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Article: Clinical approaches to preserve beta-cell function in diabetes.

Wajchenberg, Bernardo Léo

Advances in experimental medicine and biology

2010 Volume 654, Page(s) 515–535

Abstract: In type 2 diabetes (DM2) there is progressive deterioration in beta-cell function and mass. It was found that islet function was about 50% of normal at the time of diagnosis and reduction in beta-cell mass of about 60% at necropsy (accelerated apoptosis). ...

Abstract	In type 2 diabetes (DM2) there is progressive deterioration in beta-cell function and mass. It was found that islet function was about 50% of normal at the time of diagnosis and reduction in beta-cell mass of about 60% at necropsy (accelerated apoptosis). Among the interventions to preserve the beta-cells, those to lead to short-term improvement of beta-cell secretion are weight loss, metformin, sulfonylureas, and insulin. The long-term improvement was demonstrated with short-term intensive insulin therapy of newly diagnosed DM2, the use of antiapoptotic drugs such as glitazones, and the use of glucagon-like peptide-1 receptor agonists (GLP-1 mimetics), not inactivated by the enzyme dipeptidyl peptidase 4 and/or to inhibit that enzyme (GLP-1 enhancers). The incretin hormones are released from the gastrointestinal tract in response to nutrient ingestion to enhance glucose-dependent insulin secretion from the pancreas and overall maintenance of glucose homeostasis. From the two major incretins, GLP-1 and GIP (glucose-dependent insulinotropic polypeptide), only the first one or its mimetics or enhancers can be used for treatment. The GLP-1 mimetics exenatide and liraglutide as well as the DPP 4 inhibitors (sitagliptin and vildagliptin) were approved for treatment of DM2.
MeSH term(s)	Animals ; Diabetes Mellitus/drug therapy ; Diabetes Mellitus/physiopathology ; Glucagon-Like Peptide 1/analogs & derivatives ; Glucagon-Like Peptide 1/metabolism ; Glucagon-Like Peptide 1/pharmacology ; Glucose/metabolism ; Homeostasis ; Humans ; Insulin/metabolism ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Liraglutide ; Models, Biological ; PPAR gamma/metabolism ; Thiazolidinediones/pharmacology
Chemical Substances	Insulin ; PPAR gamma ; Thiazolidinediones ; Liraglutide (839I73S42A) ; Glucagon-Like Peptide 1 (89750-14-1) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2010
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-90-481-3271-3_23
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Postprandial glycemia and cardiovascular disease in diabetes mellitus.

Wajchenberg, Bernardo Léo

Arquivos brasileiros de endocrinologia e metabologia

2007 Volume 51, Issue 2, Page(s) 212–221

Abstract: This article reviews the role of fasting and postprandial glycemia to the overall glycemic control of patients with type 2 diabetes and glucose intolerance, as well as their causal relationship upon micro and macrovascular complications. Recent studies ... ...

Abstract	This article reviews the role of fasting and postprandial glycemia to the overall glycemic control of patients with type 2 diabetes and glucose intolerance, as well as their causal relationship upon micro and macrovascular complications. Recent studies have suggested that a third component of the glucose triad, the postprandial glucose excursions, might have a role in the overall glycemic load and might also reflect glycemic control. Epidemiological and intervention studies are presented in the article, supporting the conclusion that postprandial hyperglycemia in impaired glucose tolerance and diabetic subjects is a more powerful marker of cardiovascular disease risk than fasting hyperglycemia, then the treatment directed at specifically lowering postprandial glucose is crucial, as underlined by the American Diabetes Association.
MeSH term(s)	Biomarkers/blood ; Blood Glucose/analysis ; Blood Glucose/metabolism ; Coronary Disease/blood ; Coronary Disease/etiology ; Diabetes Mellitus, Type 2/blood ; Diabetic Angiopathies/blood ; Diabetic Angiopathies/etiology ; Diabetic Angiopathies/physiopathology ; Fasting ; Glucose Intolerance/blood ; Humans ; Hyperglycemia/blood ; Hyperglycemia/complications ; Meta-Analysis as Topic ; Postprandial Period ; Risk Factors ; Triglycerides/blood
Chemical Substances	Biomarkers ; Blood Glucose ; Triglycerides
Language	English
Publishing date	2007-04-27
Publishing country	Brazil
Document type	Journal Article ; Review
ZDB-ID	603919-4
ISSN	1677-9487 ; 0004-2730
ISSN (online)	1677-9487
ISSN	0004-2730
DOI	10.1590/s0004-27302007000200010
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Article ; Online: The effects of macronutrients composition on hormones and substrates during a meal tolerance test in drugnaive and sitagliptin-treated individuals with type 2 diabetes: a randomized crossover study.

