Ana M Proenza

University of the Balearic Islands, Palma, Balearic Islands, Spain

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Publications (47)148.36 Total impact

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    ABSTRACT: The aim of this study was to investigate the time-course response of retroperitoneal white adipose tissue (WAT) insulin and adiponectin signaling pathway intermediates in relation to the systemic age-associated impairment of insulin sensitivity in male and female rats. The main markers of the insulin and adiponectin signaling pathways of the retroperitoneal WAT, as well as of the systemic insulin sensitivity profile of 3-, 9- and 18-month old Wistar rats of both sexes were determined. Our results indicate that age leads to a decrease in the insulin sensitivity in both sexes that agrees with the decline in the levels of the WAT insulin signaling pathway intermediates, the increase in the adiposity index and the rise in the serum insulin resistance markers. This is accompanied by a sex-dimorphism that involves a gradual insulin signaling pathway decrease in female rats and an earlier and acute decrease in males and suggests a better insulin responsiveness in female rats at any age group. Our results confirm the idea that in rats, the insulin signaling pathway of WAT is altered at earlier ages than that of skeletal muscle and also provides further evidence of the impairment of the WAT adiponectin signaling pathway.
    Biochimie 08/2014; · 3.14 Impact Factor
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    ABSTRACT: Sexual dimorphism has been found in both mitochondrial functionality and adiponectin expression in white adipose tissue, with female rats presenting more functional mitochondria than males and greater adiponectin expression. However, little is known about the role of sex hormones in this dimorphism. The aim was to elucidate the role of sex hormones in mitochondrial biogenesis and dynamics and in adiponectin synthesis in white adipocytes, and also to provide new evidence of the link between these processes. 3T3-L1 preadipocytes were differentiated and treated either with 17-β estradiol (E2; 10 nM), progesterone (Pg), testosterone (1 μM both), or a combination of Pg or testosterone with flutamide (FLT; 10 μM) or E2 (1 μM). The markers of mitochondrial biogenesis and dynamics and adiponectin expression were analyzed. E2 induced mitochondrial proliferation and differentiation in 3T3-L1, although testosterone showed opposite effects. Pg treatment stimulated proliferation but impaired differentiation. In concerns mitochondrial dynamics, these hormones promoted fusion over fission. FLT treatment indicated that Pg elicits its effects on mitochondrial dynamics through the androgen receptor. E2 coadministration with testosterone or Pg reversed its effects. In conclusion, our results show that E2 induces stimulation of mitochondrial biogenesis in white adipocytes in vitro, especially in situations that imply an impairment of mitochondrial function, whereas testosterone would have opposite effects. Moreover, testosterone and Pg alter mitochondrial dynamics by promoting fusion over fission, while E2 stimulates both processes. All these alterations run in parallel with changes in adiponectin expression, thus suggesting the existence of a link between mitochondrial biogenesis and dynamics and adiponectin synthesis in white adipocytes.
    Journal of Molecular Endocrinology 01/2014; 52(2):203-14. · 3.58 Impact Factor
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    ABSTRACT: The aim of the study was to determine, in rats of both sexes, the effect of HF diet feeding on the expression of adipokines involved in inflammatory status and insulin sensitivity and on the levels of proteins involved in lipid handling of retroperitoneal adipose tissue. Eight-week-old Wistar rats of both sexes were fed a control diet (2.9% w/w fat) or an HF diet (30% w/w fat) for 14 weeks. Adiponectin, peroxisome proliferator-activated receptor γ and inflammatory marker mRNA levels were analyzed by real-time polymerase chain reaction. Levels of insulin receptor, glucose transporter 4, carnitine palmitoyltransferase 1, fatty acid synthase, hormone-sensitive lipase and lipoprotein lipase were determined by Western blot. HF diet feeding did not induce hyperphagia or body weight gain but did promote an increase in adiposity although only in male rats. HF diet impaired glucose tolerance and the expression of inflammatory and insulin sensitivity markers in adipose tissue of male rats, but not in female rats. Male rats seem to be more prone to disorders associated with an unbalanced composition of the diet, even in the absence of hyperphagia. In contrast, female rats counteract excessive fat intake by improving their ability to use lipid fuels, which limits adiposity and maintains insulin sensitivity. Copyright © 2012 John Wiley & Sons, Ltd.
