1,721,120 research outputs found
Flavonoids at the pharma-nutrition interface: is a therapeutic index in demand?
No full textThe consumption of flavonoid-rich foods could have beneficial effects on health. However, different classes of flavonoids have different effect on disease risk and the relationship between flavonoid intake and risk of disease appeared to be non-linear. Furthermore, contrarily to vitamins, there are no symptoms of deficiency for flavonoids; therefore, our body treats them like other xenobiotics. Therefore, a therapeutic index should be determined. Despite flavonoids are at the pharma-nutrition interface, drugs and foods are subject to different regulatory frameworks and there is no recommended daily allowance (RDA) for flavonoids. Relatively little is known about the efficacy, safety and underlying mechanisms of these bioactive compounds, especially when taken in concert with drugs. Flavonoids could act both as drugs and pro-drugs with pharmacological and toxicological promiscuity. Due to the low bioavailability, the gastrointestinal tract could be the primary target of flavonoids and metabolites. Different effects have been observed after acute and chronic consumption and bioavailability and bioactivity have high inter-individual variability. Furthermore, the difficulties in the design and in the interpretation of human intervention studies make difficult the establishment of a therapeutic index for flavonoids. Probably the concept of 'personalized nutrition' previously proposed could be the better approach. However, despite more studies are needed in order to establish a therapeutic index for each flavonoid subclasses, at the moment RDA of total flavonoids could be between 250-400 mg/d, respecting the seasonality of food source
The relationship between body weight and inflammation: Lesson from anti-TNF-α antibody therapy
No full textObesity is associated with many pathological conditions. Tumor Necrosis Factor-α (TNF-α) is one of the key mediators of inflammation involved in the obesity-related insulin resistance development. We aim to review the human evidence useful to clarify the relationship between inflammation and body weight, with particular reference to TNF-α. Genetic polymorphisms and epigenetic factors, such as diet, could affect TNF-α activity. TNF-α is associated with obesity, but also with anorexia and cachexia. Despite the role of TNF-α in obesity-related diseases, anti-TNF-α antibody therapy is associated with an increase in adiposity. In conclusion the reviewed results suggest that inflammation is more likely a consequence rather than a cause of obesit
Interaction of beta-carbolines with central dopaminergic transmission in mice: structure-activity relationships.
No full textAlthough several beta-carboline alkaloids display hallucinogenic properties in humans, their mechanism of action remains unclear. To ascertain their influence on central dopaminergic transmission, in this study we investigated the facilitating effect of low doses of various beta-carbolines on L-DOPA (250 mg/kg)-induced stereotypy in mice. Harmaline (0.075, 0.15 and 0.35 mg/kg) and harmine (0.15, 0.35 and 0.75 mg/kg) powerfully enhanced the degree of stereotypy, whereas 6-methoxy-harmalan, 6-methoxy-harman and harman were far less potent, augmenting stereotypy only at much higher doses (3 mg/kg). 6-Methoxy-tetrahydro-beta-carbolin (6-MeO-THBC) had only a weak effect at the dose of 3 mg/kg and tetrahydro-beta-carbolin (THBC) had no effect up to the dose of 3 mg/kg. The Ca2+-channel blocker nimodipine (2,5 mg/kg) only slightly antagonized harmaline (0.15 mg/kg) facilitation of L-DOPA-induced stereotypy
Association of flavonoid-rich foods and statins in the management of hypercholesterolemia: a dangerous or helpful combination?
