Navegando por Palavras-chave "leptin"

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    Adiposity in childhood cancer survivors: insights into obesity physiopathology
    (Sociedade Brasileira de Endocrinologia e Metabologia, 2009-03-01) Siviero-Miachon, Adriana Aparecida [UNIFESP]; Spinola-Castro, Angela Maria [UNIFESP]; Guerra-Junior, Gil; Universidade Federal de São Paulo (UNIFESP); Universidade Estadual de Campinas (UNICAMP)
    As childhood cancer treatment has become more effective, survival rates have improved, and a number of complications have been described while many of these patients reach adulthood. Obesity is a well-recognized late effect, and its metabolic effects may lead to cardiovascular disease. Currently, studies concerning overweight have focused on acute lymphocytic leukemia and brain tumors, since they are at risk for hypothalamic-pituitary axis damage secondary to cancer therapies (cranial irradiation, chemotherapy, and brain surgery) or to primary tumor location. Obesity and cancer have metabolic syndrome features in common. Thus, it remains controversial if overweight is a cause or consequence of cancer, and to date additional mechanisms involving adipose tissue and hypothalamic derangements have been considered, comprising premature adiposity rebound, hyperinsulinemia, leptin regulation, and the role of peroxisome proliferator-activated receptor γ. Overall, further research is still necessary to better understand the relationship between adipogenesis and hypothalamic control deregulation following cancer therapy.
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    Assessment of aerobic capacity during swimming exercise in ob/ob mice
    (Wiley-Blackwell, 2011-12-01) Almeida, W. S.; Lima, L. C. J.; Cunha, V. N. C.; Cunha, R. R.; Araujo, R. C.; Barros, C. C. [UNIFESP]; Simoes, H. G.; Campbell, C. S. G.; Univ Catolica Brasilia; Universidade Federal de São Paulo (UNIFESP)
    Obesity is a highly prevalent condition associated with several diseases. Physical exercise has been considered as a non-pharmacological tool in the treatment of obesity. However, several aspects underlying exercise evaluation and prescription in obesity and associated pathologies are still under investigation. Although many research involving exercise have been performed in animal models, there is a lack of protocols for aerobic capacity assessment in obese animals, such as the ob/ob mice. This study aimed the following: (i) to verify the possibility of determining the lactate threshold (LT) on swimming exercise in ob/ob mice and in non-obese heterozygote mice (ob/OB), through visual inspection (vLT) and polynomial adjustment (pLT); and (ii) to verify if the LT determined through these protocols corresponds to the maximal lactate steady state (MLSS). Eight ob/ob and ten ob/OB mice performed an incremental exercise test to determine vLT and pLT as well as constant-load exercise bouts to determine MLSS. There were no within-group differences between vLT, pLT and MLSS [ob/ob: similar to 5.3% body weight (BW); ob/OB: similar to 3 center dot 6%BW] with a high agreement among protocols. in conclusion, the identification of the LT and MLSS intensities was possible for both groups. These data suggest that the proposed protocols may be used in new research on the effects of different exercise intensities on some aspects of obesity. Copyright (c) 2011 John Wiley & Sons, Ltd.
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    Bradykinin inhibits hepatic gluconeogenesis in obese mice
    (Nature Publishing Group, 2012-10-01) Barros, Carlos Castilho [UNIFESP]; Haro, Anderson [UNIFESP]; Russo, Fernanda Jaqueline [UNIFESP]; Schadock, Ines; Almeida, Sandro Soares [UNIFESP]; Reis, Felipe Castellani [UNIFESP]; Moraes, Milton Rocha [UNIFESP]; Haidar, Andre [UNIFESP]; Hirata, Aparecida Emiko [UNIFESP]; Mori, Marcelo [UNIFESP]; Pereira Bacurau, Reury Frank; Wurtele, Martin [UNIFESP]; Bader, Michael; Pesquero, Joao Bosco [UNIFESP]; Araujo, Ronaldo Carvalho [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Max Delbruck Ctr Mol Med; Sch Arts Sci & Humanities
    The kallikrein-kinin system (KKS) has been previously linked to glucose homeostasis. in isolated muscle or fat cells, acute bradykinin (BK) stimulation was shown to improve insulin action and increase glucose uptake by promoting glucose transporter 4 translocation to plasma membrane. However, the role for BK in the pathophysiology of obesity and type 2 diabetes remains largely unknown. To address this, we generated genetically obese mice (ob/ob) lacking the BK B2 receptor (obB2KO). Despite similar body weight or fat accumulation, obB2KO mice showed increased fasting glycemia (162.3 +/- 28.2 mg/dl vs 85.3 +/- 13.3 mg/dl), hyperinsulinemia (7.71 +/- 1.75 ng/ml vs 4.09 +/- 0.51 ng/ml) and impaired glucose tolerance when compared with ob/ob control mice (obWT), indicating insulin resistance and impaired glucose homeostasis. This was corroborated by increased glucose production in response to a pyruvate challenge. Increased gluconeogenesis was accompanied by increased