    Cell Biochemistry and Function 10/2012; · 1.85 Impact Factor
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    ABSTRACT: Marked sex-dependent differences in mitochondrial function and redox status have been found in brown adipose tissue (BAT) of control rats. Insulin also plays a role in the development and maintenance of this tissue. The aim was to investigate sexual dimorphism in the effects of diet-induced obesity on BAT mitochondrial function, as well as on insulin signaling pathway. 10-week-old Wistar rats of both sexes were fed a control diet or a palatable high-fat diet for 26 weeks. Serum markers of insulin sensitivity were analyzed. Mitochondrial DNA (mtDNA) content, mitochondrial oxidative activities, PGC-1α mRNA levels, as well as the protein levels of insulin receptor subunit β (IRβ), glucose transporter GLUT4, β(3)-adrenergic receptor (β(3)-AR), phosphatidylinositol 3-kinase, mitochondrial transcription factor A (TFAM), cytochrome c oxidase subunit IV (COX IV), and uncoupling protein 1 (UCP1) were measured in BAT. Obese females showed impaired systemic insulin sensitivity accompanied by diminished IRβ, GLUT4, and β(3)-AR protein levels in BAT. In addition, TFAM and COX IV protein and PGC-1α mRNA levels decreased in obese females, whereas mtDNA levels increased. In obese males, oxidative and thermogenic capacities rose and no significant changes were observed in the insulin signaling pathway elements. The reduction of the insulin signaling pathway in BAT of obese females may be responsible, at least partially, for the impaired biogenesis process, which could favor the increase of body weight found in this sex. In contrast, the enhanced mitochondrial functionality in the BAT of males would avoid increased oxidative damage and the impairment of insulin signaling.
    Molecular and Cellular Biochemistry 10/2012; · 2.33 Impact Factor
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    ABSTRACT: Obesity has been related to a chronic pro-inflammatory state affecting white adipose tissue (WAT), which has a great impact on carbohydrate, lipid and energy metabolism. In turn, the dysregulation of adipokine secretion derived from the accumulation of excess lipids in adipocytes further contributes to the development of insulin resistance and can be associated with mitochondrial dysfunction. The aim of the present study was to determine whether sexual dimorphism found in the systemic insulin sensitivity profile is related to sex differences in a high-fat diet (HFD) response of gonadal WAT at mitochondrial function and inflammatory profile levels. Wistar rats (10 weeks old) of both sexes were fed a control pelleted diet (3 % (w/w) fat; n 8 for each sex) or a HFD (24 % (w/w) fat; n 8 for each sex). Serum insulin sensitivity markers, mRNA expression levels of inflammatory factors and the protein content of insulin and adiponectin signalling pathways were analysed, as well as the levels of the main markers of mitochondrial biogenesis, antioxidant defence and oxidative damage. In the present study, the periovarian depot exhibits a greater expandability capacity, along with a lower hypoxic and pro-inflammatory state, without signs of mitochondrial dysfunction or changes in its dynamics. In contrast, epididymal fat has a much more pronounced pro-inflammatory, hypoxic and insulin-resistant profile accompanied by changes in mitochondrial dynamics, probably associated with HFD-induced mitochondrial dysfunction. Thus, this explains the worse serum insulin sensitivity profile of male rats.
    The British journal of nutrition 05/2012; · 3.45 Impact Factor
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    ABSTRACT: Obesity-induced mitochondrial dysfunction in white adipose tissue (WAT) leads to a dysregulation of adipokine secretion, which is involved in insulin resistance development. Taking into account the sex differences previously found both in mitochondrial function and for the insulin sensitivity profile in different tissues, the aim of this study was to investigate whether a sex-dependent effect of a long-term high-fat diet (HFD) feeding exists on WAT mitochondrial function. Indeed, HFD effects on the levels of the key components of the insulin and adiponectin signaling pathways, and the consequences of these effects on the systemic profile of insulin sensitivity were also studied. Wistar rats of both sexes were fed a standard diet or an HFD. Serum markers of insulin sensitivity, protein, and mRNA levels of the main elements of the insulin and adiponectin signaling pathways, and the markers of mitochondrial function and biogenesis, were measured. Our results indicate that different physiological strategies are adopted by male and female rats in response to HFD. In this regard, HFD induced mitochondrial proliferation in males and mitochondrial differentiation in females, as well as a greater retroperitoneal WAT expandability capacity, which allows them to preserve a better insulin sensitivity profile than male rats for both control and HFD groups. Moreover, female WAT showed a decrease in adiponectin and insulin signaling pathway element levels. This sexual dimorphism suggests that there are different strategies for retroperitoneal WAT to maintain the energetic and metabolic homeostasis in response to HFD feeding.
