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María P. Portillo - One of the best experts on this subject based on the ideXlab platform.

  • a combination of resveratrol and quercetin induces browning in white adipose tissue of rats fed an Obesogenic Diet
    Obesity, 2017
    Co-Authors: Noemi Arias, Jonatan Miranda, Teresa M Macarulla, Catalina Pico, Paula Oliver, Andreu Palou, María P. Portillo
    Abstract:

    Objective To analyze whether a combination of quercetin (Q) and resveratrol (RSV) would induce a white adipose tissue (WAT) browning effect. Methods Thirty-six rats were fed an Obesogenic Diet and divided into four groups: control, treated with RSV (15 mg/kg body weight/day; RSV group), treated with Q (30 mg/kg body weight/day; Q group), or treated with both polyphenols (RSV + Q group). Results After 6 weeks, body and WAT weights were significantly reduced in the RSV + Q group. In perirenal WAT of the control, RSV, and Q groups, white unilocular adipocytes appeared in the majority of cells, while in the RSV + Q group numerous multilocular adipocytes with positive immunostaining for UCP1 were observed. The presence of UCP1 was confirmed by Western blot. This group also revealed increased mRNA levels of Cidea, Hocx9, Bmp4, Slc27a1, Pat2, Atgl, and Atp5d. Interscapular brown adipose tissue weight showed no differences between groups, but the Cidea mRNA level was increased in the RSV group, the Cox-2 mRNA level in the RSV + Q group, and UCP1 protein expression in the RSV and the RSV + Q groups. Conclusions This study demonstrated that the RSV + Q combination produces a brown-like remodeling effect in perirenal WAT, as well as increased UCP1 protein expression in interscapular brown adipose tissue.

  • liver delipidating effect of a combination of resveratrol and quercetin in rats fed an Obesogenic Diet
    Journal of Physiology and Biochemistry, 2015
    Co-Authors: Jonatan Miranda, María P. Portillo, Leixuri Aguirre, Teresa M Macarulla, Noemi Arias
    Abstract:

    Liver steatosis is characterized by an abnormal accumulation of triacylglycerols in this organ. This metabolic disorder is closely associated with obesity. In the present study, we aimed to analyse the effect of a combination of resveratrol and quercetin on liver steatosis in an animal model of Dietetic obesity, and to compare it with one induced by the administration of each polyphenol separately. Rats were divided into four Dietary groups of nine animals each and fed a high-fat, high-sucrose Diet: an untreated control group and three groups treated either with resveratrol (RSV; 15 mg/kg/day), with quercetin (Q; 30 mg/kg/day), or with both (RSV + Q; 15 mg resveratrol/kg/day and 30 mg quercetin/kg/day) for 6 weeks. Liver weight and triacylglycerol content decreased only in the RSV + Q group. A significant reduction in acetyl-CoA carboxylase activity was observed in RSV and RSV + Q groups, without changes in fatty acid synthase activity. A significant increase in carnitine palmitoyltransferase-1a activity was observed only in rats treated with the combination of resveratrol and quercetin, suggesting increased fatty acid oxidation. Citrate synthase, a marker of mitochondrial density, remained unchanged in all groups. No significant changes were observed in the expression of peroxisome proliferator-activated receptor α (PPARα), nuclear respiratory factor 1 (NRF-1) and transcription factor A mitochondrial (TFAM). In conclusion, resveratrol and quercetin together, combining two doses which were shown to be ineffective singly, is an interesting tool to prevent liver steatosis associated with high-fat high-sucrose feeding. The delipidating effect seems to be mediated by increased fatty acid oxidation not associated with increased mitochondriogenesis, and by reduced de novo lipogenesis.

  • The combination of resveratrol and quercetin enhances the individual effects of these molecules on triacylglycerol metabolism in white adipose tissue
    European Journal of Nutrition, 2015
    Co-Authors: Noemi Arias, Leixuri Aguirre, M. Teresa Macarulla, Iñaki Milton, María P. Portillo
    Abstract:

    Purpose The aim of this study was to analyze whether the combination of resveratrol and quercetin showed additive or synergic effects on body fat accumulation and triacylglycerol metabolism in adipose tissue from rats fed an Obesogenic Diet.

