Fabio Bessa Lima

University of São Paulo, San Paulo, São Paulo, Brazil

Are you Fabio Bessa Lima?

Claim your profile

Publications (56)180.71 Total impact

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Cachexia is a multifactorial syndrome characterized by profound involuntary weight loss, fat depletion, skeletal muscle wasting, and asthenia; all symptoms are not entirely attributable to inadequate nutritional intake. Adipose tissue and skeletal muscle loss during cancer cachexia development has been described systematically. The former was proposed to precede and be more rapid than the latter, which presents a means for the early detection of cachexia in cancer patients. Recently, pioglitazone (PGZ) was proposed to exhibit anti-cancer properties, including a reduction in insulin resistance and adipose tissue loss; nevertheless , few studies have evaluated its effect on survival. For greater insight into a potential anti-cachectic effect due to PGZ, 8-week-old male Wistar rats were subcutaneously inocu-lated with 1 mL (2×10 7) of Walker 256 tumor cells. The animals were randomly assigned to
    PLoS ONE 03/2015; 10(3):1-16. DOI:10.1371/journal.pone.0122660 · 3.53 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Melatonin, the main hormone produced by the pineal gland, is secreted in a circadian manner (24-h period) and its oscillation influences several circadian biological rhythms, such as the regulation of clock genes expression (chronobiotic effect) and the modulation of several endocrine functions in peripheral tissues. Assuming that the circadian synchronization of clock genes can play a role in the regulation of energy metabolism and it is influenced by melatonin, our study was designed to assess possible alterations as a consequence of melatonin absence on the circadian expression of clock genes in the epididymal adipose tissue of male Wistar rats, and the possible metabolic repercussions to this tissue. Our data show that pinealectomy indeed has impacts on molecular events: it abolishes the daily pattern of the expression of Clock, Per2 and Cry1 clock genes and Pparγ expression, significantly increases the amplitude of daily expression of Rev-erbα, affects the pattern of and impairs adipokine production, leading to a decrease in leptin levels. However, regarding some metabolic aspects of adipocyte functions, such as its ability to synthesize triacylglycerols from glucose along 24 hour, was not compromised by pinealectomy, although the daily profile of the lipogenic enzymes expression (ATP-citrate lyase, malic enzyme, fatty acid synthase and glucose-6-phosphate dehydrogenase) was abolished in pinealectomized animals. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Journal of Pineal Research 01/2015; DOI:10.1111/jpi.12211 · 7.81 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Palmitoleic acid was previously shown to improve glucose homeostasis by reducing hepatic glucose production and by enhancing insulin-stimulated glucose uptake in skeletal muscle. Herein we tested the hypothesis that palmitoleic acid positively modulates glucose uptake and metabolism in adipocytes. For this, both differentiated 3 T3-L1 cells treated with either palmitoleic acid (16:1n7, 200 muM) or palmitic acid (16:0, 200 muM) for 24 h and primary adipocytes from mice treated with 16:1n7 (300 mg/kg/day) or oleic acid (18:1n9, 300 mg/kg/day) by gavage for 10 days were evaluated for glucose uptake, oxidation, conversion to lactate and incorporation into fatty acids and glycerol components of TAG along with the activity and expression of lipogenic enzymes. Treatment of adipocytes with palmitoleic, but not oleic (in vivo) or palmitic (in vitro) acids, increased basal and insulin-stimulated glucose uptake and GLUT4 mRNA levels and protein content. Along with uptake, palmitoleic acid enhanced glucose oxidation (aerobic glycolysis), conversion to lactate (anaerobic glycolysis) and incorporation into glycerol-TAG, but reduced de novo fatty acid synthesis from glucose and acetate and the activity of lipogenic enzymes glucose 6-phosphate dehydrogenase and ATP-citrate lyase. Importantly, palmitoleic acid induction of adipocyte glucose uptake and metabolism were associated with AMPK activation as evidenced by the increased protein content of phospho(p)Thr172AMPKalpha, but no changes in pSer473Akt and pThr308Akt. Importantly, such increase in GLUT4 content induced by 16:1n7, was prevented by pharmacological inhibition of AMPK with compound C. In conclusion, palmitoleic acid increases glucose uptake and the GLUT4 content in association with AMPK activation.