da Silva Schreiber, Cristina / Rafacho, Alex / Silverio, Renata / Betti, Roberto / Lerário, Antonio Carlos / Lotenberg, Ana Maria Pita / Rahmann, Klara / de Oliveira, Carolina Piras / Wajchenberg, Bernardo Léo / da Luz, Protásio Lemos

Archives of endocrinology and metabolism

2022

Abstract: Objective: To evaluate the effect of sitagliptin treatment in early type 2 diabetes mellitus (T2DM) and the impact of different macronutrient compositions on hormones and substrates during meal tolerance tests (MTT).: Methods: Half of the drug-naive ... ...

Abstract	Objective: To evaluate the effect of sitagliptin treatment in early type 2 diabetes mellitus (T2DM) and the impact of different macronutrient compositions on hormones and substrates during meal tolerance tests (MTT). Methods: Half of the drug-naive patients with T2DM were randomly assigned for treatment with 100 mg of sitagliptin, q.d., or placebo for 4 weeks and then submitted to 3 consecutive MTT intercalated every 48 h. The MTTs differed in terms of macronutrient composition, with 70% of total energy from carbohydrates, proteins, or lipids. After 4 weeks of washout, a crossover treatment design was repeated. Both patients and researchers were blinded, and a repeated-measures ANOVA was employed for statistical analysis. Results: Sitagliptin treatment reduced but did not normalize fasting and post-meal glucose values in the three MTTs, with lowered area-under-glucose-curve values varying from 7% to 15%. The sitagliptin treatment also improved the insulinogenic index (+86%) and the insulin/glucose (+25%), glucagon-like peptide-1/glucose (+46%) incremental area under the curves. Patients with early T2DM maintained the lowest glucose excursion after a protein- or lipid-rich meal without any major change in insulin, C-peptide, glucagon, or NEFA levels. Conclusion: We conclude that sitagliptin treatment is tolerable and contributes to better control of glucose homeostasis in early T2DM, irrespective of macronutrient composition. The blood glucose excursion during meal ingestion is minimal in protein- or fat-rich meals, which can be a positive ally for the management of T2DM. Clinical trial no: NCT00881543.
Language	English
Publishing date	2022-05-12
Publishing country	Brazil
Document type	Journal Article
ISSN	2359-4292
ISSN (online)	2359-4292
DOI	10.20945/2359-3997000000478
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Article ; Online: The effects of macronutrients composition on hormones and substrates during a meal tolerance test in drug-naive and sitagliptin-treated individuals with type 2 diabetes

Cristina da Silva Schreiber / Alex Rafacho / Renata Silverio / Roberto Betti / Antonio Carlos Lerário / Ana Maria Pita Lotenberg / Klara Rahmann / Carolina Piras de Oliveira / Bernardo Léo Wajchenberg / Protásio Lemos da Luz

Archives of Endocrinology and Metabolism, Vol 66, Iss 3, Pp 312-

a randomized crossover study

2022 Volume 323

Abstract: ABSTRACT Objectives: To evaluate the effect of sitagliptin treatment in early type 2 diabetes mellitus (T2DM) and the impact of different macronutrient compositions on hormones and substrates during meal tolerance tests (MTT). Materials and methods: Half ...

