Anderson Marçal

Publications (13) View all

• Source

  Available from: Dennys E Cintra

  Dataset: Marçal A - British J. Nutrition

  A C Marçal, J P G Camporez, T M Lima-Salgado, D E Cintra, E H Akamine, L M Ribeiro, F N Almeida, R P Zanuto, R Curi, S C Boldrini, E A Liberti, J Fiamoncini, S M Hirabara, F C Deschamps, A R Carpinelli, C R O Carvalho
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  Available from: Anderson Marçal

  Article: Changes in food intake, metabolic parameters and insulin resistance are induced by an isoenergetic, medium-chain fatty acid diet and are associated with modifications in insulin signalling in isolated rat pancreatic islets.

  A C Marçal, J P G Camporez, T M Lima-Salgado, D E Cintra, E H Akamine, L M Ribeiro, F N Almeida, R P Zanuto, R Curi, S C Boldrini, E A Liberti, J Fiamoncini, S M Hirabara, F C Deschamps, A R Carpinelli, C R O Carvalho
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  ABSTRACT: Long-chain fatty acids are capable of inducing alterations in the homoeostasis of glucose-stimulated insulin secretion (GSIS), but the effect of medium-chain fatty acids (MCFA) is poorly elucidated. In the present study, we fed a normoenergetic MCFA diet to male rats from the age of 1 month to the age of 4 months in order to analyse the effect of MCFA on body growth, insulin sensitivity and GSIS. The 45 % MCFA substitution of whole fatty acids in the normoenergetic diet impaired whole body growth and resulted in increased body adiposity and hyperinsulinaemia, and reduced insulin-mediated glucose uptake in skeletal muscle. In addition, the isolated pancreatic islets from the MCFA-fed rats showed impaired GSIS and reduced protein kinase Bα (AKT1) protein expression and extracellular signal-related kinase isoforms 1 and 2 (ERK1/2) phosphorylation, which were accompanied by increased cellular death. Furthermore, there was a mildly increased cholinergic sensitivity to GSIS. We discuss these findings in further detail, and advocate that they might have a role in the mechanistic pathway leading to the compensatory hyperinsulinaemic status found in this animal model.
  The British journal of nutrition 11/2012; · 3.45 Impact Factor
• Article: Enhanced peroxisomal β-oxidation is associated with prevention of obesity and glucose intolerance by fish oil-enriched diets.

  J Fiamoncini, N Turner, S M Hirabara, T M L Salgado, A C Marçal, S Leslie, S M A da Silva, F C Deschamps, J Luz, G J Cooney, R Curi
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  ABSTRACT: OBJECTIVE: The effects of different amounts of omega 3-polyunsaturated fatty acids in diets with normal or high content of fat on lipid and carbohydrate metabolism were investigated. DESIGN AND METHODS: Mice were fed for 8 weeks on diets enriched with fish oil or lard at 10% or 60% of energy. Energy balance and energy expenditure were analyzed. Fatty acid (FA) oxidative capacity of the liver and the activity of enzymes involved in this pathway were assessed. RESULTS: Fish oil-fed mice had lower body weight and adiposity compared with lard-fed animals, despite having lower rates of oxygen consumption. Mice fed diets containing fish oil also displayed lower glycemia, reduced fat content in the liver, and improved glucose tolerance compared with lard-fed animals. The fish oil-containing diets increased markers of hepatic peroxisomal content and increased the generation of metabolites derived from FA β-oxidation in liver homogenates. In contrast, no changes were observed in the content of mitochondrial electron transport chain proteins or carnitine palmitoyl transferase-1 in the liver, indicating little direct effect of fish oil on mitochondrial metabolism. CONCLUSION: Collectively, our findings suggest that the energy inefficient oxidation of FAs in peroxisomes may be an important mechanism underlying the protection against obesity and glucose intolerance of fish oil administration.
  Obesity 11/2012; · 4.28 Impact Factor
• Source

  Available from: Jose Cipolla-Neto

  Article: Melatonin improves insulin sensitivity independently of weight loss in old obese rats.

  Ricardo Zanuto, Mário A Siqueira-Filho, Luciana C Caperuto, Reury F P Bacurau, Emiko Hirata, Rodrigo A Peliciari-Garcia, Fernanda Gaspar do Amaral, Anderson C Marçal, Luciene M Ribeiro, João P G Camporez, Angelo Rafael Carpinelli, Silvana Bordin, José Cipolla-Neto, Carla R O Carvalho
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  ABSTRACT: In aged rats, insulin signaling pathway (ISP) is impaired in tissues that play a pivotal role in glucose homeostasis, such as liver, skeletal muscle, and adipose tissue. Moreover, the aging process is also associated with obesity and reduction in melatonin synthesis from the pineal gland and other organs. The aim of the present work was to evaluate, in male old obese Wistar rats, the effect of melatonin supplementation in the ISP, analyzing the total protein amount and the phosphorylated status (immunoprecipitation and immunoblotting) of the insulin cascade components in the rat hypothalamus, liver, skeletal muscle, and periepididymal adipose tissue. Melatonin was administered in the drinking water for 8- and 12 wk during the night period. Food and water intake and fasting blood glucose remained unchanged. The insulin sensitivity presented a 2.1-fold increase both after 8- and 12 wk of melatonin supplementation. Animals supplemented with melatonin for 12 wk also presented a reduction in body mass. The acute insulin-induced phosphorylation of the analyzed ISP proteins increased 1.3- and 2.3-fold after 8- and 12 wk of melatonin supplementation. The total protein content of the insulin receptor (IR) and the IR substrates (IRS-1, 2) remained unchanged in all investigated tissues, except for the 2-fold increase in the total amount of IRS-1 in the periepididymal adipose tissue. Therefore, the known age-related melatonin synthesis reduction may also be involved in the development of insulin resistance and the adequate supplementation could be an important alternative for the prevention of insulin signaling impairment in aged organisms.
  Journal of Pineal Research 03/2013; · 5.79 Impact Factor
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  Available from: Anderson Marçal

  Article: Diet-induced obesity impairs AKT signalling in the retina and causes retinal degeneration.

  Anderson C Marçal, Mauro Leonelli, Jarlei Fiamoncini, Francisco C Deschamps, Maria A M Rodrigues, Rui Curi, Angelo R Carpinelli, Luiz R G Britto, Carla R O Carvalho
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  ABSTRACT: Retinopathy, a common complication of diabetes, is characterized by an unbalanced production of nitric oxide (NO), a process regulated by nitric oxide synthase (NOS). We hypothesized that retinopathy might stem from changes in the insulin receptor substrate (IRS)/PI3K/AKT pathway and/or expression of NOS isoforms. Thus, we analysed the morphology and apoptosis index in retinas of obese rats in whom insulin resistance had been induced by a high-fat diet (HFD). Immunoblotting analysis revealed that the retinal tissue of HFD rats had lower levels of AKT(1) , eNOS and nNOS protein than those of samples taken from control animals. Furthermore, immunohistochemical analyses indicated higher levels of iNOS and 4-hydroxynonenal and a larger number of apoptotic nuclei in HFD rats. Finally, both the inner and outer retinal layers of HFD rats were thinner than those in their control counterparts. When considered alongside previous results, these patterns suggest two major ways in which HFD might impact animals: direct activity of ingested fatty acids and/or via insulin-resistance-induced changes in intracellular pathways. We discuss these possibilities in further detail and advocate the use of this animal model for further understanding relationships between retinopathy, metabolic syndrome and type 2 diabetes. Copyright © 2012 John Wiley & Sons, Ltd.
  Cell Biochemistry and Function 08/2012; · 1.77 Impact Factor