    Lipids in Health and Disease 12/2014; 13(1):199. DOI:10.1186/1476-511X-13-199 · 2.31 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Several studies showed that l-leucine supplementation reduces adiposity when provided before the onset of obesity. We studied rats that were exposed to a high-fat diet (HFD) for 10 weeks before they started to receive l-leucine supplementation. Fat mass was increased in l-leucine-supplemented rats consuming the HFD. Accordingly, l-leucine produced a hypothalamic pattern of gene expression that favors fat accumulation. In conclusion, l-leucine supplementation worsened the adiposity of rats previously exposed to HFD possibly by central mechanisms.
    Nutrients 04/2014; 6(4):1364-73. DOI:10.3390/nu6041364 · 3.15 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Numerous studies address the physiology of adipose tissue (AT). The interest surrounding the physiology of AT is primarily the result of the epidemic outburst of obesity in various contemporary societies. Briefly, the two primary metabolic activities of white AT include lipogenesis and lipolysis. Throughout the last two decades, a new model of AT physiology has emerged. Although AT was considered to be primarily an abundant energy source, it is currently considered to be a prolific producer of biologically active substances, and, consequently, is now recognized as an endocrine organ. In addition to leptin, other biologically active substances secreted by AT, generally classified as cytokines, include adiponectin, interleukin-6, tumor necrosis factor-alpha, resistin, vaspin, visfatin, and many others now collectively referred to as adipokines. The secretion of such biologically active substances by AT indicates its importance as a metabolic regulator. Cell turnover of AT has also recently been investigated in terms of its biological role in adipogenesis. Consequently, the objective of this review is to provide a comprehensive critical review of the current literature concerning the metabolic (lipolysis, lipogenesis) and endocrine actions of AT.
    Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas / Sociedade Brasileira de Biofisica ... [et al.] 03/2014; 47(3):192-205. DOI:10.1590/1414-431X20132911 · 1.08 Impact Factor
  • Arquivos brasileiros de endocrinologia e metabologia 02/2014; 58(1):81-2. · 0.68 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Glucocorticoid (GC) in excess promotes the redistribution of adipose tissue from peripheral to central sites of the body. In this study we characterized an experimental condition of prolonged GC excess and investigated its effect on the lipogenic metabolism in white adipose tissue. Twenty male Wistar rats were divided into control (CON) and dexamethasone treated (DEX) groups. DEX group received dexamethasone (0.25 mg/kg/day) during 4 weeks, while CON group received saline. Animals were sacrificed and subcutaneous (SC), retroperitoneal (RP) and mesenteric (MS) fat pads were excised, weighed and processed for adipocyte isolation, morphometric cell analysis and incorporation of glucose into lipids. The treatment effectively blocked hypothalamic-pituitary-adrenal axis, as verified by a 58% decrease in plasma corticosterone levels and 19% atrophy in adrenal glands in DEX group. Animals from DEX group presented insulin resistance, glucose intolerance, dyslipidemia and increased insulin and leptin plasma levels and hypertrophied adipocytes. They showed increased lipogenesis in RP and MS depots, with increased incorporation of glucose into fatty acids of triacylglycerol. Increased activity of lipogenic enzymes ATP-citrate liase, fatty acid synthase, glucose-6-phosphate dehydrogenase and malic were only seen in the MS depot in DEX group, while gene expression of these enzymes was enhanced in SC and MS fat depots. The adaptations promoted by GC treatment in adipose metabolism seemed to be mainly due to the increased activity of enzymes that supply the NADPH required for lipogenesis than to the increase in enzymes that more directly deal with fatty acid synthesis itself. This article is protected by copyright. All rights reserved.