  • pterostilbene a dimethyl ether derivative of resveratrol reduces fat accumulation in rats fed an Obesogenic Diet
    Journal of Agricultural and Food Chemistry, 2014
    Co-Authors: Saioa Gomezzorita, Agnes M. Rimando, Alfredo Fernandezquintela, Leixuri Aguirre, Arrate Lasa, María P. Portillo
    Abstract:

    The current study aimed to demonstrate the effects of pterostilbene in rats fed an Obesogenic Diet. For this purpose, pterostilbene was administered at doses of 15 mg/kg body weight/day (PT15 group) or 30 mg/kg body weight/day (PT30 group) for 6 weeks. Pterostilbene reduced adipose tissue mass −15.1% (PT15) and −22.9% (PT30). In this tissue, it decreased malic enzyme (−39.4 and −49.5% for PT15 and PT30 groups, respectively) and fatty acid synthase (−45 and −53.4% for PT15 and PT30) activities. Acetyl-CoA carboxylase activity was reduced and AMPK activity was increased only in the PT30 group. In the liver, pterostilbene (PT30) reduced malic enzyme (−29.5%) and glucose-6-P dehydrogenase (−43.2%) activities and increased carnitine palmitoyltransferase-1a (37.5%) and acyl-coenzyme A oxidase (42.5%) activities. This increased oxidative capacity was not associated with increased mitochondriogenesis. Among biochemical serum parameters, only insulin was modified by pterostilbene (−31.6%) in the PT15 group. The am...

  • Fatty acid synthase methylation levels in adipose tissue: effects of an Obesogenic Diet and phenol compounds
    Genes & Nutrition, 2014
    Co-Authors: Ana Gracia, Xabier Elcoroaristizabal, Alfredo Fernández-quintela, Jonatan Miranda, Naiara G. Bediaga, Marian De Pancorbo, Agnes M. Rimando, María P. Portillo
    Abstract:

    DNA methylation is an epigenetic mechanism that can inhibit gene transcription. The aim of this study was to assess changes induced by an Obesogenic Diet in the methylation profile of genes involved in adipose tissue triacylglycerol metabolism, and to determine whether this methylation pattern can be altered by resveratrol and pterostilbene. Rats were divided into four groups. The control group was fed a commercial standard Diet, and the other three groups were fed a commercial high-fat, high-sucrose Diet (6 weeks): the high-fat, high-sucrose group, the resveratrol-treated group (RSV; 30 mg/kg/day), and the pterostilbene-treated group (PT; 30 mg/kg/day). Gene expression was measured by RT-PCR and gene methylation by pyrosequencing. The Obesogenic Diet induced a significant increase in adipose tissue weight. Resveratrol and pterostilbene partially prevented this effect. Methylation pattern of ppnla2 and pparg genes was similar among the experimental groups. In fasn , significant hypomethylation in −90-bp position and significant hypermethylation in −62-bp position were induced by Obesogenic feeding. Only pterostilbene reversed the changes induced by the Obesogenic Diet in fasn methylation pattern. By contrast, the addition of resveratrol to the Diet did not induce changes. Both phenolic compounds averted fasn up-regulation. These results demonstrate that the up-regulation of fasn gene induced by an Obesogenic feeding, based on a high-fat, high-sucrose Diet, is related to hypomethylation of this gene in position −90 bp. Under our experimental conditions, both molecules prevent fasn up-regulation, but this change in gene expression seems to be mediated by changes in methylation status only in the case of pterostilbene.

Christine N Metz - One of the best experts on this subject based on the ideXlab platform.