Abstract	ABSTRACT Objectives: To evaluate the effect of sitagliptin treatment in early type 2 diabetes mellitus (T2DM) and the impact of different macronutrient compositions on hormones and substrates during meal tolerance tests (MTT). Materials and methods: Half of the drug-naive patients with T2DM were randomly assigned for treatment with 100 mg of sitagliptin, q.d., or placebo for 4 weeks and then submitted to 3 consecutive MTT intercalated every 48 h. The MTTs differed in terms of macronutrient composition, with 70% of total energy from carbohydrates, proteins, or lipids. After 4 weeks of washout, a crossover treatment design was repeated. Both patients and researchers were blinded, and a repeated-measures ANOVA was employed for statistical analysis. Results: Sitagliptin treatment reduced but did not normalize fasting and post-meal glucose values in the three MTTs, with lowered area-under-glucose-curve values varying from 7% to 15%. The sitagliptin treatment also improved the insulinogenic index (+86%) and the insulin/glucose (+25%), glucagon-like peptide-1/glucose (+46%) incremental area under the curves. Patients with early T2DM maintained the lowest glucose excursion after a protein- or lipid-rich meal without any major change in insulin, C-peptide, glucagon, or NEFA levels. Conclusion: We conclude that sitagliptin treatment is tolerable and contributes to better control of glucose homeostasis in early T2DM, irrespective of macronutrient composition. The blood glucose excursion during meal ingestion is minimal in protein- or fat-rich meals, which can be a positive ally for the management of T2DM. Clinical trial no: NCT00881543
Keywords	Diabetes ; diet ; glycemia ; glucose tolerance ; incretins ; meal tolerance test ; Medicine ; R ; Diseases of the endocrine glands. Clinical endocrinology ; RC648-665
Subject code	610
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	Brazilian Society of Endocrinology and Metabolism
Document type	Article ; Online
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Article ; Online: Postprandial glycemia and cardiovascular disease in diabetes mellitus Glicemia pós-prandial e doença cardiovascular no diabetes mellitus

Bernardo Léo Wajchenberg

Arquivos brasileiros de Endocrinologia e Metabologia, Vol 51, Iss 2, Pp 212-

2007 Volume 221

Abstract	This article reviews the role of fasting and postprandial glycemia to the overall glycemic control of patients with type 2 diabetes and glucose intolerance, as well as their causal relationship upon micro and macrovascular complications. Recent studies have suggested that a third component of the glucose triad, the postprandial glucose excursions, might have a role in the overall glycemic load and might also reflect glycemic control. Epidemiological and intervention studies are presented in the article, supporting the conclusion that postprandial hyperglycemia in impaired glucose tolerance and diabetic subjects is a more powerful marker of cardiovascular disease risk than fasting hyperglycemia, then the treatment directed at specifically lowering postprandial glucose is crucial, as underlined by the American Diabetes Association. O presente artigo revisa o papel da glicemia de jejum e pós-prandial em relação ao controle glicêmico de pacientes com diabetes do tipo 2 e com intolerância à glicose, assim como sua relação causal sobre as complicações micro e macrovasculares. Estudos recentes têm sugerido que um terceiro componente na tríade glicêmica, as excursões glicêmicas pós-prandiais, podem ter influência sobre a carga glicêmica total, e podem também refletir sobre o controle glicêmico. Estudos epidemiológicos e de intervenção são apresentados neste artigo, suportando a conclusão de que a hiperglicemia pós-prandial na intolerância à glicose e em pacientes com diabetes é um marcador mais potente de risco cardiovascular do que a hiperglicemia de jejum, portanto o tratamento dirigido especificamente para reduzir a glicemia pós-prandial é crucial, conforme sugerido pela American Diabetes Association.
Keywords	Diabetes mellitus ; Glicemia de jejum alterada ; Intolerância à glicose ; Doença cardiovascular ; Glicemia pós-prandial ; Impaired fasting glucose ; Glucose intolerance ; Cardiovascular disease ; Postprandial glycemia ; Diseases of the endocrine glands. Clinical endocrinology ; RC648-665 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Internal medicine ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Language	Portuguese
Publishing date	2007-03-01T00:00:00Z
Publisher	Sociedade Brasileira de Endocrinologia e Metabologia
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Electrolyte and renal changes in severe potassium depletion.