    Acta Physiologica 01/2014; DOI:10.1111/apha.12226 · 4.25 Impact Factor
  • Rennan de Oliveira Caminhotto, Fabio Bessa Lima
    AJP Endocrinology and Metabolism 12/2013; 305(12):E1521. DOI:10.1152/ajpendo.00580.2013 · 4.51 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Here we investigated whether palmitoleic acid, a fatty acid that enhances whole body glucose disposal and suppresses hepatic steatosis, modulates triacylglycerol (TAG) metabolism in adipocytes. For this, both differentiated 3T3-L1 cells treated with either palmitoleic acid (16:1n7, 200 µM) or palmitic acid (16:0, 200 µM) for 24h and primary adipocytes from wild type or PPARα deficient mice treated with 16:1n7 (300 mg/kg/day) or oleic acid (18:1n9, 300 mg/kg/day) by gavage for 10 days were evaluated for lipolysis, TAG and glycerol 3-phosphate synthesis and gene and protein expression profile. Treatment of differentiated 3T3-L1 cells with 16:1n7, but not 16:0, increased basal and isoproterenol-stimulated lipolysis, mRNA levels of adipose triglyceride lipase (ATGL) and hormone sensitive lipase (HSL) and protein content of ATGL and pSer660-HSL. Such increase in lipolysis induced by 16:1n7, which can be prevented by pharmacological inhibition of PPARα, was associated with higher rates of PPARα binding to DNA. In contrast to lipolysis, both 16:1n7 and 16:0 increased fatty acid incorporation into TAG and glycerol 3-phosphate synthesis from glucose, without affecting glyceroneogenesis and glycerokinase expression. Corroborating in vitro findings, treatment of wild type, but not PPARα deficient mice with 16:1n7 increased primary adipocytes basal and stimulated lipolysis and ATGL and HSL mRNA levels. In contrast to lipolysis, however, 16:1n7 treatment increased fatty acid incorporation into TAG and glycerol 3-phosphate synthesis from glucose in both wild type and PPARα deficient mice. In conclusion, palmitoleic acid increases adipocyte lipolysis and lipases by a mechanism that requires a functional PPARα.
    AJP Endocrinology and Metabolism 09/2013; 305(9). DOI:10.1152/ajpendo.00082.2013 · 4.51 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The adaptations to physical training are reversible with inactivity. Although significant reductions in maximal oxygen uptake (VO2Max) are observed following detraining, its consequences to the adipose tissue are poorly known. Our aim was therefore to investigate effects of discontinuing training (detraining) on the metabolism and adipocyte cellularity of rat periepididymal (PE) adipose tissue. Male Wistar rats, aged 6 weeks, were divided into 3 groups (studied for 12 weeks) under the following conditions: (1) trained (T) throughout the period; (2) detrained (D), trained (first 8 weeks) and detrained (last 4 weeks); and (3) age-matched sedentary (S). Training consisted of treadmill running sessions (1 h/day, 5 d/week, 50-60% VO2Max). The PE adipocyte size enlarged. The cross-sectional area (in µm(2)) was larger in D than in the T and S groups (3474 ± 68.8; 1945.7 ± 45.6; 2492.4 ± 49.08, respectively, p<0.05). Compared with T, the isolated adipose cells (D rats) showed a 48% increase in both basal and maximally insulin-stimulated lipogenesis and in isoproterenol-stimulated lipolysis. A 15% reduction in apoptotic adipocytes was observed in groups T and D compared to S. The levels of adiponectin (3x) and PPAR-gamma (2x) gene expression were up-regulated in D vs. S. PREF-1 gene expression was 3-fold higher in T vs. S. From these results, we hypothesize that adipogenesis was stimulated in group D and accompanied by significant hypertrophy and increased lipogenic capacity of the adipocytes. And with the reduced fat cell apoptosis in D and T rats, it raises the possibility that these changes are obesogenic.