  • the effects of prenatal metformin on Obesogenic Diet induced alterations in maternal and fetal fatty acid metabolism
    Nutrition & Metabolism, 2016
    Co-Authors: Kemoy Harris, Neeraj Desai, Madhu Gupta, Prodyot K Chatterjee, Burton Rochelson, Christine N Metz
    Abstract:

    Maternal obesity may program the fetus and increase the susceptibility of the offspring to adult diseases. Metformin crosses the placenta and has been associated with decreased inflammation and reversal of fatty liver in obese leptin-deficient mice. We investigated the effects of metformin on maternal and fetal lipid metabolism and hepatic inflammation using a rat model of Diet-induced obesity during pregnancy. Female Wistar rats (6–7 weeks old) were fed normal or high calorie Diets for 5 weeks. After mating with normal-Diet fed males, half of the high calorie-fed dams received metformin (300 mg/kg, daily); dams (8 per group) continued Diets through gestational day 19. Maternal and fetal livers and fetal brains were analyzed for fatty acids and for fatty acid metabolism-related gene expression. Data were analyzed by ANOVA followed by Dunnett’s post hoc testing. When compared to control-lean maternal livers, Obesogenic-Diet-exposed maternal livers showed significantly higher saturated fatty acids (14:0 and 16:0) and monounsaturated fatty acids (16:1n7 and 18:1n9) and lower polyunsaturated (18:2n6 and 20:4n6 [arachidonic acid]) and anti-inflammatory n3 polyunsaturated fatty acids (18:3n3 and 22:6n3 [docosahexaenoic acid]) (p < 0.05). Metformin did not affect Diet-induced changes in maternal livers. Fetal livers exposed to the high calorie Diet showed significantly increased saturated fatty acids (18:0) and monounsaturated fatty acids (18:1n9 and 18:1n7) and decreased polyunsaturated fatty acids (18:2n6, 20:4n6 and 22:6n3) and anti-inflammatory n3 polyunsaturated fatty acids, along with increased gene expression of fatty acid metabolism markers (Fasn, D5d, D6d, Scd1, Lxrα). Metformin significantly attenuated Diet-induced inflammation and 18:1n9 and 22:6n3 in fetal livers, as well as n3 fatty acids (p < 0.05). Prenatal Obesogenic Diet exposure significantly increased fetal liver IFNγ levels (p < 0.05), which was reversed by maternal metformin treatment (p < 0.05). Consumption of a high calorie Diet significantly affected maternal and fetal fatty acid metabolism. It reduced anti-inflammatory polyunsaturated fatty acids in maternal and fetal livers, altered gene expression of fatty acid metabolism markers, and induced inflammation in the fetal livers. Prenatal metformin attenuated some Diet-induced fatty acid changes and inflammation in the fetal livers without affecting maternal livers, suggesting that maternal metformin may impact fetal/neonatal fatty acid/lipid metabolism.

  • The effects of prenatal metformin on Obesogenic Diet-induced alterations in maternal and fetal fatty acid metabolism
    Nutrition & Metabolism, 2016
    Co-Authors: Kemoy Harris, Neeraj Desai, Madhu Gupta, Prodyot K Chatterjee, Burton Rochelson, Christine N Metz
    Abstract:

    Maternal obesity may program the fetus and increase the susceptibility of the offspring to adult diseases. Metformin crosses the placenta and has been associated with decreased inflammation and reversal of fatty liver in obese leptin-deficient mice. We investigated the effects of metformin on maternal and fetal lipid metabolism and hepatic inflammation using a rat model of Diet-induced obesity during pregnancy. Female Wistar rats (6–7 weeks old) were fed normal or high calorie Diets for 5 weeks. After mating with normal-Diet fed males, half of the high calorie-fed dams received metformin (300 mg/kg, daily); dams (8 per group) continued Diets through gestational day 19. Maternal and fetal livers and fetal brains were analyzed for fatty acids and for fatty acid metabolism-related gene expression. Data were analyzed by ANOVA followed by Dunnett’s post hoc testing. When compared to control-lean maternal livers, Obesogenic-Diet-exposed maternal livers showed significantly higher saturated fatty acids (14:0 and 16:0) and monounsaturated fatty acids (16:1n7 and 18:1n9) and lower polyunsaturated (18:2n6 and 20:4n6 [arachidonic acid]) and anti-inflammatory n3 polyunsaturated fatty acids (18:3n3 and 22:6n3 [docosahexaenoic acid]) (p 

C Coudray - One of the best experts on this subject based on the ideXlab platform.