Pereira, Virgílio Gonçalves / Wajchenberg, Bernardo Léo / Quintão, Eder Rocha / Machado, Marcelo Marcondes

Metabolism: clinical and experimental

2014 Volume 14, Issue 7, Page(s) 800–812

Abstract: This report describes electrolyte changes and some clinical aspects of the renal disease associated with the loss of potassium through the gastrointestinal tract in 2 patients with diarrhea. In one of them, the diarrhea resulted from non-tropical sprue, ... ...

Abstract	This report describes electrolyte changes and some clinical aspects of the renal disease associated with the loss of potassium through the gastrointestinal tract in 2 patients with diarrhea. In one of them, the diarrhea resulted from non-tropical sprue, in the other, from non-beta islet-cell adenoma of pancreas. In both patients, some observations were repeated after potassium repletion.
MeSH term(s)	Adenoma/complications ; Adenoma/pathology ; Adenoma/surgery ; Adenoma, Islet Cell ; Diarrhea/complications ; Diarrhea/drug therapy ; Diarrhea/etiology ; Diarrhea/pathology ; Electrolytes/blood ; Female ; Humans ; Kidney/pathology ; Kidney Diseases ; Male ; Middle Aged ; Pancreas ; Pancreatic Neoplasms/complications ; Pancreatic Neoplasms/pathology ; Pancreatic Neoplasms/surgery ; Paralysis/etiology ; Potassium/pharmacology ; Potassium/therapeutic use ; Potassium Deficiency/etiology ; Potassium Deficiency/pathology ; Tetany/etiology ; Treatment Outcome
Chemical Substances	Electrolytes ; Potassium (RWP5GA015D)
Language	English
Publishing date	2014-07-27
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	80230-x
ISSN	1532-8600 ; 0026-0495
ISSN (online)	1532-8600
ISSN	0026-0495
DOI	10.1016/0026-0495(65)90007-7
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Article ; Online: Disfunção Endotelial no Diabetes do Tipo 2

Wajchenberg Bernardo Léo

Arquivos brasileiros de Endocrinologia e Metabologia, Vol 46, Iss 5, Pp 514-

2002 Volume 519

Abstract: A principal etiologia para a mortalidade e grande morbidade dos diabéticos é a ateroesclerose. A hipótese para a lesão inicial da ateroesclerose é a disfunção endotelial, pelo reconhecimento de que o endotélio tem um papel fundamental na manutenção das ... ...

Abstract	A principal etiologia para a mortalidade e grande morbidade dos diabéticos é a ateroesclerose. A hipótese para a lesão inicial da ateroesclerose é a disfunção endotelial, pelo reconhecimento de que o endotélio tem um papel fundamental na manutenção das características de fluidez do sangue, tônus vascular e sua permeabilidade, sendo o óxido nítrico derivado do endotélio (e-NO) o principal protetor contra a moléstia ateroesclerótica por inibir as diversas vias envolvidas na aterogênese. A disfunção endotelial identificada como um marcador precoce de moléstia cardiovascular poderá prever coronariopatia no futuro, mesmo antes que alterações ateroescleróticas evidentes apareçam nas artérias. Assim, medidas da função endotelial poderiam identificar indivíduos com risco para moléstia cardiovascular, como determinar a vaso-dilatação endotélio-dependente pelo fluxo após isquemia induzida, que requer a produção de e-NO. Além disso, pode-se também avaliar a reatividade vascular da microcirculação bem como dosar os marcadores bioquímicos da função endotelial. Finalmente, pode-se fazer a mensuração da espessura da camada médio-intimal de grandes artérias, como as carótidas, um marcador indireto da função do endotélio. A disfunção endotelial tem sido documentada no diabetes (DM), em indivíduos com resistência à insulina ou com alto risco para desenvolver DM do tipo 2, nos quais a hiperglicemia está associada a um aumento do estresse oxidativo, levando a um incremento na formação de radicais oxigênio tais como o superóxido, que reage com o e-NO, levando à sua degradação. No DM do tipo 1 o estado diabético predispõe para a alteração endotelial mas não é suficiente para causá-lo, outros agentes tendo provavelmente um papel. No tipo 2 estão presentes os efeitos do envelhecimento, hipertensão arterial e outros fatores e, em contraste à disfunção no tipo 1, esta pode ser observada anos antes da manifestação da vasculopatia, associada com a resistência à insulina.
Keywords	Diabetes do tipo 1 ; Diabetes do tipo 2 ; Disfunção endotelial ; Ateroesclerose ; Óxido nítrico ; Estresse oxidativo ; Resistência à insulina ; Diseases of the endocrine glands. Clinical endocrinology ; RC648-665 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Internal medicine ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Language	Portuguese
Publishing date	2002-01-01T00:00:00Z
Publisher	Sociedade Brasileira de Endocrinologia e Metabologia
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Disfunção Endotelial no Diabetes do Tipo 2 Endothelial Dysfunction in Type 2 Diabetes Mellitus