hepatic mRNA expression of forkhead box protein 01 (FoxO1, four-fold), peroxisome proliferator-activated receptor gamma co-activator 1-alpha (seven-fold), phosphoenolpyruvate carboxykinase (PEPCK, three-fold) and glucose-6-phosphatase (eight-fold). FoxO1 nuclear exclusion was also impaired, as the obB2KO mice showed increased levels of this transcription factor in the nucleus fraction of liver homogenates during random feeding. Intraportal injection of BK in lean mice was able to decrease the hepatic mRNA expression of FoxO1 and PEPCK. in conclusion, BK modulates glucose homeostasis by affecting hepatic glucose production in obWT. These results point to a protective role of the KKS in the pathophysiology of type 2 diabetes mellitus. Laboratory Investigation (2012) 92, 1419-1427; doi:10.1038/labinvest.2012.105; published online 6 August 2012
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    Efeitos do exercício crônico sobre a concentração circulante da leptina e grelina em ratos com obesidade induzida por dieta
    (Sociedade Brasileira de Medicina do Exercício e do Esporte, 2008-06-01) Eguchi, Ricardo [UNIFESP]; Cheik, Nadia Carla; Oyama, Lila Missae [UNIFESP]; Nascimento, Claudia Maria da Penha Oller do [UNIFESP]; Mello, Marco Tulio de [UNIFESP]; Tufik, Sergio [UNIFESP]; Dâmaso, Ana Raimunda [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Centro Universitário do Triângulo
    Obesity is becoming one of the biggest worldwide epidemics. Therefore, knowing its etiology and mechanisms that regulate its development is of great relevance for its treatment. Thus, the aim of the present study was to evaluate the effects of obesity induced by the palatable hyperlipidic diet and of the chronic physical activity in rats, on the adiposity and the serum concentration of regulating hormones of the energy balance (leptin and ghrelin). 32 male Wistar rats were divided in four groups: Sedentary fed with chow diet (SN), sedentary fed with cafeteria diet (SC), trained fed with chow diet (TN) and trained fed with cafeteria diet (TC). The cafeteria diet led to a significant increase of central (RET) and visceral (EPI) adiposity (p<0.05). Conversely,the exercise training minimized the effect of the cafeteria diet, diminishing the central and visceral adiposity. Leptin was also increased in the groups fed with the cafeteria diet, suggesting increase of the resistance to the action of this hormone. Chronic physical activity did not hinder the development of hyperleptinemia. Reduction in the serum ghrelin concentration was observed only in the normocaloric group. Therefore,it has been concluded that the quality of diet and the quantity of adipose tissue mass behaved as important regulators of the serum concentration of leptin and ghrelin, reinforcing the importance of a suitable diet and continuous physical activity in the maintenance of body weight in the combat to the deleterious effects of obesity.
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    Effect of angiotensin converting enzyme inhibitor enalapril on body weight and composition in young rats
    (Elsevier B.V., 2008-02-01) Santos, Edson L. [UNIFESP]; Souza, Kely de Picoli [UNIFESP]; Guimarães, Paola Bianchi [UNIFESP]; Reis, Felipe Castellani Gomes [UNIFESP]; Silva, Sylvia Maria Affonso [UNIFESP]; Costa-Neto, Claudio M.; Luz, Jacqueline [UNIFESP]; Pesquero, João Bosco [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)
    Obesity is considered a worldwide public health problem showing an increased prevalence in developing countries, with urgent need for new and more efficient drugs and therapies. Enalapril, an angiotensin-I converting enzyme inhibitor (ACEi), is classically used in antihypertensive therapies, however, earlier publications have shown that this drug could also have significant impact on body weight in rats as well as in humans, besides reducing blood pressure. the effect of this drug in the white adipose tissue has been neglected for long time, even considering that most components of the renin-angiotensin and kallikrein-kinin system are expressed in this tissue. Furthermore, the adipose tissue is considered today as one of the most important sites for endocrine/inflammatory regulation of appetite and energy output and AngII has been linked to the metabolism in this tissue. Therefore, we analyzed the influence of chronic enalapril treatment in normotensive rats at earlier ages, evaluating body weight, energy homeostasis, lipid profile and serum levels of the hormones leptin and insulin, in the presence of a standard or a palatable hyperlipidic diet regimen for one month. Our results show that enalapril treatment is able to reduce body fat on both diets, without alteration in serum lipid profile. Furthermore, animals receiving enalapril showed reduction in food intake, leptin level and energy intake. in summary, these findings show for the first time that the ACEi enalapril reduces body fat in young normotensive rats and highlights a novel target to treat obesity and associated diseases. (c) 2007 Elsevier B.V. All rights reserved.
