Carnosine: Potential aid for diabetes and cardiovascular disease
Notice bibliographique
Résumé
In 2015 more than 250 scientific papers published in international journals analyzed the potential beneficial effects of oral administration of carnosine in a wide range of diseases. There is strong evidence that demonstrates the ability of carnosine to improve cellular metabolism and muscle performance. Carnosine is a powerful antioxidant, acts as a buffer system of pH slowing muscular acidosis, and increases the release of nitric oxide enhancing endothelial function (1). The interest around this dipetide (β-alanyl-l-histidine) present in large amounts in skeletal muscle is derived from the demonstration that in humans the oral administration of carnosine increases exercise tolerance and functional capacity in both healthy subjects and recently in patients with heart failure and depression (2, 3). Animal studies have suggested that oral supplementation of carnosine can prevent diabetes and non-cardiovascular complications associated with this disease such as diabetes-induced nephropathy and ocular diseases (4, 5). There is a strong relationship between cardiovascular disease and diabetes (5). The identification of novel treatments for diabetes and the control of risk factors for obesity, metabolic syndrome, and sedentary lifestyle are still the objectives of the research. The article by de Courten et al. (6) in this issue examines for the first time the effect of oral administration of carnosine in overweight subjects randomized to receive 2 mg per day of carnosine or placebo for 3 months. The results show carnosine's ability to hamper insulin resistance and associated fasting hyperinsulinemia. In addition, carnosine supplementation normalized 2-h glucose and decreased 2-h insulin levels in individuals with impaired glucose tolerance. Although this study was methodologically well conducted, there are some important limitations: 1) the number of patients is limited and the cardiovascular risk profile was rather low because there were no patients with hypertension and lipid profile was normal; 2) the authors used indirect methods to calculate the plasma levels of insulin and its release; 3) it is unclear whether any changes in the diet were able to alter the impact of carnosine in the final results. Despite these observations, this preliminary data confirm the results of many studies that attribute carnosine's ability to prevent the formation of advanced lipoxidation end-products (ALEs) and advanced glycoxidation end-products (AGEs) (1). These molecules are associated with cell aging and are directly involved in the processes that induce hyperglycemia and subsequently diabetes; they have also been associated with the early onset of microvascular complications typical of diabetes. The mechanisms by which AGEs alter cell activity by stimulating atherosclerosis and diabetes include: glycation of intracellular proteins, activation through specific receptor (RAGE) that increases the secretion of endothelin-1, vascular endothelial growth factor (VEGF), and numerous cytokines. Hipkiss et al. have widely documented the ability of carnosine to inhibit the formation of AGEs and ALEs (7). Carnosine has also showed the ability to regulate the autonomic nervous system by preserving or increasing β-cells within the pancreas. This mechanism is responsible for the increase in pancreatic insulin secretion and the subsequent reduction of release of glucagon. The study by de Courten et al. (6) suggests the use of carnosine proved free of side effects as a potential treatment for the reduction of hyperglycemia and hyperinsulinemia in individuals at risk of developing diabetes. The authors are to be commended for their study which adds another piece to the puzzle of the complex relationships among carnosine and metabolism. These data in sedentary individuals with overweight and obesity still require replication in other large studies before carnosine supplementation can become part of the standard medical approach for the metabolic syndrome.
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Prédiction distillée sur la base complète
Imitation des enseignantsNi prévalence calibrée, ni vérité terrain. Validation humaine à venir. Apprise à partir de 10 348 étiquettes directes de Codex et de 10 348 étiquettes directes de Gemma. Le mode candidate est l'union des têtes enseignantes seuillées; le consensus est leur intersection. Ces sorties portent le statut machine_predicted_unvalidated et ne sont ni des étiquettes humaines ni des étiquettes directes de modèles de pointe.
Scores Codex et Gemma par catégorie
| Catégorie | Codex | Gemma |
|---|---|---|
| Métarecherche | 0,000 | 0,000 |
| Méta-épidémiologie (sens strict) | 0,000 | 0,000 |
| Méta-épidémiologie (sens large) | 0,001 | 0,001 |
| Bibliométrie | 0,000 | 0,000 |
| Études des sciences et des technologies | 0,000 | 0,000 |
| Communication savante | 0,000 | 0,000 |
| Science ouverte | 0,000 | 0,000 |
| Intégrité de la recherche | 0,001 | 0,001 |
| Charge utile insuffisante (le modèle a refusé de juger) | 0,000 | 0,000 |
Scores machine (provisoires)
Les deux têtes enseignantes du modèle étudiant, lues sur ce travail. Un score ordonne la base pour la relecture; il n'affirme jamais une catégorie, et le statut de validation accompagne chaque rangée tel quel.
Scores de référence d'un modèle non mature (critères de maturité non atteints, 7 itérations). Un score ordonne; il n'affirme jamais une catégorie.
score_only:v0-immature-baseline · tel quel depuis la passe de notation : score_only signifie que le nombre peut ordonner les travaux, et qu'aucune étiquette de catégorie n'en découleClassification
machine, non validéePrédiction automatique; un appel candidat d’une seule tête enseignante, pas un consensus.
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