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1.
Proc Nutr Soc ; 78(3): 340-350, 2019 08.
Artículo en Inglés | MEDLINE | ID: mdl-30967168

RESUMEN

Some food bioactives potentially exert anti-obesity effects. Anthocyanins (ACN), catechins, ß-glucan (BG) and n-3 long chain PUFA (LCPUFA) are among the most promising candidates and have been considered as a strategy for the development of functional foods counteracting body weight gain. At present, clinical trials, reviews and meta-analyses addressing anti-obesity effects of various bioactives or bioactive-rich foods show contradictory results. Abdominal obesity is an important criterion for metabolic syndrome (MetS) diagnosis along with glucose intolerance, dyslipidaemia and hypertension. Food bioactives are supposed to exert beneficial effects on these parameters, therefore representing alternative therapy approaches for the treatment of MetS. This review summarises outcomes on MetS biomarkers in recent clinical trials supplementing ACN, catechins, BG and n-3 LCPUFA, focusing mainly on anti-obesity effects. Overall, it is clear that the level of evidence for the effectiveness varies not only among the different bioactives but also among the different putative health benefits suggested for the same bioactive. Limited evidence may be due to the low number of controlled intervention trials or to inconsistencies in trial design, i.e. duration, dose and/or the method of bioactive supplementation (extracts, supplements, rich or enriched food). At present, the question 'Are bioactives effective in weight management and prevention of metabolic syndrome?' remains inconclusive. Thus, a common effort to harmonise the study design of intervention trials focusing on the most promising bioactive molecules is urgently needed to strengthen the evidence of their potential in the treatment of obesity, MetS and related diseases.


Asunto(s)
Fármacos Antiobesidad , Metabolismo Energético , Síndrome Metabólico , Fitoquímicos , Antocianinas , Fármacos Antiobesidad/farmacología , Fármacos Antiobesidad/uso terapéutico , Catequina , Metabolismo Energético/efectos de los fármacos , Metabolismo Energético/fisiología , Ácidos Grasos Omega-3 , Humanos , Síndrome Metabólico/metabolismo , Síndrome Metabólico/fisiopatología , Síndrome Metabólico/terapia , Fitoquímicos/farmacología , Fitoquímicos/uso terapéutico , beta-Glucanos
2.
Biochim Biophys Acta ; 1453(1): 35-40, 1999 Jan 06.
Artículo en Inglés | MEDLINE | ID: mdl-9989243

RESUMEN

Magnesium (Mg) plays an essential role in fundamental cellular reactions and the importance of the immuno-inflammatory processes in the pathology of Mg deficiency has been recently reconsidered. The purpose of the present study was to assess the effect of different stages of Mg deficiency on endotoxin response and tumor necrosis factor-alpha (TNF alpha) production. Weaning male Wistar rats were pair fed either a Mg-deficient or a control diet. At day 7, lipopolysaccharide (LPS) induced no lethal effects in control rats but resulted in 70% mortality in Mg-deficient rats within 3 h. The vulnerability of Mg-deficient rats to LPS was associated with higher TNF alpha plasma values. Mg-deficient animals that received magnesium supplementation before endotoxin challenge had significantly increased survival. At day 2, control and Mg-deficient rats were also subjected to endotoxin challenge with or without magnesium pre-treatment. A significant increase in TNF alpha plasma level was observed in Mg-deficient rats compared to rats fed the control diet. Mg-deficient rats that received magnesium replacement therapy before endotoxin challenge had significantly lower TNF alpha plasma values than those receiving saline before endotoxin. Thus, the results of this experiment suggest that the activated or primed state of immune cells is an early event occurring in Mg deficiency.


Asunto(s)
Deficiencia de Magnesio/metabolismo , Factor de Necrosis Tumoral alfa/biosíntesis , Animales , Endotoxinas , Magnesio/sangre , Magnesio/farmacología , Deficiencia de Magnesio/sangre , Deficiencia de Magnesio/inducido químicamente , Masculino , Ratas , Ratas Wistar , Factor de Necrosis Tumoral alfa/análisis
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