    Journal of Applied Physiology 05/2013; 115(3). DOI:10.1152/japplphysiol.01272.2012 · 3.43 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Kinins participate in the pathophysiology of obesity and type 2 diabetes by mechanisms which are not fully understood. Kinin B1 receptor knockout mice (B1−/−) are leaner and exhibit improved insulin sensitivity. Methodology/Principal Findings Here we show that kinin B1 receptors in adipocytes play a role in controlling whole body insulin action and glucose homeostasis. Adipocytes isolated from mouse white adipose tissue (WAT) constitutively express kinin B1 receptors. In these cells, treatment with the B1 receptor agonist des-Arg9-bradykinin improved insulin signaling, GLUT4 translocation, and glucose uptake. Adipocytes from B1−/− mice showed reduced GLUT4 expression and impaired glucose uptake at both basal and insulin-stimulated states. To investigate the consequences of these phenomena to whole body metabolism, we generated mice where the expression of the kinin B1 receptor was limited to cells of the adipose tissue (aP2-B1/B1−/−). Similarly to B1−/− mice, aP2-B1/B1−/− mice were leaner than wild type controls. However, exclusive expression of the kinin B1 receptor in adipose tissue completely rescued the improved systemic insulin sensitivity phenotype of B1−/− mice. Adipose tissue gene expression analysis also revealed that genes involved in insulin signaling were significantly affected by the presence of the kinin B1 receptor in adipose tissue. In agreement, GLUT4 expression and glucose uptake were increased in fat tissue of aP2-B1/B1−/− when compared to B1−/− mice. When subjected to high fat diet, aP2-B1/B1−/− mice gained more weight than B1−/− littermates, becoming as obese as the wild types. Conclusions/Significance Thus, kinin B1 receptor participates in the modulation of insulin action in adipocytes, contributing to systemic insulin sensitivity and predisposition to obesity.
    PLoS ONE 09/2012; 7(9). DOI:10.1371/journal.pone.0044782 · 3.53 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Intracellular peptides generated by the proteasome and oligopeptidases have been suggested to function in signal transduction and to improve insulin resistance in mice fed a high-caloric diet. The aim of this study was to identify specific intracellular peptides in the adipose tissue of Wistar rats that could be associated with the physiological and therapeutic control of glucose uptake. Using semiquantitative mass spectrometry and LC/MS/MS analyses, we identified ten peptides in the epididymal adipose tissue of the Wistar rats; three of these peptides were present at increased levels in rats that were fed a high-caloric Western diet (WD) compared with rats fed a control diet (CD). The results of affinity chromatography suggested that in the cytoplasm of epididymal adipose tissue from either WD or CD rats, distinctive proteins bind to these peptides. However, despite the observed increase in the WD animals, the evaluated peptides increased insulin-stimulated glucose uptake in 3T3-L1 adipocytes treated with palmitate. Thus, intracellular peptides from the adipose tissue of Wistar rats can bind to specific proteins and facilitate insulin-induced glucose uptake in 3T3-L1 adipocytes.
    Proteomics 06/2012; 12(17):2668-81. DOI:10.1002/pmic.201200051 · 3.97 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Diabetes mellitus is a product of low insulin sensibility and pancreatic β-cell insufficiency. Rats with streptozotocin-induced diabetes during the neonatal period by the fifth day of age develop the classic diabetic picture of hyperglycemia, hypoinsulinemia, polyuria, and polydipsia aggravated by insulin resistance in adulthood. In this study, we investigated whether the effect of long-term treatment with melatonin can improve insulin resistance and other metabolic disorders in these animals. At the fourth week of age, diabetic animals started an 8-wk treatment with melatonin (1 mg/kg body weight) in the drinking water at night. Animals were then killing, and the sc, epididymal (EP), and retroperitoneal (RP) fat pads were excised, weighed, and processed for adipocyte isolation for morphometric analysis as well as for measuring glucose uptake, oxidation, and incorporation of glucose into lipids. Blood samples were collected for biochemical assays. Melatonin treatment reduced hyperglycemia, polydipsia, and polyphagia as well as improved insulin resistance as demonstrated by constant glucose disappearance rate and homeostasis model of assessment-insulin resistance. However, melatonin treatment was unable to recover body weight deficiency, fat mass, and adipocyte size of diabetic animals. Adiponectin and fructosamine levels were completely recovered by melatonin, whereas neither plasma insulin level nor insulin secretion capacity was improved in diabetic animals. Furthermore, melatonin caused a marked delay in the sexual development, leaving genital structures smaller than those of nontreated diabetic animals. Melatonin treatment improved the responsiveness of adipocytes to insulin in diabetic animals measured by tests of glucose uptake (sc, EP, and RP), glucose oxidation, and incorporation of glucose into lipids (EP and RP), an effect that seems partially related to an increased expression of insulin receptor substrate 1, acetyl-coenzyme A carboxylase and fatty acid synthase. In conclusion, melatonin treatment was capable of ameliorating the metabolic abnormalities in this particular diabetes model, including insulin resistance and promoting a better long-term glycemic control.