Bernardo Léo Wajchenberg

Arquivos brasileiros de Endocrinologia e Metabologia, Vol 46, Iss 5, Pp 514-

2002 Volume 519

Abstract	A principal etiologia para a mortalidade e grande morbidade dos diabéticos é a ateroesclerose. A hipótese para a lesão inicial da ateroesclerose é a disfunção endotelial, pelo reconhecimento de que o endotélio tem um papel fundamental na manutenção das características de fluidez do sangue, tônus vascular e sua permeabilidade, sendo o óxido nítrico derivado do endotélio (e-NO) o principal protetor contra a moléstia ateroesclerótica por inibir as diversas vias envolvidas na aterogênese. A disfunção endotelial identificada como um marcador precoce de moléstia cardiovascular poderá prever coronariopatia no futuro, mesmo antes que alterações ateroescleróticas evidentes apareçam nas artérias. Assim, medidas da função endotelial poderiam identificar indivíduos com risco para moléstia cardiovascular, como determinar a vaso-dilatação endotélio-dependente pelo fluxo após isquemia induzida, que requer a produção de e-NO. Além disso, pode-se também avaliar a reatividade vascular da microcirculação bem como dosar os marcadores bioquímicos da função endotelial. Finalmente, pode-se fazer a mensuração da espessura da camada médio-intimal de grandes artérias, como as carótidas, um marcador indireto da função do endotélio. A disfunção endotelial tem sido documentada no diabetes (DM), em indivíduos com resistência à insulina ou com alto risco para desenvolver DM do tipo 2, nos quais a hiperglicemia está associada a um aumento do estresse oxidativo, levando a um incremento na formação de radicais oxigênio tais como o superóxido, que reage com o e-NO, levando à sua degradação. No DM do tipo 1 o estado diabético predispõe para a alteração endotelial mas não é suficiente para causá-lo, outros agentes tendo provavelmente um papel. No tipo 2 estão presentes os efeitos do envelhecimento, hipertensão arterial e outros fatores e, em contraste à disfunção no tipo 1, esta pode ser observada anos antes da manifestação da vasculopatia, associada com a resistência à insulina. The main cause for mortality and the great morbidity in diabetes (DM) is atherosclerosis. A hypothesis for the initial lesion of atherosclerosis is endothelial dysfunction by recognizing that the endothelium plays a fundamental role in the maintenance of blood fluidity, vessel wall tone and permeability, the endothelium-derived nitric oxide (e-NO) being the main protector against atherosclerotic disease by inhibiting key pathways involved in atherogenesis. Endothelial dysfunction identified as an early marker of cardiovascular disease (CVD) could predict coronary artery disease in the future before the development of evident atherosclerotic changes in the arteries. Thus, the evaluation of endothelial function would identify subjects at high risk for CVD, such as determining flow-mediated endothelium-dependent vasodilatation, following induced ischemia, which requires the production of e-NO. Furthermore, it could also be assessed the vascular reactivity of the microcirculation as well as the biochemical markers of endothelial activity. Finally, it could also be measured the thickness of intima-media of large arteries, such as the carotids, an indirect measurement of the endothelial function. Endothelial dysfunction has been documented in DM, in individuals with insulin resistance or at high risk for future development of type 2 DM. In the DM subjects the hyperglycemia is associated with increased oxidative stress leading to increased formation of oxygen radicals such as super-oxide, which reacts with NO, causing it to be degraded. Although the diabetic state in type 1 DM predisposes to endothelial dysfunction it is not sufficient to cause it, other agents are likely to play a role. In type 2, the effects of aging, hyperelipidemia, hypertension and other factors add to the complexity of the problem and in contrast to the type 1 DM dysfunction, it could be observed years before the manifestation of the disease, associated with insulin resistance.
Keywords	Diabetes do tipo 1 ; Diabetes do tipo 2 ; Disfunção endotelial ; Ateroesclerose ; Óxido nítrico ; Estresse oxidativo ; Resistência à insulina ; Type 2 diabetes ; Type 1 diabetes ; Endothelial dysfunction ; Atherosclerosis ; Nitric oxide ; Oxidative stress ; Insulin resistance ; Diseases of the endocrine glands. Clinical endocrinology ; RC648-665 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Internal medicine ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Language	Portuguese
Publishing date	2002-10-01T00:00:00Z
Publisher	Sociedade Brasileira de Endocrinologia e Metabologia
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: O perfil lipídico e a síndrome metabólica.