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    Efficient method for obtaining Lep(ob)/Lep(ob)-derived animal models using adipose tissue transplantations
    (Nature Publishing Group, 2009-08-01) Barros, C. C. [UNIFESP]; Almeida, S. S. [UNIFESP]; Mori, M. A. [UNIFESP]; Valero, V. B. [UNIFESP]; Haro, A. S. [UNIFESP]; Batista, E. C. [UNIFESP]; Rosa, T. S.; Bacurau, Reury Frank Pereira; Wuertele, M. [UNIFESP]; Araujo, R. C. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Mogi das Cuzes; Universidade de São Paulo (USP)
    Background: Leptin-deficient mice (Lep(ob)/Lep(ob), also known as ob/ob) are of great importance for studies of obesity, diabetes and other correlated pathologies. Thus, generation of animals carrying the Lep(ob) gene mutation as well as additional genomic modifications has been used to associate genes with metabolic diseases. However, the infertility of Lep(ob)/Lep(ob) mice impairs this kind of breeding experiment.Objective: To propose a new method for production of Lep(ob)/Lep(ob) animals and Lep(ob)/Lep(ob)-derived animal models by restoring the fertility of Lep(ob)/Lep(ob) mice in a stable way through white adipose tissue transplantations.Methods: for this purpose, 1 g of peri-gonadal adipose tissue from lean donors was used in subcutaneous transplantations of Lep(ob)/Lep(ob) animals and a crossing strategy was established to generate Lep(ob)/Lep(ob)-derived mice.Results: the presented method reduced by four times the number of animals used to generate double transgenic models (from about 20 to 5 animals per double mutant produced) and minimized the number of genotyping steps (from 3 to 1 genotyping step, reducing the number of Lep gene genotyping assays from 83 to 6).Conclusion: the application of the adipose transplantation technique drastically improves both the production of Lep(ob)/Lep(ob) animals and the generation of Lep(ob)/Lep(ob)-derived animal models. International Journal of Obesity (2009) 33, 938-944; doi: 10.1038/ijo.2009.95; published online 16 June 2009
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    In vitro evaluation of leptin fragments activity on the ob receptor
    (Wiley-Blackwell, 2008-05-01) Oliveira, Vani Xavier de; Fazio, Marcos Antonio [UNIFESP]; Santos, Edson Lucas [UNIFESP]; Pesquero, Joao Bosco [UNIFESP]; Miranda, Antonio [UNIFESP]; Universidade Federal do ABC (UFABC); Universidade Federal de São Paulo (UNIFESP)
    In an attempt to identify regions in the leptin molecule responsible for its bioactivity, we tested six related-leptin peptide fragments denoted: Ae-hLEP(23-47)-NH(2) (I), Ac-hLEP(48-71)-NH(2) (II), Ac-hLEP(72-88)-NH(2) (III), Ac-hLEP(92-115)-NH(2) (IV), Ac-[Ser(117)]-hLEP(116-140)-NH(2) (V), Ac-hLEP(141-164)-NH(2) (VI) and their correspondent disulfide bridged dimer forms. the activity of the fragments was evaluated in comparision to leptin, by their ability to interact with leptin receptor using a cytosensor microphysiometer. Our results indicated that the fragments IV and V and [D-Leu(4)]-OB(3) and its human sequence analog were recognized by leptin receptor present in HP-75 cells, in agreement with the results obtained by other workers, validating that this region of the molecule contain the functional epitope of the leptin molecule. Copyright (C) 2007 European Peptide Society and John Wiley & Sons, Ltd.
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    Influence of dexamethasone and weight loss on the regulation of serum leptin levels in obese individuals
    (Associação Brasileira de Divulgação Científica, 2001-04-01) Lerario, D.d.g. [UNIFESP]; Ferreira, Sandra Roberta Gouvea [UNIFESP]; Miranda, Walkiria Lopes [UNIFESP]; Chacra, Antonio Roberto [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    The adipocyte hormone leptin is thought to serve as a signal to the central nervous system reflecting the status of fat stores. Serum leptin levels and adipocyte leptin messenger RNA levels are clearly increased in obesity. Nevertheless, the factors regulating leptin production are not fully understood. The aim of this study was to determine the effects of in vivo administration of the synthetic glucocorticoid dexamethasone and weight loss on serum leptin levels in two independent protocols. Twenty-five obese subjects were studied (18 women and 7 men, mean age 26.6 ± 6 years, BMI 31.1 ± 2.5 kg/m², %fat 40.3 ± 8.3) and compared at baseline to 22 healthy individuals. Serum levels of leptin, insulin, proinsulin and glucose were assessed at baseline and after ingestion of dexamethasone, 4 mg per day (2 mg, twice daily) for two consecutive days. To study the effects of weight loss on serum leptin, 17 of the obese subjects were submitted to a low-calorie dietary intervention trial for 8 weeks and again blood samples were collected. Serum leptin levels were significantly higher in the obese group compared to the control group and a high positive correlation between leptinemia and the magnitude of fat mass was found (r = 0.88, P<0.0001). After dexamethasone, there was a significant increase in serum leptin levels (22.9 ± 12.3 vs 51.4 ± 23.3 ng/ml, P<0.05). Weight loss (86.1 ± 15.1 vs 80.6 ± 14.2 kg, P<0.05) led to a reduction in leptin levels (25.13 ± 12.8 vs 15.9 ± 9.1 ng/ml, P<0.05). We conclude that serum leptin levels are primordially dependent on fat mass magnitude. Glucocorticoids at supraphysiologic levels are potent secretagogues of leptin in obese subjects and a mild fat mass reduction leads to a disproportionate decrease in serum leptin levels. This suggests that, in addition to the changes in fat mass, complex nutritional and hormonal interactions may also play an important role in the regulation of leptin levels.