    Endocrinology 02/2012; 153(5):2178-88. DOI:10.1210/en.2011-1675 · 4.72 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Weight gain and metabolic abnormalities are serious side effects associated with the use of several second generation antipsychotics (SGA). The adipose tissue has been considered a direct SGA target involved in the development of these adverse effects. Recent studies, mainly using murine cells, have suggested that SGA increase both adipogenesis of preadipocytes and lipid accumulation in mature adipocytes. However, to date there has been little research comparing the effects of antipsychotics with different propensities to induce weight gain on human in vitro models of white adipose tissue neoformation and metabolism. The present study aimed to investigate the effects of antipsychotics either strongly associated with weight gain, such as the SGA clozapine and olanzapine, or not, such as the SGA ziprasidone and the classical antipsychotic haloperidol, on proliferation and adipocyte differentiation of human adipose-derived stem cells (ADSCs) and lipogenesis in human mature adipocytes. Whereas ziprasidone induced elevated levels of cell death during adipogenesis and could not be investigated further, we observed that clozapine, olanzapine and haloperidol had slight stimulatory effects on the transcriptional program of ADSCs adipogenesis. However, the observed changes in adipocyte-specific genes were not accompanied by a significant increase in triglyceride accumulation within differentiated adipocytes. Our data also showed that these three antipsychotics displayed inhibitory effects on the proliferation rates of undifferentiated ADSCs. Regarding mature adipocyte metabolism, we observed that olanzapine slightly inhibited insulin-stimulated lipogenesis at the highest concentration used, and haloperidol exerted the strongest inhibitory effects on both basal and insulin-stimulated lipogenesis. Taken together, our results suggest that a direct and potent effect of clozapine and olanzapine on adipose tissue biology is not an important mechanism by which these SGA induce metabolic disturbances in humans. On the other hand, the haloperidol-mediated downregulation of the lipogenic capacity of human adipose tissue may be a possible mechanism contributing to its lower propensity to induce serious metabolic side effects.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 08/2011; 35(8):1884-90. DOI:10.1016/j.pnpbp.2011.07.017 · 4.03 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Previous studies show that exercise training and caloric restriction improve cardiac function in obesity. However, the molecular mechanisms underlying this effect on cardiac function remain unknown. Thus, we studied the effect of exercise training and/or caloric restriction on cardiac function and Ca(2+) handling protein expression in obese rats. To accomplish this goal, male rats fed with a high-fat and sucrose diet for 25 weeks were randomly assigned into 4 groups: high-fat and sucrose diet, high-fat and sucrose diet and exercise training, caloric restriction, and exercise training and caloric restriction. An additional lean group was studied. The study was conducted for 10 weeks. Cardiac function was evaluated by echocardiography and Ca(2+) handling protein expression by Western blotting. Our results showed that visceral fat mass, circulating leptin, epinephrine, and norepinephrine levels were higher in rats on the high-fat and sucrose diet compared with the lean rats. Cardiac nitrate levels, reduced/oxidized glutathione, left ventricular fractional shortening, and protein expression of phosphorylated Ser(2808)-ryanodine receptor and Thr(17)-phospholamban were lower in rats on the high-fat and sucrose diet compared with lean rats. Exercise training and/or caloric restriction prevented increases in visceral fat mass, circulating leptin, epinephrine, and norepinephrine levels and prevented reduction in cardiac nitrate levels and reduced:oxidized glutathione ratio. Exercise training and/or caloric restriction prevented reduction in left ventricular fractional shortening and in phosphorylation of the Ser(2808)-ryanodine receptor and Thr(17)-phospholamban. These findings show that exercise training and/or caloric restriction prevent cardiac dysfunction in high-fat and sucrose diet rats, which seems to be attributed to decreased circulating neurohormone levels. In addition, this nonpharmacological paradigm prevents a reduction in the Ser(2808)-ryanodine receptor and Thr(17)-phospholamban phosphorylation and redox status.
