metabolic syndrome and NAFLD are not completely understood. High fructose intake impairs copper status, and copper-fructose interactions have been well documented in rats. Altered copper-fructose metabolism leads to exacerbated experimental metabolic syndrome and NAFLD. A growing body of evidence has demonstrated that copper levels are low in NAFLD patients. Moreover, hepatic and serum copper levels are inversely correlated with the severity of NAFLD. Thus, high fructose consumption and low copper availability are considered two important risk factors in NAFLD. However, the causal effect of copper-fructose interactions as well as the effects of fructose intake on copper status remain to be evaluated in humans. The aim of this review is to summarize the role of copper-fructose interactions in the pathogenesis of the metabolic syndrome and discuss the potential underlying mechanisms. This review will shed light on the role of copper homeostasis and high fructose intake and point to copper-fructose interactions as novel mechanisms in the fructose induced NAFLD.

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Myosteatosis in NAFLD patients correlates with plasma Cathepsin D

BioMolecular Concepts ◽

10.1515/bmc-2021-0004 ◽

2021 ◽

Vol 12 (1) ◽

pp. 27-35

Author(s):

Lingling Ding ◽

Toon. J. I. De Munck ◽

Yvonne Oligschlaeger ◽

Inês Magro dos Reis ◽

Jef Verbeek ◽

...

Keyword(s):

Metabolic Syndrome ◽

Hepatic Steatosis ◽

Lipid Accumulation ◽

Cathepsin D ◽

Fatty Liver Disease ◽

Positive Association ◽

Metabolic Disturbances ◽

Nonalcoholic Fatty Liver ◽

Hepatic Lipid Accumulation

Abstract Previously, we have shown that hepatic lipid accumulation induces the secretion of cathepsin D (CTSD), and that plasma CTSD levels are associated with increased inflammation and disease severity in nonalcoholic fatty liver disease (NAFLD). Although it is clear that the liver is a major source of plasma CTSD, it is unknown whether other metabolically active organs such as the muscle, also associate with plasma CTSD levels in NAFLD patients. Therefore, the aim of this study was to explore the relation between lipid accumulation in the muscle (myosteatosis) and plasma CTSD levels in forty-five NAFLD patients. We observed that hepatic steatosis positively associated with plasma CTSD levels, confirming the previously established link between plasma CTSD and the liver. Furthermore, a positive association between myosteatosis and plasma CTSD levels was observed, which was independent of sex, age, BMI, waist circumference and hepatic steatosis. By establishing a positive association between myosteatosis and plasma CTSD levels, our findings suggest that, in addition to the liver, the muscle is also linked to plasma CTSD levels in NAFLD patients. The observed link between myosteatosis and plasma CTSD levels supports the concept of a significant role of the skeletal muscle in metabolic disturbances in metabolic syndrome-related disorders.

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Aging Increases Susceptibility to High Fat Diet-Induced Metabolic Syndrome in C57BL/6 Mice: Improvement in Glycemic and Lipid Profile after Antioxidant Therapy

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/1987960 ◽

2016 ◽

Vol 2016 ◽

pp. 1-17 ◽

Cited By ~ 19

Author(s):

Valéria Nunes-Souza ◽

Cheila Juliana César-Gomes ◽

Lucas José Sá Da Fonseca ◽

Glaucevane Da Silva Guedes ◽

Salete Smaniotto ◽

...

Keyword(s):

Oxidative Stress ◽

Metabolic Syndrome ◽

Lipid Peroxidation ◽

Insulin Sensitivity ◽

Glucose Tolerance ◽

High Fat Diet ◽

High Fat ◽

Hepatic Lipid ◽

Hepatic Lipid Peroxidation ◽

Old Mice

Nonalcoholic fatty liver disease (NAFLD) has been considered a novel component of the metabolic syndrome (MetS), with the oxidative stress participating in its progression. This study aimed to evaluate the metabolic profile in young and old mice with MetS, and the effects of apocynin and tempol on glycemic and lipid parameters. Young and old C57BL/6 mice with high fat diet- (HFD-) induced MetS received apocynin and tempol 50 mg·kg−1/day in their drinking water for 10 weeks. After HFD, the young group showed elevated fasting glucose, worsened lipid profile in plasma, steatosis, and hepatic lipid peroxidation. Nevertheless, the old group presented significant increase in fasting insulin levels, insulin resistance, plasma and hepatic lipid peroxidation, and pronounced steatosis. The hepatic superoxide dismutase and catalase activity did not differ between the groups. Tempol and apocynin seemed to prevent hepatic lipid deposition in both groups. Furthermore, apocynin improved glucose tolerance and insulin sensitivity in old mice. In summary, old mice are more susceptible to HFD-induced metabolic changes than their young counterparts. Also, the antioxidant therapy improved insulin sensitivity and glucose tolerance, and in addition, apocynin seemed to prevent the HFD-induced hepatic fat deposition, suggesting an important role of oxidative stress in the induction of NAFLD.

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