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    Kinin B-1 receptor stimulation modulates leptin homeostasis. Evidence for an insulin-dependent mechanism
    (Elsevier B.V., 2008-02-01) Mori, Marcelo A. [UNIFESP]; Araujo, Ronaldo C. [UNIFESP]; Pesquero, Joao B. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Kinins are potent vasoactive and inflammatory peptides generated by kallikreins in blood and tissues that bind to specific receptors named B-1 and B-2. On the other hand, leptin is an adipocytokine that displays broad effects on energy balance, inflammation and vascular tone. Here we demonstrate that the intravenous administration of the kinin B-1 receptor agonist des-Arg(9)-bradykinin (DBK) in mice leads to significant increase in serum leptin levels. However, incubation of isolated white adipose tissue with DBK was not sufficient to induce leptin release or leptin mRNA overexpression. On the contrary, long-term DBK treatment in isolated fat tissue impaired insulin-mediated actions on leptin secretion and expression. in order to verify whether the in vivo effect of B-1 receptor stimulation on leptin release was also dependent on blood insulin levels, DBK was injected in animals in hyperinsulinemic state. in this case, however, DBK was not able to potentiate leptinemia. Therefore, our results show that the B-1 receptor stimulation may modulate leptin homeostasis in an insulin-dependent manner. These new findings contribute to a better understanding of the processes involving leptin regulation and highlight the involvement of kinins with metabolic processes. (c) 2007 Elsevier B.V. All rights reserved.
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    Leptin as a link between the immune system and kidney-related diseases: leading actor or just a coadjuvant?
    (Wiley-Blackwell, 2012-08-01) Moraes-Vieira, P. M. M.; Bassi, E. J.; Araujo, R. C. [UNIFESP]; Camara, N. O. S.; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    Food intake and nutritional status modify the physiological responses of the immune system to illness and infection and regulate the development of chronic inflammatory processes, such as kidney disease. Adipose tissue secretes immune-related proteins called adipokines that have pleiotropic effects on both the immune and neuroendocrine systems, linking metabolism and immune physiology. Leptin, an adipose tissue-derived adipokine, displays a variety of immune and physiological functions, and participates in several immune responses. Here, we review the current literature on the role of leptin in kidney diseases, linking adipose tissue and the immune system with kidney-related disorders. the modulation of this adipose hormone may have a major impact on the treatment of several immune- and metabolic-related kidney diseases.
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    Leptin assessment in acute lymphocytic leukemia survivors: Role of cranial radiotherapy?
    (Lippincott Williams & Wilkins, 2007-11-01) Siviero-Miachon, Adriana Aparecida [UNIFESP]; Spinola-Castro, Angela Maria [UNIFESP]; Tosta-Hernandez, Patricia Debora Cavalcanti [UNIFESP]; Lee, Maria Lucia de Martino; Petrilli, Antonio Sergio; Universidade Federal de São Paulo (UNIFESP)
    Leptin has been hypothesized to play a role in the development of obesity in leukemia survivors, particularly those who have received cranial radiotherapy. This cross-sectional study evaluated the relationship between leptin levels and body mass index (BMI) in a sample of 26 acute lymphocytic leukemia survivors of both sexes, treated with and without cranial irradiation, aged 7.6 to 17 years, at a mean 3.4 +/- 2.0 years off treatment. There were significantly more males among the irradiated group (P < 0.001), even though no differences were encountered in pubertal stage (P = 1.000), BMI standard deviation score (mean SD) (0.68 +/- 1.00 vs. 1.19 +/- 0.78; P = 0.164), or leptin concentrations (17.01 +/- 17.04 vs. 23.3 +/- 13.4; P = 0.309). Nonetheless, there was a positive correlation between the natural logarithm of leptin and BMI standard deviation score [t(22) = 2.348, P = 0.028], however, no differences were recorded among irradiated and nonirradiated patients [F(2,22) = 0.384, P = 0.685]. When this relationship was compared between sexes, a significant difference was encountered [F(2,22) = 4.907, P 0.017], with males having the strongest association (R-males(2) = 65.5%, R-females(2) = 34.7% ).Leptin is a reliable adiposity index as it strongly correlates with BMI. Overall, the current data suggest that cranial irradiation did not play a role upon this relationship; however, sex differences influenced positively this correlation.