    Hypertension 10/2010; 56(4):629-35. DOI:10.1161/HYPERTENSIONAHA.110.156141 · 7.63 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Considering that melatonin has been implicated in body weight control, this work investigated whether this effect involves the regulation of adipogenesis. 3T3-L1 preadipocytes were induced to differentiate in the absence or presence of melatonin (10(-3) m). Swiss-3T3 cells ectopically and conditionally (Tet-off system) over-expressing the 34 kDa C/EBPbeta isoform (Swiss-LAP cells) were employed as a tool to assess the mechanisms of action at the molecular level. Protein markers of the adipogenic phenotype were analyzed by Western blot. At 36 hr of differentiation of 3T3-L1 preadipocytes, a reduction of PPARgamma expression was detected followed by a further reduction, at day 4, of perilipin, aP2 and adiponectin protein expression in melatonin-treated cells. Real-time PCR analysis also showed a decrease of PPARgamma (60%), C/EBPalpha (75%), adiponectin (30%) and aP2 (40%) mRNA expression. Finally, we transfected Swiss LAP cells with a C/EBPalpha gene promoter/reporter construct in which luciferase expression is enhanced in response to C/EBPbeta activity. Culture of such transfected cells in the absence of tetracycline led to a 2.5-fold activation of the C/EBPalpha promoter. However, when treated with melatonin, the level of C/EBPalpha promoter activation by C/EBPbeta was reduced by 50% (P = 0.05, n = 6). In addition, this inhibitory effect of melatonin was also reflected in the phenotype of the cells, since their capacity to accumulate lipids droplets was reduced as confirmed by the poor staining with Oil Red O. In conclusion, melatonin at a concentration of 10(-3 ) m works as a negative regulator of adipogenesis acting in part by inhibiting the activity of a critical adipogenic transcription factor, C/EBPbeta.
    Journal of Pineal Research 09/2009; 47(3):221-7. DOI:10.1111/j.1600-079X.2009.00705.x · 7.81 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Obesity is one of the major Public Health problems. Obese individuals are more susceptible to develop cardiovascular diseases and type 2 diabetes mellitus. The obesity results from the increase in size and number of the adipocytes. The balance between adipogenesis and adiposity determines the degree of obesity. Mature adipocytes secrete adipokines, such as TNFalpha, IL-6, leptine and adiponectin, and lipokine, the palmitoleic acid omega-7. The production of adipokines is increased in obesity, contributing to the onset of peripheral insulin resistance. The knowledge about the molecular events that regulate the differentiation of pre-adipocytes and mesenchymal stem cells into adipocytes (adipogenesis) is important for the comprehension of the genesis of obesity. Activation of transcription factor PPARgamma plays an essential role in the adipogenesis. Certain fatty acids are PPARgamma ligands and can control adipogenesis. Moreover, some fatty acids act as signaling molecules regulating their differentiation into adipocytes or death. Accordingly, the lipid composition of the diet and PPARgamma agonists can regulate the balance between adipogenesis and death of adipocytes and, therefore, the obesity.
    Arquivos brasileiros de endocrinologia e metabologia 07/2009; 53(5):582-94. · 0.68 Impact Factor
  • Medicine &amp Science in Sports &amp Exercise 01/2009; 41. DOI:10.1249/01.MSS.0000355481.46162.ae · 4.46 Impact Factor
  • Source
    Arquivos Brasileiros de Endocrinologia & Metabologia 01/2009; 53(5). DOI:10.1590/S0004-27302009000500011 · 0.68 Impact Factor
  • Fabio Bessa Lima
    Arquivos brasileiros de endocrinologia e metabologia 09/2008; 52(6):927-8. · 0.68 Impact Factor