  • a mitochondrial targeted ubiquinone modulates muscle lipid profile and improves mitochondrial respiration in Obesogenic Diet fed rats
    British Journal of Nutrition, 2016
    Co-Authors: C Coudray, Gilles Fouret, Jennifer Rieusset, Jerome Lecomte, Carla Ferreri, Karen Lambert, Agnieszka Blachniozabielska, Raymond Ebabe Elle, Eric Badia, Michael P Murphy
    Abstract:

    The prevalence of the metabolic syndrome components including abdominal obesity, dyslipidaemia and insulin resistance is increasing in both developed and developing countries. It is generally accepted that the development of these features is preceded by, or accompanied with, impaired mitochondrial function. The present study was designed to analyse the effects of a mitochondrial-targeted lipophilic ubiquinone (MitoQ) on muscle lipid profile modulation and mitochondrial function in Obesogenic Diet-fed rats. For this purpose, twenty-four young male Sprague-Dawley rats were divided into three groups and fed one of the following Diets: (1) control, (2) high fat (HF) and (3) HF+MitoQ. After 8 weeks, mitochondrial function markers and lipid metabolism/profile modifications in skeletal muscle were measured. The HF Diet was effective at inducing the major features of the metabolic syndrome--namely, obesity, hepatic enlargement and glucose intolerance. MitoQ intake prevented the increase in rat body weight, attenuated the increase in adipose tissue and liver weights and partially reversed glucose intolerance. At the muscle level, the HF Diet induced moderate TAG accumulation associated with important modifications in the muscle phospholipid classes and in the fatty acid composition of total muscle lipid. These lipid modifications were accompanied with decrease in mitochondrial respiration. MitoQ intake corrected the lipid alterations and restored mitochondrial respiration. These results indicate that MitoQ protected Obesogenic Diet-fed rats from some features of the metabolic syndrome through its effects on muscle lipid metabolism and mitochondrial activity. These findings suggest that MitoQ is a promising candidate for future human trials in the metabolic syndrome prevention.

  • the mitochondrial targeted antioxidant mitoq increases liver mitochondrial cardiolipin content in Obesogenic Diet fed rats
    Biochimica et Biophysica Acta, 2015
    Co-Authors: Gilles Fouret, Beatrice Bonafos, Evanthia Tolika, Jerome Lecomte, Manar Aoun, Michael P Murphy, Carla Ferreri, Chryssostomos Chatgilialoglu, Eric Dubreucq, C Coudray
    Abstract:

    Abstract Cardiolipin (CL), a unique mitochondrial phospholipid, plays a key role in several processes of mitochondrial bioenergetics as well as in mitochondrial membrane stability and dynamics. The present study was designed to determine the effect of MitoQ, a mitochondrial-targeted antioxidant, on the content of liver mitochondrial membrane phospholipids, in particular CL, and its fatty acid composition in Obesogenic Diet-fed rats. To do this, twenty-four 6 week old male Sprague Dawley rats were randomized into three groups of 8 animals and fed for 8 weeks with either a control Diet, a high fat Diet (HF), or a HF Diet with MitoQ (HF + MitoQ). Phospholipid classes and fatty acid composition were assayed by chromatographic methods in liver and liver mitochondria. Mitochondrial bioenergetic function was also evaluated. While MitoQ had no or slight effects on total liver fatty acid composition and phospholipid classes and their fatty acid composition, it had major effects on liver mitochondrial phospholipids and mitochondrial function. Indeed, MitoQ both increased CL synthase gene expression and CL content of liver mitochondria and increased 18:2n-6 (linoleic acid) content of mitochondrial phospholipids by comparison to the HF Diet. Moreover, mitochondrial CL content was positively correlated to mitochondrial membrane fluidity, membrane potential and respiration, as well as to ATP synthase activity, while it was negatively correlated to mitochondrial ROS production. These findings suggest that MitoQ may decrease pathogenic alterations to CL content and profiles, thereby preserving mitochondrial function and attenuating the development of some of the features of metabolic syndrome in Obesogenic Diet-fed rats.