    Metabolism: clinical and experimental 03/2012; 61(8):1108-17. · 3.10 Impact Factor
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    ABSTRACT: Sexual dimorphism has been previously found both in mitochondrial biogenesis and function and in adiponectin expression of retroperitoneal WAT. However, little is known about the E2 effects on WAT mitochondrial function. Accordingly, the aim of this study was to examine in greater depth the role of estrogens in sexual dimorphism. This was accomplished by studying the effects of ovariectomy and E2 replacement on retroperitoneal WAT mitochondrial function. Fourteen-week-old female and ovariectomized (OVX) female Wistar rats were used in this study. The ovariectomy was performed at 5 weeks of age and at 10 weeks of age OVX rats were divided into two experimental groups: OVX, and OVX treated with 17β-estradiol (E2) (OVX+E2). Subcutaneous injections of E2 (10 μg/kg/48 h) were administered to the OVX+E2 rats for 4 weeks previous to the sacrifice whereas OVX rats were treated only with the vehicle. Levels of the main markers for mitochondrial biogenesis and function and those representatives of the antioxidant defense system and insulin sensitivity were determined. Additionally, the mRNA levels of the α and β estrogen receptors and of some adipocyte differentiation markers were studied. Our results indicate that retroperitoneal WAT was able to adapt itself to ovariectomy without any changes in mitochondrial function markers or for the adiponectin levels. However, E2 supplementation led to an unexpected decrease in: TFAM protein levels, in LPL, PPARγ and adiponectin gene expression and in the systemic HMW adiponectin levels. This decrease is probably due to the down-regulation of the ERα mRNA expression to avoid an over-stimulation by E2.
    Steroids 02/2012; 77(6):659-65. · 2.80 Impact Factor
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    ABSTRACT: Mitochondrial dysfunction is thought to play a crucial role in the etiology of insulin resistance, in which skeletal muscle is the main tissue contributor. Sex differences in skeletal muscle insulin and antioxidant responses to high-fat-diet (HFD) feeding have been described. The aim of this study was to elucidate whether there is a sex dimorphism in the effects of HFD feeding on skeletal muscle mitochondrial biogenesis and on the adiponectin signaling pathway, as well as the influence of the muscle type (oxidative or glycolytic). Gastrocnemius and soleus muscles of male and female Wistar rats of 2 months of age fed with a high-fat-diet (HFD) or a low fat diet for 26 weeks were used. Mitochondrial biogenesis and oxidative damage markers, oxidative capacity and antioxidant defences were analyzed. Serum insulin sensitivity parameters and the levels of proteins involved in adiponectin signaling pathway were also determined. HFD feeding induced mitochondrial biogenesis in both sexes, but to a higher degree in male rats. Although HFD female rats showed greater antioxidant protection and maintained a better insulin sensitivity profile than their male counterparts, both sexes showed an impaired response to adiponectin, which was more evident in gastrocnemius muscle. We conclude that HFD rats may induce skeletal muscle mitochondrial biogenesis as an attempt to compensate the deleterious consequences of adiponectin and insulin resistance on oxidative metabolism, and that the effects of HFD feeding are sex-dependent and muscle-type specific.
    Nutrition & Metabolism 02/2012; 9:15. · 3.16 Impact Factor
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    ABSTRACT: Ectopic deposition of lipids in liver and other extrahepatic tissues alters their function and occurs once adipose tissue fat storage capacity is exceeded. We investigated sexual dimorphism in the effects of dietary obesity on the liver insulin signaling pathway, as well as its connection to differences in hepatic fat accumulation. Ten-week-old Wistar rats of both sexes were fed a standard diet or a high-fat diet for 26 weeks. Insulin, adipokine levels, and glucose tolerance were measured. Lipid content, PPARα mRNA expression and protein levels of insulin receptor subunit β (IRβ), IR substrate 2 (IRS-2), Ser/Thr kinase A (Akt), and pyruvate dehydrogenase kinase isozyme 4 (PDK4) were measured in liver. In control rats, serum parameters and hepatic levels of IRβ, IRS-2, and Akt proteins pointed to a profile of better insulin sensitivity in females. In response to dietary treatment, female rats exhibited a greater increase in body mass and adiposity and lower liver fat accumulation than males, but maintained better glucose tolerance. The reduced insulin signaling capacity in the liver of obese female rats seems to prevent lipid accumulation and probably lipotoxicity-associated hepatic disorders.