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    Leptin Modulates Allograft Survival by Favoring a Th2 and a Regulatory Immune Profile
    (Wiley-Blackwell, 2013-01-01) Moraes-Vieira, P. M. M.; Bassi, E. J.; Larocca, R. A.; Castoldi, A.; Burghos, M.; Lepique, A. P.; Quintana, F. J.; Araújo, Ronaldo de Carvalho [UNIFESP]; Basso, A. S. [UNIFESP]; Strom, T. B.; Camara, N. O. S. [UNIFESP]; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); Harvard Univ; Beth Israel Deaconess Med Ctr; Transplant Inst
    Leptin, an adipose-secreted hormone, links metabolism and immunity. Our aim was to determine whether leptin affects the alloimmune response. We used an allogeneic skin transplant model as a means to analyze the allograft immune response in Lepob/ob and wild-type mice. Leptin deficiency results in an increased frequency of Treg and Th2 cells and a prolonged graft survival. These effects of leptin deficiency indicate the importance of leptin and obesity in modulating the allograft immune responses. Our data suggest a possible explanation for the increased susceptibility of hyperleptinemic obese patients to acute and chronic graft rejection.
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    Metabolic and haemodynamic effects of metformin in patients with type 2 diabetes mellitus and hypertension
    (Blackwell Science Ltd, 2001-10-01) Uehara, M. H.; Kohlmann, NEB; Zanella, M. T.; Ferreira, SRG; Universidade Federal de São Paulo (UNIFESP)
    Background: Since metformin improves insulin sensitivity, it has been indicated for patients with diabetes and hypertension, which are insulin-resistant conditions. in contrast to its well-known effects on carbohydrate metabolism, its potential for reducing blood pressure (BP) and its effect on leptin levels have been investigated less frequently.Patients and Methods: A double-blind, randomized, placebo-controlled trial was carried out with 26 overweight diabetic subjects with mild-to-moderate hypertension to assess the effects of metformin-induced glycaemic control on BP and metabolic parameters. After a 4-week placebo period, when BP was stabilized by calcium channel blockers, they received either metformin (MG) or placebo (PG) for 12 weeks.Results: Neither group showed any change in weight throughout the study. Only metformin-treated patients reduced fasting plasma glucose (8.54+1.72 to 7.54+1.33 mmol/l, p<0.05), although HbA(1c) had decreased in both groups (PG: 6.73.0 to 5.9 +/-2.6%; MG: 5.3 +/-1.5 to 4.6 +/-0.9%; p<0.05). the initial office mean BPs were similar and decreased at the end of the treatment period in both groups, reaching statistical significance only in MG (105.78.0 to 99.2 +/-9.3 mmHg, p<0.05). No difference was observed when comparing baseline and final values obtained by 24-h ambulatory BP monitoring. Metformin induced a reduction in both insulinaemia (71.062.4 to 38.0 +/- 23.0 pmol/l, p<0.05) and the insulin resistance index (3.52.7 to 1.8 +/-1.0, p<0.05). the two groups had similar baseline leptin levels which remained unchanged after treatment (PG: 16.87.9 to 21.4 +/- 14.6 mug/l; MG: 18.5 +/- 10.3 to 18.4 +/-8.9 mug/l). Dopamine levels increased significantly only in metformin-treated subjects.Conclusions: Reductions in both the insulin levels and the resistance index reinforced metformin capacity to improve peripheral sensitivity. Moreover, such benefits were not accompanied by any hypotensive effects. Since leptin levels were affected neither by metformin per se nor by the induced insulinaemia reduction, our data support the role of body weight as the major determinant of circulating leptin levels.
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    Metabolic profile and cardiovascular risk patterns of an Indian tribe living in the Amazon Region of Brazil
    (Wayne State Univ Press, 2003-02-01) Tavares, E. F.; Vieira, JPB; Andriolo, A.; Sanudo, A.; Gimeno, SGA; Franco, L. J.; Universidade Federal de São Paulo (UNIFESP)
    The Parkateje Indians, belonging to the Je group and inhabiting the Mae Maria Reservation in the southeast of the state of Para in the Amazon Region of Brazil, have suffered rapid and intensive cultural changes in recent years. This survey was designed to characterize the metabolic profile and the frequency of cardiovascular risk factors in this community. Ninety subjects (90.0% of the adult population without admixture) were investigated. Anthropometric measurements were performed and the following clinical characteristics measured: glycemia, serum insulin and proinsulin (fasting and 2-hr post 75 g of glucose load), beta-cell function (%B) and insulin sensitivity (%S) estimated by HOMA, HbA1c, GAD65 antibody, serum lipids, uric acid, creatinine, leptin, and blood pressure. Information about alcohol use, smoking, and medical history was obtained through individual interviews. the prevalences were: overweight, 67.8%; obesity, 14.4%; central obesity, 72.2%; hypertension, 4.4%; dyslipidemia, 44.4%; hyperuricemia, 5.6%; GAD65 antibody positivity, 4.4%; smoking, 25.6%; chronic alcohol use, 0.0%. One case of impaired glucose tolerance (1.1%) and one case of impaired fasting glycemia (1.1%) were diagnosed during this study and one case of diabetes (1.1%) was diagnosed previously. the diabetic woman was excluded from the analyses involving HbA1c, glycemia, insulin, proinsulin, %B, and %S. All creatinine values were normal. Blood pressure did not correlate with age, anthropometric measurements, insulin, proinsulin, and natural logarithm (In) transformed %S. After adjustment for age and sex, there were positive correlations between total cholesterol and body mass index (BMI; r = 0.24), triglycerides and BMI (r = 0.44), triglycerides and waist-to-hip ratio (WHR; r = 0.52), in leptin and BMI (r = 0.41), in leptin and WHR (r = 0.29), uric acid and systolic blood pressure (r = 0.34), uric acid and triglycerides (r = 0.22). Systolic (r = 0.04; r = 0.70) and diastolic (r = 0.14; p = 0.18) blood pressure did not correlate with BMI. Ln leptin had a weak positive correlation with 2-hr insulin (r = 0.14) adjusted for age, sex, and BMI. the multiple linear regression model containing the variables sex, BMI, and 2-hr insulin concentrations explained 77.2% of the variation of in leptin. in conclusion, the high rates of cardiovascular risk factors found among these Indians point to there being a high-risk group to develop diabetes and cardiovascular diseases. To reduce this risk they need to receive preventive interventions.
