Gender Related Differences in Paraoxonase 1 Response to High‐fat Diet‐induced Oxidative Stress

Thomàs-Moyà, Elena; Gómez-Pérez, Yolanda; Fiol, Miguel; Gianotti, Magdalena; Lladó, Isabel; Proenza, Ana M.

doi:10.1038/oby.2008.340

Cited by 33 publications

(27 citation statements)

References 56 publications

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“…This is in agreement with studies using short dietary treatments and similar diets, where the excess of body weight was found to be genderdependent [43]. However, in spite of this greater body weight, HFD female rats showed a less marked lipid accumulation in liver, which could be related to higher adipose tissue expandability, such as is pointed out by the adiposity index.…”

Section: Diet-induced Obesity Effectssupporting

confidence: 80%

Long-term High-fat-diet Feeding Impairs Mitochondrial Biogenesis in Liver of Male and Female Rats

Nadal-Casellas

Amengual-Cladera

Proenza

et al. 2010

Cell Physiol Biochem

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Background/Aims: Mitochondrial biogenesis includes both mitochondrial proliferation and differentiation and its regulation under different physiological conditions is not clear. Given the sexual dimorphism previously found in mitochondrial function, the aim of this study was to investigate the gender-dependent effect of chronic high-fat-diet (HFD) feeding on rat liver mitochondrial function and biogenesis. Methods: Ten-week old male and female rats were fed a HFD (26% fat) or a control diet (2.9% fat) for 26 weeks. Mitochondrial morphology was studied. Mitochondrial DNA and protein content, hydrogen peroxide production, oxidative capacity, antioxidant defenses, as well as markers of oxidative damage and mitochondrial biogenesis were analyzed. Results: Female rats showed higher levels of mitochondrial protein and an enhanced oxidative capacity per mitochondrion than males. In both genders, HFD feeding increased mtDNA content and decreased mitochondrial differentiation markers. Conclusion: In comparison to male rats, females show higher oxidative capacity as a consequence of their greater mitochondrial differentiation under both control and obese status. In response to HFD feeding, the oxidative capacity of the whole mitochondrial population is maintained in both genders. This is obtained by means of an enhancement of mitochondrial proliferation, which counteracts the diet-induced impairment of the function of each mitochondrion.

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Section: Diet-induced Obesity Effectssupporting

confidence: 80%

Long-term High-fat-diet Feeding Impairs Mitochondrial Biogenesis in Liver of Male and Female Rats

Nadal-Casellas

Amengual-Cladera

Proenza

et al. 2010

Cell Physiol Biochem

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“…Similarly, Kujiraoka et al (28) found no correlation of serum clusterin with BMI in a study on Japanese adults with coronary artery disease and type 2 diabetes. In rats, diet-induced obesity had no effect on plasma clusterin levels (29). Our results obtained in plasma samples do not necessarily indicate that the binding of leptin to clusterin is irrelevant for the regulation of leptin activity and body weight.…”

Section: Discussionsupporting

confidence: 48%

Effect of Obesity on Plasma Clusterin: A Proposed Modulator of Leptin Action

et al. 2011

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Clusterin, a protein constituent of HDL, was recently shown to bind plasma leptin in vitro and has been proposed to modulate leptin activity. To gain insight into a possible role for plasma clusterin in human obesity, we measured plasma clusterin, leptin, soluble leptin receptor (sObR), and lipoproteins in 70 obese adolescents (12.4 Ϯ 1.6 y; BMI-SD score (SDS-BMI) 2.35 Ϯ 0.47) before and after 3 wk of weight reduction in a dietary camp and in 44 normal weight controls. Binding of plasma leptin to HDL or clusterin was studied using ultracentrifugation and immunoaffinity chromatography. During weight reduction, clusterin decreased from 14.6 Ϯ 4.1 to 10.3 Ϯ 2.9 mg/dL, p Ͻ 0.001) in obese adolescents, whereas sObR increased. However, baseline plasma clusterin in obese adolescents did not differ from controls. Clusterin did not correlate with SDS-BMI, weight loss, leptin, or lipoproteins. Only ϳ1% of plasma leptin was associated with clusterin/apoA-I complexes or with HDL. Our results do not support a role for plasma clusterin as an important leptin-binding protein or modulator of leptin action. The decrease of plasma clusterin during weight reduction may be an effect of the hypocaloric diet rather than being directly linked to weight loss. (Pediatr Res 69: 237-242, 2011)

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“…29 Paraoxonase activity has been suggested to play a role as an antioxidant defense. 30 In our study, the decreased serum PON1 activity induced by EG treatment could be related to the oxidative stress generated by oxalate accumulation. 2 Thus, PON1 protection against oxidation has been reported to result in a partial, time-dependent inactivation of the enzyme.…”

Section: Discussionmentioning

confidence: 90%

Phytotherapy in a rat model of hyperoxaluria: the antioxidant effects of quercetin involve serum paraoxonase 1 activation

Amengual-Cladera

Nadal-Casellas

Gómez-Pérez

et al. 2011

Exp Biol Med (Maywood)

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Serum paraoxonase 1 (PON1) has been reported to be an important contributor to the antioxidant and anti-inflammatory activities of HDL, avoiding LDL oxidation. The activity of this enzyme is reduced in patients with renal insufficiency, caused by elevated oxidative stress and disturbances of apolipoprotein metabolism. Therapeutic utilization of antioxidants to control renal oxidative stress may be an effective therapy in renal protection. The aim was to investigate the protective effects of several antioxidant compounds against the oxidative stress associated to renal failure induced by ethylene glycol (EG), focusing on the possible role of serum PON1 activity. Fifty-four male Wistar rats were randomly assigned to six groups (n = 9): an untreated control (C) group, an EG-treated group, a catechin (CAT)-treated group, an epicatechin (EPI)-treated group, a quercetin (QUE)-treated group and a folk herbal extract (FHE)-treated group. After 16 d of treatment, calcium oxalate lithiasis was induced in the rats using EG. After eight days (treatment + EG), the animals were sacrificed. EG treatment impaired kidney composition, increased oxidative damage, and decreased serum paraoxonase and arylesterase activities. CAT, QUE and the FHE Fagolitos improved oxidative status by enhancing antioxidant defenses - superoxide dismutase and PON1 activities - and reducing oxidative damage, thus reinforcing the idea of a possible role of PON1 in the protective effects of QUE against the deleterious consequences of oxidative stress in kidney.

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Gender Related Differences in Paraoxonase 1 Response to High‐fat Diet‐induced Oxidative Stress

Cited by 33 publications

References 56 publications

Long-term High-fat-diet Feeding Impairs Mitochondrial Biogenesis in Liver of Male and Female Rats

Long-term High-fat-diet Feeding Impairs Mitochondrial Biogenesis in Liver of Male and Female Rats

Effect of Obesity on Plasma Clusterin: A Proposed Modulator of Leptin Action

Phytotherapy in a rat model of hyperoxaluria: the antioxidant effects of quercetin involve serum paraoxonase 1 activation

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