    Biochemistry and Cell Biology 01/2012; 90(2):164-72. · 2.92 Impact Factor
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    ABSTRACT: 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.
    Experimental Biology and Medicine 09/2011; 236(10):1133-8. · 2.80 Impact Factor
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    ABSTRACT: The objective of the study was to investigate whether sex differences in oxidative stress-associated insulin resistance previously reported in rats could be attributed to a possible sex dimorphism in pancreas redox status. Fifteen-month-old male and female Wistar rats were fed a control diet or a high-fat diet for 14 weeks. Serum glucose, lipids, and hormone levels were measured. Insulin immunohistochemistry and morphometric analysis of islets were performed. Pancreas triglyceride content, oxidative damage, and antioxidant enzymatic activities were determined. Lipoprotein lipase, hormone-sensitive lipase, and uncoupling protein 2 (UCP2) levels were also measured. Male rats showed a more marked insulin resistance profile than females. In control female rats, pancreas Mn-superoxide dismutase activity and UCP2 levels were higher, and oxidative damage was lower compared with males. High-fat-diet feeding decreased pancreas triglyceride content in female rats and UCP2 levels in male rats. High-fat-diet female rats showed larger islets than both their control and sex counterparts. These results confirm the existence of a sex dimorphism in pancreas oxidative status in both control and high-fat-diet feeding situations, with female rats showing higher protection against oxidative stress, thus maintaining pancreatic function and contributing to a lower risk of insulin resistance.
    Pancreas 07/2011; 40(5):682-8. · 2.95 Impact Factor
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    ABSTRACT: Taking into account the sexual dimorphism previously reported regarding mitochondrial function and biogenesis in brown adipose tissue, the aim of the present study was to go further into these differences by investigating the effect of ovariectomy and 17-β estradiol (E2) replacement on brown adipose tissue mitochondrial function. In this study, fourteen-week-old control female and ovariectomized female Wistar rats were used. Rats were ovariectomized at 5 weeks of age and were treated every 2 days with placebo (OVX group) or E2 (10 μg/kg) (OVX+E2 group) for 4 weeks before sacrifice. We studied the levels of oxidative capacity, antioxidant defence and oxidative damage markers in brown adipose tissue. Moreover, the levels of key elements of mitochondrial biogenesis as well as UCP1 protein levels, as an index of mitochondrial thermogenic capacity, were also determined. In response to ovariectomy, mitochondrial proliferation increased, resulting in less functional mitochondria, since oxidative capacity and antioxidant defences decreased. Although E2 supplementation was able to restore the serum levels of E2 shown by control rats, the treatment reverted the effects of the ovariectomy only in part, and oxidative and antioxidant capacities in OVX+E2 rats did not reach the levels shown by control females. Taking these results into account, we suggest that ovarian hormones are responsible, at least in part, for the sexual dimorphism in BAT mitochondrial function. However, other signals produced by ovary, rather than E2, would play an important role in the control of mitochondrial function in BAT.
    Steroids 04/2011; 76(10-11):1051-6. · 2.80 Impact Factor
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    ABSTRACT: Aging is associated with a progressive decline of skeletal muscle function and insulin sensitivity. Sex differences in the insulin response to different physiological situations have been found, leading to the development of type 2 diabetes. The aim of this study was to investigate the changes in insulin sensitivity with age in male and female rats and to elucidate whether there are sex differences in the alteration profiles of systemic insulin sensitivity parameters, adiposity, skeletal muscle oxidative damage, and the insulin signaling pathway. The gastrocnemius and soleus muscles of male and female rats of 3, 9, and 18 months of age were used. The decrease of insulin sensitivity with age was higher in female than in male rats. However, the increase of both serum insulin levels and adiposity with age shows a different profile in both sexes and suggests an earlier onset of age-related impairment of insulin sensitivity in male than in female rats. Sex differences in insulin signaling key protein levels were found mainly in the most aged rats, suggesting that sex differences in these proteins would be manifested at more advanced ages than differences in the insulin-sensitivity serum profile. In addition, the gastrocnemius muscle showed more age-associated oxidative damage and insulin resistance impact than the soleus in both sexes. These results suggest the sex differences found in the impairment of insulin sensitivity of aged rats would not be attributable to differences between sexes in the time course of the levels of key proteins of the skeletal muscle insulin signaling pathway, at least in the first 18 months of life.