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    Nutritional recovery with rice bran did not modify energy balance and leptin and insulin levels
    (Sociedade Brasileira de Endocrinologia e Metabologia, 2010-03-01) Martins, Maria Salete F.; Oyama, Lila Missae [UNIFESP]; Latorraca, Marcia Q.; Gomes-da-Silva, Maria Helena G.; Nascimento, Claudia Maria da Penha Oller do [UNIFESP]; Universidade Federal de Mato Grosso Faculdade de Nutrição; Universidade Federal de São Paulo (UNIFESP)
    OBJECTIVE: To investigate the effect of nutritional recovery with rice bran on energy balance, leptin and insulin levels. METHODS: Weaned Wistar rats were fed on a 17% (Control - C) or 0.5% (Aproteic - A) protein diet for 12d. After this, rats were kept on a C diet (C) or recovered with control (Recovered Control - RC) or control plus recovered rice bran diet (Recovered Rice Bran - RRB). RESULTS: Despite the increased food intake, group A exhibited lower carcass fat associated to low serum leptin. RRB and RC groups showed lower carcass weight and energy intake and expenditure. Energy expenditure was positively associated with food intake and carcass weight. Negative correlations between HOMA-IR and energy expenditure and energy intake were observed. CONCLUSION: Nutritional recovery with rice bran did not modify energy balance, leptin and insulin levels.
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    Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation
    (Amer Physiological Soc, 2010-03-01) Forcina Martins, Paulo Jose [UNIFESP]; Marques, Marina Soares [UNIFESP]; Tufik, Sergio [UNIFESP]; D'Almeida, Vania [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Martins PJ, Marques MS, Tufik S, D'Almeida V. Orexin activation precedes increased NPY expression, hyperphagia, and metabolic changes in response to sleep deprivation. Am J Physiol Endocrinol Metab 298: E726-E734, 2010. First published January 5, 2010; doi:10.1152/ajpendo.00660.2009.-Several pieces of evidence support that sleep duration plays a role in body weight control. Nevertheless, it has been assumed that, after the identification of orexins (hypocretins), the molecular basis of the interaction between sleep and energy homeostasis has been provided. However, no study has verified the relationship between neuropeptide Y (NPY) and orexin changes during hyperphagia induced by sleep deprivation. in the current study we aimed to establish the time course of changes in metabolite, endocrine, and hypothalamic neuropeptide expression of Wistar rats sleep deprived by the platform method for a distinct period (from 24 to 96 h) or sleep restricted for 21 days (SR-21d). Despite changes in the stress hormones, we found no changes in food intake and body weight in the SR-21d group. However, sleep-deprived rats had a 25-35% increase in their food intake from 72 h accompanied by slight weight loss. Such changes were associated with increased hypothalamus mRNA levels of prepro-orexin (PPO) at 24 h followed by NPY at 48 h of sleep deprivation. Conversely, sleep recovery reduced the expression of both PPO and NPY, which rapidly brought the animals to a hypophagic condition. Our data also support that sleep deprivation rapidly increases energy expenditure and therefore leads to a negative energy balance and a reduction in liver glycogen and serum triacylglycerol levels despite the hyperphagia. Interestingly, such changes were associated with increased serum levels of glucagon, corticosterone, and norepinephrine, but no effects on leptin, insulin, or ghrelin were observed. in conclusion, orexin activation accounts for the myriad changes induced by sleep deprivation, especially the hyperphagia induced under stress and a negative energy balance.
