RESUMO
ABSTRACT Background: Systemic blockade of TNF-α in Rheumatoid arthritis with insulin resistance seems to produce more improvement in insulin sensitivity in normal weight patients with Rheumatoid arthritis than in obese patients with Rheumatoid arthritis, suggesting that systemic-inflammation and obesity are independent risk factors for insulin resistance in Rheumatoid arthritis patients. Objectives: To evaluate the insulin resistance in: normal weight patients with Rheumatoid arthritis, overweight patients with Rheumatoid arthritis, obese Rheumatoid arthritis patients, and matched control subjects with normal weight and obesity; and its association with major cytokines involved in the pathogenesis of the disease. Methods: Assessments included: body mass index, insulin resistance by Homeostasis Model Assessment, ELISA method, and enzymatic colorimetric assay. Results: Outstanding results from these studies include: (1) In Rheumatoid arthritis patients, insulin resistance was well correlated with body mass index, but not with levels of serum cytokines. In fact, levels of cytokines were similar in all Rheumatoid arthritis patients, regardless of being obese, overweight or normal weight (2) Insulin resistance was significantly higher in Rheumatoid arthritis with normal weight than in normal weight (3) No significant difference was observed between insulin resistances of Rheumatoid arthritis with obesity and obesity (4) As expected, levels of circulating cytokines were significantly higher in Rheumatoid arthritis patients than in obesity. Conclusions: Obesity appears to be a dominant condition above inflammation to produce IR in RA patients. The dissociation of the inflammation and obesity components to produce IR suggests the need of an independent therapeutic strategy in obese patients with RA.
RESUMO Introdução: O bloqueio sistêmico do Fator de Necrose Tumoral-α (TNF-α) nos indivíduos com artrite reumatoide (AR) com resistência à insulina (RI) parece produzir mais melhoria na sensibilidade à insulina em pacientes com AR com peso normal do que em pacientes obesos com AR. Isso sugere que a inflamação sistêmica e a obesidade são fatores de risco independentes para a RI em pacientes com AR. Objetivos: Avaliar a resistência à insulina em pacientes com peso normal com AR (AR-PN), pacientes com sobrepeso com AR (AR-SP), pacientes com AR obesos (AR-OB) e indivíduos controle com peso normal (PN) e obesidade (OB) pareados; e a associação com as principais citocinas envolvidas na patogênese da doença. Métodos: As avaliações incluíram: índice de massa corporal (IMC), resistência à insulina com o modelo de avaliação da homeostase (Homa-IR), método Elisa e ensaio colorimétrico enzimático. Resultados: Os resultados marcantes do presente estudo incluíram: (1) Em pacientes com AR, a RI estava bem correlacionada com o Índice de Massa Corporal (quanto maior o IMC, maior a RI), mas não com os níveis séricos de citocinas. Na verdade, os níveis de citocinas eram semelhantes em todos os pacientes com AR, independentemente de serem obesos, com sobrepeso ou peso normal. (2) A RI foi significativamente maior no grupo AR-PN do que no grupo PN. (3) Não houve diferença estatisticamente significativa entre a RI de pacientes AR-OB e OB. (4) Como esperado, os níveis circulantes de citocinas foram significativamente maiores em pacientes com AR do que em OB. Conclusões: A obesidade parece ser uma condição mais importante do que a inflamação em produzir RI em pacientes com AR. A dissociação dos componentes da inflamação e da obesidade na produção de RI sugere a necessidade de uma estratégia terapêutica independente em pacientes obesos com AR.
Assuntos
Humanos , Feminino , Adulto , Artrite Reumatoide/sangue , Resistência à Insulina/imunologia , Fator de Necrose Tumoral alfa/sangue , Obesidade/sangue , Artrite Reumatoide/complicações , Ensaio de Imunoadsorção Enzimática , Índice de Massa Corporal , Estudos de Casos e Controles , Interleucina-6/sangue , Interleucina-1beta/sangue , Pessoa de Meia-Idade , Obesidade/complicaçõesRESUMO
BACKGROUND: Systemic blockade of TNF-α in Rheumatoid arthritis with insulin resistance seems to produce more improvement in insulin sensitivity in normal weight patients with Rheumatoid arthritis than in obese patients with Rheumatoid arthritis, suggesting that systemic-inflammation and obesity are independent risk factors for insulin resistance in Rheumatoid arthritis patients. OBJECTIVES: To evaluate the insulin resistance in: normal weight patients with Rheumatoid arthritis, overweight patients with Rheumatoid arthritis, obese Rheumatoid arthritis patients, and matched control subjects with normal weight and obesity; and its association with major cytokines involved in the pathogenesis of the disease. METHODS: Assessments included: body mass index, insulin resistance by Homeostasis Model Assessment, ELISA method, and enzymatic colorimetric assay. RESULTS: Outstanding results from these studies include: (1) In Rheumatoid arthritis patients, insulin resistance was well correlated with body mass index, but not with levels of serum cytokines. In fact, levels of cytokines were similar in all Rheumatoid arthritis patients, regardless of being obese, overweight or normal weight (2) Insulin resistance was significantly higher in Rheumatoid arthritis with normal weight than in normal weight (3) No significant difference was observed between insulin resistances of Rheumatoid arthritis with obesity and obesity (4) As expected, levels of circulating cytokines were significantly higher in Rheumatoid arthritis patients than in obesity. CONCLUSIONS: Obesity appears to be a dominant condition above inflammation to produce IR in RA patients. The dissociation of the inflammation and obesity components to produce IR suggests the need of an independent therapeutic strategy in obese patients with RA.
Assuntos
Artrite Reumatoide/sangue , Resistência à Insulina/imunologia , Obesidade/sangue , Fator de Necrose Tumoral alfa/sangue , Adulto , Artrite Reumatoide/complicações , Índice de Massa Corporal , Estudos de Casos e Controles , Ensaio de Imunoadsorção Enzimática , Feminino , Humanos , Interleucina-1beta/sangue , Interleucina-6/sangue , Pessoa de Meia-Idade , Obesidade/complicaçõesRESUMO
Because an unbalanced diet is an important risk factor for several illnesses, interest has increased in finding novel health-promoting foods. Amaranth produces seeds that not only have substantial nutritional properties but that also contain phytochemical compounds as rutin and nicotiflorin and peptides with antihypertensive and anticarcinogenic activities. We report that a cancer-preventive peptide in amaranth has activities similar to those of soybean lunasin. The amaranth lunasin-like peptide, however, requires less time than the soybean lunasin to internalize into the nucleus of NIH-3T3 cells, and inhibits histone acetylation (H(3) and H(4) in a 70 and 77%, respectively). The amaranth lunasin-like peptide inhibited the transformation of NIH-3T3 cells to cancerous foci. The open reading frame (ORF) of amaranth lunasin corresponds to a bifunctional inhibitor/lipid-transfer protein (LTP). LTPs are a family of proteins that in plants are implicated in different functions, albeit all linked to developmental processes and biotic and abiotic stress resistance. Our results open new intriguing questions about the function of lunasin in plants and support that amaranth is a food alternative containing natural peptides with health-promoting benefits.