    Rejuvenation Research 01/2011; 14(2):153-61. · 2.92 Impact Factor
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    ABSTRACT: High-fat (HF) diet feeding usually leads to hyperphagia and body weight gain, but macronutrient proportions in the diet can modulate energy intake and fat deposition. The mechanisms of fat accumulation and mobilization may differ significantly between depots, and gender can also influence these differences. To investigate, in rats of both sexes, the effect of an isocaloric intake of a diet with an unbalanced proportion of macronutrients on fatty acid composition of visceral and subcutaneous adipose tissues and how this is influenced by both dietary fatty acids and levels of proteins involved in tissue lipid handling. Eight-week-old Wistar rats of both sexes were fed a control diet (3% w/w fat) or high-fat diet (30% w/w fat) for 14 weeks. Fatty acid composition was analyzed by gas-chromatography and levels of LPL, HSL, α2-AR, β3-AR, PKA and CPT1 were determined by Western blot. The HF diet did not induce hyperphagia or body weight gain, but promoted an increase of adiposity index only in male rats. HF diet produced an increase of the proportion of MUFA and a decrease in that of PUFA in both adipose depots and in both sexes. The levels of proteins involved in the adrenergic control of the lipolytic pathway increased in the gonadal fat of HF females, whereas LPL levels increased in the inguinal fat of HF males and decreased in that of females. Sexual dimorphism in adiposity index reflects a differential sex response to dietary fatty acid content and could be related to the levels of the proteins involved in tissue lipid management.
    Lipids in Health and Disease 01/2011; 10:52. · 2.31 Impact Factor
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    ABSTRACT: Obesity is linked to systemic oxidative stress and, although brown adipose tissue (BAT) plays a crucial role in energy balance, BAT redox status effects on obesity have not been studied previously. Female rats exhibit a greater BAT thermogenic capacity, attributed to enhanced mitochondrial differentiation, than males. The aim of this study was to investigate whether the mitochondrial sexual dimorphism is related to differences in BAT redox status and to assess its role in the regulation of body weight gain in response to chronic high fat diet (HFD) feeding. Ten-week-old Wistar rats of both genders were fed a pelleted control diet or HFD for 26 weeks. Although mitochondria of female rats produced higher levels of hydrogen peroxide than those of males, females exhibited lower oxidative damage, attributed to greater glutathione peroxidase activity and higher glutathione content. In response to HFD, body weight increased markedly in females, but oxidative capacity increased only in males, thus maintaining improved BAT redox status compared with females. In conclusion, the sexual dimorphism in BAT redox status found in control animals is attenuated by the HFD. The enhanced oxidative capacity of HFD males can be related to their greater resistance to body weight gain.
    Stress (Amsterdam, Netherlands) 10/2010; 14(2):174-84. · 3.21 Impact Factor
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    ABSTRACT: 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. 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. 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. 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.
    Cellular Physiology and Biochemistry 01/2010; 26(3):291-302. · 3.42 Impact Factor
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    ABSTRACT: To evaluate the influence of the pro-oxidant and proinflammatory state related to dietary obesity on serum paraoxonase 1 (PON1) activity in male and female rats. Adult Wistar rats of both genders were fed on a high-fat diet to induce weight gain or standard diet for 14 weeks. Body weight was assessed weekly and food intake fortnightly throughout the dietary treatment. Biometrical parameters and serum lipid profile, glucose, insulin, and adipokine levels were measured. To assess the effect of dietary obesity on oxidative stress, levels of liver and serum thiobarbituric acid reactive substances, liver protein carbonyl groups, liver antioxidant enzymes activities, and serum PON1 activities were measured. High-fat diet feeding induced a significant body weight gain in both male and female rats, as well as a reduction of liver antioxidant protection. High-fat diet increased serum lipid peroxides in male rats and reduced serum PON1 activities and serum apolipoprotein A-I (apoA-I) levels in females, although did not alter serum PON1 or apolipoprotein J (apoJ) levels. Our results reveal a gender dimorphism in the high-fat diet-induced reduction of serum PON1 activity, which is likely to be related to the greater obese and proinflammatory state achieved in female rats. We suggest that the enhanced oxidative stress caused by dietary increased body weight, on leading to high-density lipoprotein (HDL), apoA-I or PON1 oxidation could entail the destabilization of the PON1 association to HDL or a direct inactivation of PON1 enzymatic activity, thus accounting for the decreased serum PON1 activities observed in female rats.