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    Perfil da leptina e adiponectina na perda auditiva neurossensorial súbita idiopática
    (Universidade Federal de São Paulo (UNIFESP), 2016-12-15) Maranhao, Andre Souza de Albuquerque [UNIFESP]; Penido, Norma de Oliveira Penido [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Objective: To investigate the profile of leptin and adiponectin in onset of idiopathic sudden sensorineural hearing loss as also study their prognostic influence on hearing recovery of patients. Methods: A prospective cohort study, controlled, was conducted. Patients with idiopathic sudden sensorineural hearing loss, seen from August 2013 to March 2015, followed by outpatient clinic of Department of Otorhinolaryngology and Head and Neck Surgery, Paulista School of Medicine/ Federal University of São Paulo. We evaluated the initial and final audiometric parameters, the latter being obtained after at least 30 days after the end of treatment and/or hearing stabilization (minimum follow-up of 30 days). Two blood samples were collected, one prior to treatment and another at least 1 month after the end of treatment, in order to determine the serum levels of the adipokines: leptin and adiponectin. Patients were divided into 2 groups: significant hearing recovery (RSA) and non-significant hearing recovery (RNSA). Results: Twentyfour patients with ISSHL met the inclusion criteria of the study group. 17 (71%) were females and 7 (29%) were male. The mean age was 53.6 years, with a median of 56.5 years, standard deviation of 13.7, minimum age 20 years and maximum age of 76 years. The control group consisted of 22 individuals, 15 (68%) females and 7 (32%) were male. The mean age was 52.5 years, with a median of 54 years, standard deviation of 13.5, minimum age of 28 years and maximum age of 73 years. Leptin serum concentration in the control group was 33.2 ng/ml, in the RSA group 48.5ng/ml (p=0.20) and in the RNSA group 33.7 ng/ml (p=0.61). The serum concentration of adiponectin in the control group was 7.1 ?g/ml, in the RSA group it was 5.2 ?g/ml (p=0.30) and in the RNSA group 4.6 ?g/ml (p=0.10). The leptin initial plasma concentration in the RSA group was 48.5 ng/ml and the final concentration was 32.3ng/ml (p<0.002) and in the RNSA group the initial concentration was 32.7 ng/ml and the final concentration was 26.7ng/ml (p=0.07). There was no statistically significant difference in plasma concentrations of adiponectin within each group. Blood levels of adipokines before and after treatment between the RSA and RNSA groups had no statistically significant difference. Conclusion: The serum concentrations of leptin and adiponectin in the onset of sudden idiopathic sensorineural hearing loss do not differ from individuals without this condition. Serum leptin concentration significantly reduced in patients with idiopathic sudden sensorineural hearing loss wich evolved with good auditory prognosis.
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    Plaqueta e leptina em adolescentes com obesidade
    (Sociedade Brasileira de Pediatria, 2008-12-01) Foschini, Denis [UNIFESP]; Santos, Ronaldo Vagner Thomatieli dos [UNIFESP]; Prado, Wagner Luiz do [UNIFESP]; Piano, Aline de [UNIFESP]; Lofrano, Mara Cristina [UNIFESP]; Martins, Aniela C. [UNIFESP]; Carnier, June; Caranti, Danielle Arisa [UNIFESP]; Sanches, Priscila de Lima [UNIFESP]; Tock, Lian [UNIFESP]; Mello, Marco Tulio de [UNIFESP]; Tufik, Sergio [UNIFESP]; Dâmaso, Ana Raimunda [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade Metodista de São Paulo Faculdade de Educação Física e Fisioterapia; Universidade de Pernambuco Escola Superior de Educação Física Programa de Mestrado Associado
    OBJECTIVE: To analyze the influence of obesity status on immune cell count and concentration of the hormones cortisol and leptin, in order to establish a relationship among the variables analyzed. METHODS: We recruited 27 obese [body mass index (BMI) ≥ 95th percentile[ and 21 non-obese (BMI ≤ 75th percentile) adolescent boys and girls, aged 15-19 years at the post-pubertal stage. BMI was calculated as body weight divided by height squared, and body composition was estimated by plethysmography in the Bod PodTM system. Blood samples were collected to analyze leukocytes, neutrophils, lymphocytes, monocytes, platelets, cortisol, and leptin. The Kolmogorov-Smirnov test was performed, followed by the independent Student t test in case of normal distribution. Significance values were set at p < 0.05 and expressed as means ± standard deviation. The statistical package SPSS for Windows version 12.0 was used. RESULTS: There was no difference between obese and non-obese adolescents in terms of leukocyte, neutrophil, lymphocyte, monocyte and cortisol serum concentrations. The group of obese adolescents presented higher platelet and leptin concentrations (p < 0.01). The prevalence of hyperleptinemia was 25.92% in the obese adolescents (15.38% in boys and 35.7% in girls). CONCLUSIONS: Obese adolescents have higher platelet and leptin concentrations in comparison with non-obese adolescents. It was also found that obese girls presented a higher prevalence of hyperleptinemia than obese boys.