No full textStatins and dietary modifications are the cornerstone of hypercholesterolemia management. Although it is well known that possible adverse effect of statins can occur due to drug-drug interactions, food-drug interactions are a commonly overlooked aspect. In particular, flavonoids could interfere with statins' bioavailability through different mechanisms, such as competition with cytochrome P450 (CYP) enzymes, esterases, uridine diphosphate glucuronosyltransferases and transporters (P-glycoprotein, multi-drug resistance-associated proteins, organic anion transporting polypeptides, breast cancer-resistance protein and monocarboxylate transporters). Transporters are characterized by low substrate specificity and flavonoid- rich foods could interfere with the bioavailability of all statins at this level. On the other hand, in addition to being substrates of drug metabolism/ transport systems, flavonoids are also able to modulate gene expression of enzymes and transporters. Therefore, long-term transcriptional induction may increase the clearance of statins, despite flavonoids act as competitive inhibitors after bolus consumption. In humans, major interactions were observed between grapefruit juice and statins that are substrates of P-glycoprotein/CYP3A, but other fruit juices also affect the bioavailability of statins that are not metabolised by CYP. Even if flavonoids could play a role in the prevention of hypercholesterolemia, the question whether there's a helpful or dangerous association between flavonoid-rich foods and statins, due to the interactions between flavonoid-rich foods and statins and the potential associated adverse effects of statins, remain unanswered. Therefore, the anamnesis of patients must include detailed information about their eating habits and the present review suggests monitoring and reporting any possible case of interaction between a prescribed statin and food
Effect of cocoa products and flavanols on platelet aggregation in humans: a systematic review
No full textPrevious evidence suggested an active role of cocoa products and flavanols in modulating platelet aggregation. However, cocoa flavanols are characterized by a low bioavailability that can deeply affect their presence in biological fluids and raise questions on their biological effect in humans. We performed a systematic search on Medline, Embase, Cochrane and ProQuest databases, until April 2015, on the effect of cocoa products on platelet aggregation in human intervention studies. We identified 13 interventions, of which only five involved repeated administration. Different effects were observed on the basis of the platelet aggregation test used, whereas neither a longer duration of treatment nor a higher dose was associated with a higher inhibition of platelet aggregation. In conclusion, the reviewed results suggest that consumption of cocoa products in bolus administration positively affects platelet aggregation in both healthy subjects and diseased patients. On the other hand, more evidence is required in order to assess the effect of long-term cocoa product ingestion and to identify the bioactive components involve
Acute effects of aflatoxins on guinea pig ileum
No full textPrevious studies on the aflatoxins have focused mainly on their chronic toxic effects. In this study we investigated the acute gastrointestinal effects of four common aflatoxins on isolated guinea pig ileum. AFB(1) (EC(50) 4.6+/-0.4 microM) and AFB(2) (EC(50)17+/-4.4 microM) contracted isolated guinea pig ileum in a dose-dependent manner, whereas AFG(1) and AFG(2) evoked no contractions. Atropine (5.9 nM 11.8 and 23.6 nM) antagonized AFB(1)-induced contractions in a dose-dependent manner. Pretreatment with the nicotinic ganglionic blocker, hexamethonium (up to 55 microM), left AFB(1)-induced contractions unchanged. In contrast, tetrodotoxin (0.3 microM), blocked AFB(1) contractile activity. The two inhibitors of ACh release, morphine (0.3 microM) and clonidine (0.4 microM), antagonized EC(50) AFB(1)-induced contractions, and apamin, a drug that increases neuronal excitability, facilitated the EC(50) AFB(1)-induced contractile effect. The choline uptake blocker, hemicholinium (17.4 microM) markedly reduced AFB(1)-induced contractions. These results suggest that aflatoxins induce their contractile effect indirectly through the cholinergic system by stimulating acetylcholine release from the postganglionic parasympathetic nerve endings. The acute actions of aflatoxins on isolated guinea pig ileum could explain their acute gastrointestinal effects in humans and animals
Interactions between prebiotics, probiotics, polyunsaturated fatty acids and polyphenols: diet or supplementation for metabolic syndrome prevention?
No full textThe metabolic syndrome can be prevented by the Mediterranean diet, characterized by fiber, omega-3 polyunsaturated fatty acids and polyphenols. However, the composition of the Mediterranean diet, which can be viewed as a natural multiple supplement, is poorly controlled, and its beneficial effects poorly predictable. The metabolic syndrome is associated with intestinal dysbiosis and the gut microbioma seems to be the main target and player in the interactions occurring between probiotics, prebiotics, omega 3 polyunsaturated fatty acids, and polyphenols. From the reviewed evidence, it is reasonable to manage growth and metabolism of gut microflora with specific prebiotics and polyphenols. Even though the healthy properties of functional foods and nutraceuticals still need to be fully elucidated, available data suggest that well-designed supplements, containing the better ratio of omega-3 polyunsaturated fatty acids and antioxidants, specific probiotic strains, and selected polyphenols and prebiotics, could be useful in metabolic syndrome prevention and treatment..........
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