Lerario, Antonio Carlos / Betti, Roberto Tadeu Barcellos / Wajchenberg, Bernardo Leo

Revista da Associacao Medica Brasileira (1992)

2009 Volume 55, Issue 3, Page(s) 232–233

Title translation	Lipid profile and metabolic syndrome. .
MeSH term(s)	Cholesterol, HDL/blood ; Humans ; Metabolic Syndrome/blood ; Metabolic Syndrome/diagnosis ; Metabolic Syndrome/etiology ; Triglycerides/blood
Chemical Substances	Cholesterol, HDL ; Triglycerides
Language	Portuguese
Publishing date	2009-09-01
Publishing country	Brazil
Document type	Editorial
ZDB-ID	731969-1
ISSN	0104-4230 ; 0004-5241 ; 0102-843X
ISSN	0104-4230 ; 0004-5241 ; 0102-843X
DOI	10.1590/s0104-42302009000300002
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Article ; Online: Tecido adiposo como glândula endócrina

Bernardo Léo Wajchenberg

Arquivos brasileiros de Endocrinologia e Metabologia, Vol 44, Iss 1, Pp 13-

2000 Volume 20

Abstract: O conceito de que os adipócitos são células secretórias surgiu nos últimos anos. Os adipócitos sintetizam e liberam uma variedade de peptídeos e não-peptídeos, bem com expressam outros fatores além de sua capacidade de depositar e mobilizar ... ...

Abstract	O conceito de que os adipócitos são células secretórias surgiu nos últimos anos. Os adipócitos sintetizam e liberam uma variedade de peptídeos e não-peptídeos, bem com expressam outros fatores além de sua capacidade de depositar e mobilizar triglicerídios, retinóides e colesterol. Estas propriedades permitem uma interação do tecido adiposo como outros órgãos, bem como outras células adiposas. A observação importante de que adipócitos secretam leptina como o produto do gene ob estabeleceu o tecido adiposo como um órgão endócrino que se comunica com o sistema nervoso central. The author has studied the hormonal secretion by the adipose tissue, related to fat metabolism, blood coagulation, steroids and energetic balance, such as leptin and adiponectin, and autocrine-paracrine relationships.
Keywords	Tecido gorduroso ; Hormônios secretantes ; Fatores autócrinos e parácrinos ; Fat tissue ; Hormonal secretion ; Autocrine-paracrine relationships ; Diseases of the endocrine glands. Clinical endocrinology ; RC648-665 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Internal medicine ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
Language	Portuguese
Publishing date	2000-02-01T00:00:00Z
Publisher	Sociedade Brasileira de Endocrinologia e Metabologia
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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