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1.
J Nutr Biochem ; 110: 109127, 2022 12.
Artigo em Inglês | MEDLINE | ID: mdl-35977667

RESUMO

Fatty acid esters of hydroxyl fatty acids (FAHFAs) are a new family of endogenous lipids that exert anti-inflammatory action. Among the various FAHFA isomers, the dietary source of oleic acid-hydroxy stearic acid (OAHSA) and its anti-inflammatory functions are poorly understood. This study investigated the composition of OAHSA isomers in dietary oils and the impact of 12-OAHSA on obesity-induced inflammation. Liquid chromatography with tandem mass spectrometry analysis revealed that various dietary oils, including fish oil, corn oil, palm oil, soybean oil, and olive oil, present a wide variation in OAHSA profiles and amounts. The highest amounts of total OAHSAs are present in olive oil including 12-OAHSA. Compared to vehicle-treated obese mice, administration of 12-OAHSA significantly improved glucose homeostasis, independent of body weight. 12-OAHSA-treated mice displayed significantly reduced accumulation of CD11c+ adipose tissue macrophages, and CD4+/CD8+ adipose tissue T lymphocytes. Concomitantly, the expression of pro-inflammatory cytokine genes and the nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway were significantly decreased in the 12-OAHSA-treated adipose tissue, while the expression of the anti-inflammatory gene Il10 was markedly increased. Moreover, in vitro cell culture experiments showed that 12-OAHSA significantly inhibited the lipopolysaccharides-induced inflammatory response in macrophages by suppressing the nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway. Collectively, these results indicated that 12-OAHSA, as a component of olive oil, mitigates obesity-induced insulin resistance by regulating AT inflammation. Therefore, 12-OAHSA could be used as a novel nutritional intervention against obesity-associated metabolic dysregulation.


Assuntos
Obesidade , Ácido Oleico , Camundongos , Animais , Azeite de Oliva/farmacologia , Obesidade/metabolismo , Inflamação/prevenção & controle , Inflamação/metabolismo , Ácidos Graxos/metabolismo , Ácidos Esteáricos , Óleo de Milho , Anti-Inflamatórios/farmacologia , Anti-Inflamatórios/uso terapêutico
2.
J Med Food ; 21(7): 665-671, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-29969359

RESUMO

Red pepper seed, a by-product of red pepper, has been reported to have antioxidant and antiobesity activities. However, its role in diabetes has not yet been highly investigated. Glucose homeostasis is mainly maintained by insulin, which suppresses glucose production in the liver and enhances glucose uptake in peripheral tissues. In this study, we investigated the underlying mechanisms through which red pepper seed extract (RPSE) affects glucose production in AML12 hepatocytes and glucose uptake in C2C12 myotubes. RPSE reduced glucose production in a dose-dependent manner in AML12 cells. The levels of glucose 6 phosphatase, phosphoenolpyruvate carboxykinase, and critical enzymes for hepatic gluconeogenesis were decreased by RPSE. Gluconeogenesis regulating proteins, Akt and forkhead box protein O1, were also activated by RPSE. In addition, RPSE increased glucose uptake in C2C12 via inducing translocation of glucose transporter type 4 from cytosol to plasma membrane. Analysis of the insulin-dependent pathway showed that the activities of insulin receptor substrate 1, phosphatidylinositol 3-kinase, and Akt were significantly stimulated by RPSE. In conclusion, RPSE might improve glucose homeostasis by reducing hepatic gluconeogenesis and increasing peripheral glucose uptake. Results obtained also suggest that RPSE can be a compelling antidiabetic nutraceutical.


Assuntos
Capsicum/química , Gluconeogênese/efeitos dos fármacos , Glucose/metabolismo , Fígado/efeitos dos fármacos , Músculo Esquelético/efeitos dos fármacos , Extratos Vegetais/farmacologia , Animais , Linhagem Celular , Fatores de Transcrição Forkhead/genética , Fatores de Transcrição Forkhead/metabolismo , Transportador de Glucose Tipo 4/genética , Transportador de Glucose Tipo 4/metabolismo , Glucose-6-Fosfatase/genética , Glucose-6-Fosfatase/metabolismo , Hepatócitos/efeitos dos fármacos , Hepatócitos/metabolismo , Insulina/metabolismo , Fígado/metabolismo , Camundongos , Músculo Esquelético/metabolismo , Fosfoenolpiruvato Carboxiquinase (ATP)/genética , Fosfoenolpiruvato Carboxiquinase (ATP)/metabolismo , Proteínas Proto-Oncogênicas c-akt/genética , Proteínas Proto-Oncogênicas c-akt/metabolismo , Sementes/química , Transdução de Sinais/efeitos dos fármacos
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