  • mitochondrial targeted antioxidant mitoq ameliorated metabolic syndrome features much better than apocynin and allopurinol in Obesogenic Diet fed rats
    Assises du Département AlimH, 2014
    Co-Authors: C Coudray, Gilles Fouret, Jennifer Rieusset, Beatrice Bonafos, Beatrice Chabi, Etienne Raymond Ebabe Elle, David Crouzier, Jeanne Ramos, Elena Marcela Badea, Neven Zarkovich
    Abstract:

    Mitochondrial-targeted antioxidant MitoQ ameliorated metabolic syndrome features much better than Apocynin and Allopurinol in Obesogenic Diet-fed rats. Assises du Departement AlimH

J A Martinez - One of the best experts on this subject based on the ideXlab platform.

  • Supplementation with methyl donors during lactation to high-fat-sucrose-fed dams protects offspring against liver fat accumulation when consuming an Obesogenic Diet.
    Journal of Developmental Origins of Health and Disease, 2014
    Co-Authors: Paul Cordero, Javier Campion, Fermin I Milagro, J A Martinez
    Abstract:

    Methyl donor supplementation has been reported to prevent obesity-induced liver fat accumulation in adult rats. We hypothesized that this protection could be mediated by perinatal nutrition. For this purpose, we assessed the response to an Obesogenic Diet (high-fat-sucrose, HFS) during adulthood depending on maternal Diet during lactation. Female Wistar rats fed control Diet during pregnancy were assigned to four postpartum Dietary groups: control, control supplemented with methyl donors (choline, betaine, folic acid, vitamin B12), HFS and HFS supplemented with methyl donors. At weaning, the male offspring was transferred to a chow Diet and at week 12th assigned to a control or a HFS Diet during 8 weeks. The offspring whose mothers were fed HFS during lactation showed increased adiposity (19%, P

  • Transcriptomic and epigenetic changes in early liver steatosis associated to obesity: Effect of Dietary methyl donor supplementation
    Molecular Genetics and Metabolism, 2013
    Co-Authors: Paul Cordero, Javier Campion, Fermin I Milagro, J A Martinez
    Abstract:

    Abstract Non-alcoholic fatty liver disease is a primary hepatic manifestation of obesity and an important adverse metabolic syndrome trait. Animal models of Diet-induced obesity promote liver fat accumulation putatively associated with alterations in epigenetic profile. Dietary methyl donor-supplementation may protect against this disturbance during early developmental stages affecting the molecular basis of gene regulation. The aim of this study was to investigate the transcriptomic and epigenetic mechanisms implicated in liver fat accumulation as a result of an Obesogenic Diet and the putative preventive role of Dietary methyl donors. Forty-eight male Wistar rats were assigned into four Dietary groups for 8 weeks; control, control methyl-donor-supplemented with a Dietary cocktail containing betaine, choline, vitamin B 12 and folic acid, high-fat-sucrose and high-fat-sucrose methyl-donor-supplemented. Liver fat accumulation induced by a HFS Diet was prevented by methyl donor supplementation in HFS-fed animals. A liver mRNA microarray, subsequently validated by real time-qPCR, showed modifications in some biologically relevant genes involved in obesity development and lipid metabolism (Lepr, Srebf2, Agpat3 and Esr1). Liver global DNA methylation was decreased by methyl donor supplementation in control-fed animals. Methylation levels of specific CpG sites from Srebf2, Agpat3 and Esr1 promoter regions showed changes due to the Obesogenic Diet and the supplementation with methyl donors. Interestingly, Srebf2 CpG23_24 methylation levels (− 167 bp and − 156 bp with respect to the transcriptional start site) correlated with HDLc plasma levels, whereas Esr1 CpG14 (− 2623 bp) methylation levels were associated with body and liver weights and fat content. Furthermore HFS Diet-induced liver fat accumulation was prevented by methyl donor supplementation. In conclusion, both Obesogenic Diet and methyl donor supplementation modified the mRNA hepatic profile as well as the methylation of specific gene promoters and total DNA.

