Iron bioavailability of common beans (Phaseolus vulgaris L.) intrinsically labeled with (59)Fe.

A radiobioassay was performed in rats with or without iron depletion to evaluate the iron bioavailability of diets enriched with common beans and with "multimixture", a nutritional supplement based on parts of foods that are not usually eaten. The full-body (59)Fe level was determined after 5h, the absorbed (59)Fe level was determined after 48 h, and the amount of (59)Fe retained was determined after 7 days. Iron bioavailability was assessed by the full-body radioactivity of the animals, determined using a solid scintillation detector. The iron bioavailability of common beans was higher in the iron-depleted animals (55.7%) than in the non-depleted animals (25.12%) because of the higher absorption rate in the iron-depleted animals. The multimixture did not influence dietary iron bioavailability. In addition, the iron bioavailability of common beans was similar to that observed in the standard source of iron for Wistar rats. Hence, common beans may be considered an adequate dietary iron source because of its high bioavailability.

Development of nonalcoholic hepatopathy: contributions of oxidative stress and advanced glycation end products.

Advanced glycation end products (AGEs) are generated spontaneously in cells; however, under conditions of hyperglycemia and lipid peroxidation, their levels are higher than usual, which contribute to the development of diseases such as the nonalcoholic fatty liver disease (NAFLD). NAFLD is associated with oxidative stress (OS), which is linked to the transition of steatosis to steatohepatitis due to lipid peroxidation. The AGE-receptor interaction in hepatic stellate cells leads to an increase in reactive oxygen species and enhances the proliferation and activation of these cells, worsening liver fibrosis and disease progression. In this vicious cycle, there is production of (carboxymethyl)lysine, a biomarker for products of advanced glycation and lipid peroxidation, being a shared component between the two pathways. In this review, we aim to compile evidence to support the basic molecular mechanisms of AGEs and OS generation and their influence, independently or combined, on the evolution of NAFLD. The deeper understanding of the interrelations of AGEs + OS may help to elucidate the pathogenic pathways of NAFLD and to devise rational therapeutic interventions for this disease, with an expected positive impact on quality of life of patients.

[Hepatoprotective effect of diheptanoin and tritreptanoin chronic consumption against steatosis in rats]. / Efeito hepatoprotetor do consumo crônico de dieptanoína e trieptanoína contra a esteatose em ratos.

OBJECTIVE: To evaluate the effect of chronic consumption of di- and triheptanoin on hepatic steatosis (HS) in rats. METHODOLOGY: Wistar rats were submitted to a diet AIN-93 with 0, 30 or 50% of its oil substituted with an oil rich in di- and triheptanoin, groups TAGC(7)0, TAGC(7)30 and TAGC(7)50 respectively, for nine months. The control group received Labina(R). Liver histology, hepatic lesion and function proofs, glycemia and lipid profile, were performed. Variance analyses, F-test, Dunnet s test and uni- and multivariate regression analyses were performed (p<0.05). RESULTS: TAGC(7)0, TAGC(7)30 and TAGC(7)50 developed HS; 80% of severe cases in TAGC(7)0, as against 40% in TAGC(7)50. The absolute (ALW) and relative (RLW) liver weights were higher in TAGC(7)0 and TAGC(7)30, and glycemia was greater in TAGC(7)30 and TAGC(7)50, than in the Control. Total cholesterol, LDL-c, LDL-c/HDL-c and total proteins were higher in the Control. The experimental oil reduced RLW and showed a tendency in the reduction of body weight, ALW, percentage of hepatic lipids and the severity of HS. The explanatory variables in relation to HS were final weight, glycemia, albumin, HDL-c, LDL-c, LDL-c/HDL-c, VLDL-c and alkaline phosphatase. CONCLUSIONS: It is suggested that di- and triheptanoin have a hepatoprotector effect against HS, in rats, in a dose-dependent manner.

Efeito hepatoprotetor do consumo crônico de dieptanoína e trieptanoína contra a esteatose em ratos / Hepatoprotective effect of diheptanoin and tritreptanoin chronic consumption against steatosis in rats

OBJETIVO: Avaliar o efeito do consumo crônico de di e trieptanoínas sobre a esteatose hepática (EH) em ratos. METODOLOGIA: Ratos Wistar submetidos à dieta AIN-93 com 0 por cento, 30 por cento ou 50 por cento de substituição do óleo por óleo rico em di e trieptanoína, grupos TAGC(7)0, TAGC(7)30 e TAGC(7)50, respectivamente, por nove meses. O grupo-controle recebeu ração Labina®. Analisaram-se histologia e provas de função e lesão hepática, glicemia e perfil lipídico sérico. Realizaram-se análise de variância, teste F, teste de Dunnet e análises de regressão uni e multivariadas (p < 0,05). RESULTADOS: TAGC(7)0, TAGC(7)30 e TAGC(7)50 desenvolveram EH; 80 por cento de casos graves no TAGC(7)0 contra 40 por cento no TAGC(7)50. Os pesos absoluto (PAF) e relativo do fígado (PRF) foram maiores em TAGC(7)0 e TAGC(7)30 e a glicemia foi maior em TAGC(7)30 e TAGC(7)50, que no grupo-controle. Colesterol total, LDL-c, LDL-c/HDL-c e proteínas totais foram maiores no grupo-controle. O óleo experimental reduziu o PRF e determinou tendência de redução do peso corporal, PAF, percentual de lipídios hepáticos e graus de EH (GHE). As variáveis explicativas para GHE foram peso final, glicemia, albumina, HDL-c, LDL-c, LDL-c/HDL-c, VLDL-c e fosfatase alcalina. CONCLUSÕES: Sugere-se que di e trieptanoínas exerçam efeito hepatoprotetor contra a EH, em ratos, em uma feição dose-dependente.

OBJECTIVE: to evaluate the effect of chronic consumption of di- and triheptanoin on hepatic steatosis (HS) in rats. METHODOLOGY: Wistar rats were submitted to a diet AIN-93 with 0, 30 or 50 percent of its oil substituted with an oil rich in di- and triheptanoin, groups TAGC(7)0, TAGC(7)30 and TAGC(7)50 respectively, for nine months. The control group received Labina®. Liver histology, hepatic lesion and function proofs, glycemia and lipid profile, were performed. Variance analyses, F-test, Dunnet´s test and uni- and multivariate regression analyses were performed (p<0.05). RESULTS: TAGC(7)0, TAGC(7)30 and TAGC(7)50 developed HS; 80 percent of severe cases in TAGC(7)0, as against 40 percent in TAGC(7)50. The absolute (ALW) and relative (RLW) liver weights were higher in TAGC(7)0 and TAGC(7)30, and glycemia was greater in TAGC(7)30 and TAGC(7)50, than in the Control. Total cholesterol, LDL-c, LDL-c/HDL-c and total proteins were higher in the Control. The experimental oil reduced RLW and showed a tendency in the reduction of body weight, ALW, percentage of hepatic lipids and the severity of HS. The explanatory variables in relation to HS were final weight, glycemia, albumin, HDL-c, LDL-c, LDL-c/HDL-c, VLDL-c and alkaline phosphatase. CONCLUSIONS: It is suggested that di- and triheptanoin have a hepatoprotector effect against HS, in rats, in a dose-dependant manner.