    Obesity 08/2008; 16(10):2232-8. · 3.92 Impact Factor
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    ABSTRACT: Muscle resistance to insulin plays a key role in the metabolic dysregulation associated to obesity. A pro-inflammatory and pro-oxidant status has been proposed to be the link between dietary obesity and insulin resistance. Given the gender differences previously found in mitochondrial function and oxidative stress, the aim of the present study was to investigate whether this gender dimorphism leads to differences in the development of high-fat-diet-induced insulin resistance in rat skeletal muscle. Male and female rats of 15 months of age were fed with a high-fat-diet (32% fat) for 14 weeks. Control male rats showed a more marked insulin resistance status compared to females, as indicated by the glucose tolerance curve profile and the serum insulin, resistin and adiponectin levels. High-fat-diet feeding induced an excess of body weight of 16.2% in males and 38.4% in females, an increase in both muscle mitochondrial hydrogen peroxide production and in oxidative damage, together with a decrease in the Mn-superoxide dismutase activity in both genders. However, high-fat-diet fed female rats showed a less marked insulin resistance profile than males, higher mitochondrial oxygen consumption and cytochrome c oxidase activity, and a better capacity to counteract the oxidative-stress-dependent insulin resistance through an overexpression of both muscle UCP3 and GLUT4 proteins. These results point to a gender dimorphism in the insulin resistance status and in the response of skeletal muscle to high-fat-diet feeding which could be related to a more detrimental effect of age in male rats.
    Cellular Physiology and Biochemistry 02/2008; 22(5-6):539-48. · 3.42 Impact Factor
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    ABSTRACT: High fat diets (HFD) usually lead to hyperphagia and body weight gain. However, macronutrient proportions in the diet can modulate energy intake and body fat deposition. The aim of the study was to investigate muscle and liver oxidative metabolism in response to an isocaloric intake of a HFD and to elucidate the possible gender-dependent response. Eight week-old male and female rats were fed either standard chow or HFD for 14 weeks. Energy intake, body weight and whole animal oxygen consumption were determined periodically. Mitochondrial oxygen consumption, hydrogen peroxide production, TBARS levels, Cytochrome-c-oxidase, Citrate synthase and antioxidant enzyme activities were measured in muscle and liver. UCP1 and UCP3 protein levels were analyzed in brown adipose tissue and muscle, respectively. Male rats showed higher energy efficiency, enhanced adiposity, greater hydrogen peroxide production and less effective antioxidant machinery compared to females. HFD feeding increased energy expenditure but did not modify either tissue oxidative metabolism or oxidative damage in either gender. HFD animals over-expressed uncoupling proteins in order to maintain energy balance (brown adipose tissue UCP1) and to avoid oxidative stress (skeletal muscle UCP3), thus counteracting the alterations induced by the modification of the proportion of macronutrients in the diet.
    Cellular Physiology and Biochemistry 02/2008; 22(1-4):327-36. · 3.42 Impact Factor
  • Biochimica Et Biophysica Acta-bioenergetics - BBA-BIOENERGETICS. 01/2008; 1777.

Publication Stats

439 Citations
148.36 Total Impact Points

Institutions

  • 1992–2014
    • University of the Balearic Islands
      • • Laboratory of Molecular Biology, Nutrition and Biotechnology (LBNB)
      • • Department of Fundamental Biology and Health Sciences
      Palma, Balearic Islands, Spain
  • 2006
    • Hospital Son Dureta
      Palma, Balearic Islands, Spain
  • 2000
    • Institut de Génétique Moléculaire de Montpellier
      Montpelhièr, Languedoc-Roussillon, France