  • Dietary supplementation with methyl donors reduces fatty liver and modifies the fatty acid synthase dna methylation profile in rats fed an Obesogenic Diet
    Genes and Nutrition, 2013
    Co-Authors: Paul Cordero, Ana M Gomezuriz, Javier Campion, Fermin I Milagro, J A Martinez
    Abstract:

    Non-alcoholic fatty liver disease (NAFLD) is one of the first hepatic manifestations of metabolic syndrome, whose progression can lead to cirrhosis and hepatic carcinoma. Interestingly, methyl donor supplementation could improve Obesogenic Diet-induced hepatic triglyceride accumulation. The aim of this research is to describe methyl donor effects on a high-fat-sucrose (HFS) Diet in both sexes and epigenetic changes induced on fatty acid synthase (FASN) promoter methylation pattern as well as gene expression of NAFLD key metabolic genes. Twenty-four male and 28 female Wistar rats were assigned to three Dietary groups: control, HFS, and HFS supplemented with methyl donors (choline, betaine, vitamin B12, and folic acid). After 8 weeks of treatment, somatic, biochemical, mRNA, and epigenetic measurements were performed. Rats fed the HFS Diet presented an overweight phenotype and alterations in plasma biochemical measurements. Methyl donor supplementation reverted the HFS-Diet-induced hepatic triglyceride accumulation. Analysis of FASN promoter cytosine methylation showed changes in both sexes due to the Obesogenic Diet at −1,096, −780, −778, and −774 CpG sites with respect to the transcriptional start site. Methyl donor supplementation modified DNA methylation at −852, −833, −829, −743, and −733 CpGs depending on the sex. RT-PCR analysis confirmed that FASN expression tended to be altered in males. Our findings reinforce the hypothesis that methyl donor supplementation can prevent hepatic triglyceride accumulation induced by Obesogenic Diets in both sexes. Changes in liver gene expression profile and epigenetic-mediated mechanisms related to FASN DNA hypermethylation could be involved in methyl donor-induced NAFLD improvement.

  • Maternal weight gain induced by an Obesogenic Diet affects adipose accumulation, liver weight, and insulin homeostasis in the rat offspring depending on the sex
    Journal of Endocrinological Investigation, 2012
    Co-Authors: Paul Cordero, Javier Campion, Fermin I Milagro, Ana M. Gómez-Úriz, J A Martinez
    Abstract:

    Background: The aim of this research was to analyze the influence of the maternal Dietary intake before pregnancy, as well as the parental impact on the response to a transgenerational high-fat-Diet in rats. Methods: Ten female Wistar rats were fed a standard or a high-fat-sucrose (HFS) Diet in the 8 weeks prior to pregnancy. Adult offsprings were assigned to a control or Obesogenic Diet for 8 weeks. Then, rat tissues and plasma samples were collected for analyzing tissue weight, liver triglycerides, and biochemical parameters such as triglycerides, HDL cholesterol, glucose, and insulin levels. Results: The offspring of rats fed a HFS Diet gained less weight when they were fed the same Diet than those fed a HFS Diet combined with maternal control Diet. Insulin levels were higher in rats fed a HFS Diet (p

  • maternal weight gain induced by an Obesogenic Diet affects adipose accumulation liver weight and insulin homeostasis in the rat offspring depending on the sex
    Journal of Endocrinological Investigation, 2012
    Co-Authors: Paul Cordero, Ana M Gomezuriz, Javier Campion, Fermin I Milagro, J A Martinez
    Abstract:

    Background: The aim of this research was to analyze the influence of the maternal Dietary intake before pregnancy, as well as the parental impact on the response to a transgenerational high-fat-Diet in rats. Methods: Ten female Wistar rats were fed a standard or a high-fat-sucrose (HFS) Diet in the 8 weeks prior to pregnancy. Adult offsprings were assigned to a control or Obesogenic Diet for 8 weeks. Then, rat tissues and plasma samples were collected for analyzing tissue weight, liver triglycerides, and biochemical parameters such as triglycerides, HDL cholesterol, glucose, and insulin levels. Results: The offspring of rats fed a HFS Diet gained less weight when they were fed the same Diet than those fed a HFS Diet combined with maternal control Diet. Insulin levels were higher in rats fed a HFS Diet (p<0.05) in both sexes; however, maternal HFS Diet reversed, partially in males and totally in females, this hormonal imbalance. In male newborns, Diet-induced maternal weight gain before pregnancy significantly influenced visceral (R2=0.373) and subcutaneous (R2=0.239) adipose deposition as well as liver weight (R2=0.130). Paternal genetic make-up was also a relevant factor affecting adiposity in both sexes (R2=0.333 in visceral fat; R2=0.183 in subcutaneous fat in males, and 0.292 and 0.282, respectively in females) as well as plasma triglycerides (R2=0.193 in males and R2=0.251 in females). Conclusions: The genetic parental background and pre-natal maternal Diet are important factors in the response to a hypercaloric Diet and affect body composition and glucose homeostasis traits, including insulin secretion and homeostatic model assessment index.

Gilles Fouret - One of the best experts on this subject based on the ideXlab platform.

  • spirulina platensis and silicon enriched spirulina equally improve glucose tolerance and decrease the enzymatic activity of hepatic nadph oxidase in Obesogenic Diet fed rats
    Food & Function, 2018
    Co-Authors: Joris Vide, Gilles Fouret, Beatrice Bonafos, Melha Benlebna, Joel Poupon, Bernard Jover, Francois Casas, Nicolas Jouy, Christine Feilletcoudray, Sylvie Gaillet
    Abstract:

    The prevalence of metabolic syndrome components, such as obesity, glucose intolerance and hepatic steatosis, is rapidly increasing and becoming a major issue of public health. The present work was designed to determine the effects of Spirulina platensis (Sp) algae and silicon-enriched Sp on major metabolic syndrome components in Obesogenic Diet-fed rats. Forty male Wistar rats were divided into 4 groups. Ten rats were fed a control Diet and 30 rats were fed a high fat (HF) Diet. The HF groups were divided into three groups and supplemented with placebo or Sp or Si-enriched Sp for 12 weeks. Dietary intake and body weight were recorded. Oral glucose tolerance test and surrogate metabolic syndrome (insulin, leptin, adiponectin and lipids), mitochondrial function (enzymatic activity of respiratory chain complexes and β-hydroxyacyl-CoA dehydrogenase), NADPH oxidase activity and several long-established oxidative stress markers were measured in the blood and liver. The HF Diet induced obesity, glucose intolerance, hepatic steatosis and huge metabolic alterations, associated with higher NADPH oxidase activity and lower hepatic sulfhydryl group and glutathione contents. Otherwise, the Sp and Sp + Si supplements showed some interesting effects on rat characteristics and particularly on blood and hepatic metabolic parameters. Indeed, the intake of Sp or Sp + Si mainly improved glucose tolerance and decreased the enzymatic activity of hepatic NADPH oxidase. Overall, Si supplementation of spirulina does not appear to have more beneficial effects than spirulina alone. Other experiments with different species of rats/mice, different Diets or different durations of Diet intake should be undertaken to confirm or invalidate these results.

  • a mitochondrial targeted ubiquinone modulates muscle lipid profile and improves mitochondrial respiration in Obesogenic Diet fed rats
    British Journal of Nutrition, 2016
    Co-Authors: C Coudray, Gilles Fouret, Jennifer Rieusset, Jerome Lecomte, Carla Ferreri, Karen Lambert, Agnieszka Blachniozabielska, Raymond Ebabe Elle, Eric Badia, Michael P Murphy
    Abstract:

    The prevalence of the metabolic syndrome components including abdominal obesity, dyslipidaemia and insulin resistance is increasing in both developed and developing countries. It is generally accepted that the development of these features is preceded by, or accompanied with, impaired mitochondrial function. The present study was designed to analyse the effects of a mitochondrial-targeted lipophilic ubiquinone (MitoQ) on muscle lipid profile modulation and mitochondrial function in Obesogenic Diet-fed rats. For this purpose, twenty-four young male Sprague-Dawley rats were divided into three groups and fed one of the following Diets: (1) control, (2) high fat (HF) and (3) HF+MitoQ. After 8 weeks, mitochondrial function markers and lipid metabolism/profile modifications in skeletal muscle were measured. The HF Diet was effective at inducing the major features of the metabolic syndrome--namely, obesity, hepatic enlargement and glucose intolerance. MitoQ intake prevented the increase in rat body weight, attenuated the increase in adipose tissue and liver weights and partially reversed glucose intolerance. At the muscle level, the HF Diet induced moderate TAG accumulation associated with important modifications in the muscle phospholipid classes and in the fatty acid composition of total muscle lipid. These lipid modifications were accompanied with decrease in mitochondrial respiration. MitoQ intake corrected the lipid alterations and restored mitochondrial respiration. These results indicate that MitoQ protected Obesogenic Diet-fed rats from some features of the metabolic syndrome through its effects on muscle lipid metabolism and mitochondrial activity. These findings suggest that MitoQ is a promising candidate for future human trials in the metabolic syndrome prevention.

  • the mitochondrial targeted antioxidant mitoq increases liver mitochondrial cardiolipin content in Obesogenic Diet fed rats
    Biochimica et Biophysica Acta, 2015
    Co-Authors: Gilles Fouret, Beatrice Bonafos, Evanthia Tolika, Jerome Lecomte, Manar Aoun, Michael P Murphy, Carla Ferreri, Chryssostomos Chatgilialoglu, Eric Dubreucq, C Coudray
    Abstract:

    Abstract Cardiolipin (CL), a unique mitochondrial phospholipid, plays a key role in several processes of mitochondrial bioenergetics as well as in mitochondrial membrane stability and dynamics. The present study was designed to determine the effect of MitoQ, a mitochondrial-targeted antioxidant, on the content of liver mitochondrial membrane phospholipids, in particular CL, and its fatty acid composition in Obesogenic Diet-fed rats. To do this, twenty-four 6 week old male Sprague Dawley rats were randomized into three groups of 8 animals and fed for 8 weeks with either a control Diet, a high fat Diet (HF), or a HF Diet with MitoQ (HF + MitoQ). Phospholipid classes and fatty acid composition were assayed by chromatographic methods in liver and liver mitochondria. Mitochondrial bioenergetic function was also evaluated. While MitoQ had no or slight effects on total liver fatty acid composition and phospholipid classes and their fatty acid composition, it had major effects on liver mitochondrial phospholipids and mitochondrial function. Indeed, MitoQ both increased CL synthase gene expression and CL content of liver mitochondria and increased 18:2n-6 (linoleic acid) content of mitochondrial phospholipids by comparison to the HF Diet. Moreover, mitochondrial CL content was positively correlated to mitochondrial membrane fluidity, membrane potential and respiration, as well as to ATP synthase activity, while it was negatively correlated to mitochondrial ROS production. These findings suggest that MitoQ may decrease pathogenic alterations to CL content and profiles, thereby preserving mitochondrial function and attenuating the development of some of the features of metabolic syndrome in Obesogenic Diet-fed rats.

  • mitochondrial targeted antioxidant mitoq ameliorated metabolic syndrome features much better than apocynin and allopurinol in Obesogenic Diet fed rats
    Assises du Département AlimH, 2014
    Co-Authors: C Coudray, Gilles Fouret, Jennifer Rieusset, Beatrice Bonafos, Beatrice Chabi, Etienne Raymond Ebabe Elle, David Crouzier, Jeanne Ramos, Elena Marcela Badea, Neven Zarkovich
    Abstract:

    Mitochondrial-targeted antioxidant MitoQ ameliorated metabolic syndrome features much better than Apocynin and Allopurinol in Obesogenic Diet-fed rats. Assises du Departement AlimH