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    Reduced neuronal nitric oxide synthase expression contributes to cardiac oxidative stress and nitroso-redox imbalance in ob/ob mice
    (Elsevier B.V., 2007-05-01) Saraiva, Roberto M. [UNIFESP]; Minhas, Khalid M.; Zheng, Meizi; Pitz, Eleanor; Treuer, Adriana; Gonzalez, Daniel; Schuleri, Karl H.; Vandegaer, Koenraad M.; Barouch, Lili A.; Hare, Joshua M.; Johns Hopkins Med Inst; Universidade Federal de São Paulo (UNIFESP); Univ Miami
    Disruption of leptin signaling in the heart may contribute to obesity-related cardiac disease, as leptin deficient (ob/ob) mice display cardiac hypertrophy, increased cardiac apoptosis and reduced survival. Since leptin maintains a tonic level of neuronal nitric oxide synthase (NOS1) expression in the brain, we hypothesized that leptin deficiency would decrease 1 cardiac expression, in turn activating xanthine oxidoreductase (XOR) and creating nitroso-redox imbalance. We studied 2- to 6-month-old ob/ob (n = 26) and C57B1/6 controls (n = 27). Cardiac NOS1 protein abundance (P < 0.01) and mRNA expression (P = 0.03) were reduced in ob/ob (n = 10 and 6, respectively), while NOS3 protein abundance and mRNA expression were unaltered. Importantly, cardiac NOS1 protein abundance was restored towards normal in ob/ob mice after leptin treatment (n = 3; P < 0.05 vs leptin untreated ob/ob mice). NO metabolite (nitrite and nitrate) production within the myocardium was also reduced in ob/ob mice (n = 5; P = 0.02). Furthermore, oxidative stress was increased in ob/ob mice as GSH/GSSG ratio was decreased (n = 4; P = 0.02). Whereas XOR activity measured by Amplex Red fluorescence was increased (n = 8; P = 0.04), XOR and NADPH oxidase subunits protein abundance were not changed in ob/ob mice (n = 6). Leptin deficiency did not disrupt NOS1 subcellular localization, as NOS1 co-localized with ryanodine receptor but not with caveolin-3. in conclusion, leptin deficiency is linked to decreased cardiac expression of NOSI and NO production, with a concomitant increase in XOR activity and oxidative stress, resulting in nitroso-redox imbalance. These data offer novel insights into potential mechanisms of myocardial dysfunction in obesity. (c) 2006 Elsevier Inc. All rights reserved.
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    Sleep pattern is associated with adipokine levels and nutritional markers in resident physicians
    (Informa Healthcare, 2014-12-01) Mota, Maria Carliana; Waterhouse, Jim; De-Souza, Daurea Abadia; Rossato, Luana Thomazetto; Silva, Catarina Mendes; Jeha Araujo, Maria Bernadete; Tufik, Sergio [UNIFESP]; Mello, Marco Tulio de [UNIFESP]; Crispim, Cibele Aparecida [UNIFESP]; Universidade Federal de Uberlândia (UFU); Liverpool John Moores Univ; Universidade Federal de São Paulo (UNIFESP)
    Shift work and long hours of work are common in medical training and have been associated with a higher propensity for developing nutritional problems and obesity. Changes in leptin and ghrelin concentrations - two hormones that contribute importantly to the central regulation of food intake - are poorly described in this population. the aim of this study was to identify possible negative associations between sleep patterns, nutritional status and serum levels of adipokines. the study included 72 resident physicians (52 women and 20 men) who underwent the following assessments: nutritional assessment (3-day dietary recall evaluated by the Adapted Healthy Eating Index), anthropometric variables, fasting metabolism, physical activity level, sleep quality and sleepiness. Resident physicians with poor sleep quality reported greater weight gain after the beginning of residency (5.1 and 3.0 kg, respectively; p=0.01) and higher frequency of abnormal waist circumference (44.2 and 17.6%, respectively; p=0.04) than those with better sleep quality. Mean ghrelin concentration was greater in volunteers with poor sleep quality (64.6 +/- 67.8 and 26.2 +/- 25.0 pg/mL, respectively; p=0.04). Women identified as having excessive daytime sleepiness had lower levels of leptin (9.57 +/- 10.4 ng/mL versus 16.49 +/- 11.4 ng/mL, respectively; p = 0.03) than those without excessive sleepiness. Furthermore, correlations were found between hours of additional work per week and: intake of cereals, bread and pasta (r = 0.22, p = 0.01); intake of servings of fruits (r = -0.20; p = 0.02) and beans (r = -0.21; p = 0.01); and global score for Adapted Healthy Eating Index (r = -0.23; p = 0.008; Table 3). the sleep quality total score correlated with servings of beans (r = -0.22; p = 0.01) and servings of oils (r = 0.23; p = 0.008). Significant correlations were found between mean of time of sleep and servings of cereals, bread and pasta (r =0.20; p = 0.02), servings of meat (r = -0.29; p = 0.02) and cholesterol levels (r = 0.27; p = 0.03). These observations indicate that sleep patterns and long working hours of resident physicians are negatively associated with biological markers related to central food control, the lipid profile, cholesterol levels and eating healthy foods. These factors may predispose these shift workers to become overweight and develop metabolic disorders.