Postprandial hyperglycemia and oxidative stress are important factors that worsen the health condition of patients with type 2 diabetes. We recently showed that extracts from Ceiba pentandra mitigate hyperglycemia in dexamethasone- and high diet/streptozotocin-induced diabetes. Herein, we evaluated the postprandial regulatory properties and the antioxidant effects of the aqueous (AE) and methanol (ME) extracts from the stem bark of Ceiba pentandra. The phytochemical analysis of AE and ME was performed using the LC-MS technique and the total phenolic and flavonoid assays. Both extracts were tested for their ability to inhibit superoxide anion (O2•ـ), hydrogen peroxide (H2O2), protein oxidation, alpha-amylase, and alpha-glucosidase activities. The mode of enzyme inhibition was also determined in a kinetic study. AE and ME were both rich in phenolic and flavonoid compounds. ME was 2.13 and 1.91 times more concentrated than AE in phenolic and flavonoid compounds, respectively. LC-MS allowed the identification of 5 compounds in both extracts. ME and AE inhibited O2•ـ with IC50 of 51.81 and 34.26 μg/ml, respectively. On H2O2, they exhibited IC50 of 44.84 and 1.78 μg/ml, respectively. Finally, they exhibited IC50 of 120.60 and 140.40 μg/ml, respectively, in the inhibition of protein oxidation induced by H2O2, while showing IC50 of 39.26 and 97.95 μg/ml on the protein oxidation induced by AAPH. ME and AE inhibited alpha-amylase with IC50 of 6.15 and 54.52 μg/ml, respectively. These extracts also inhibited alpha-glucosidase, demonstrating IC50 of 76.61 and 86.49 μg/ml. AE exhibited a mixed noncompetitive inhibition on both enzymes, whereas ME exhibited a competitive inhibition on α-amylase and a pure noncompetitive inhibition on α-glucosidase. These results demonstrate that ME and AE scavenge reactive oxygen species and prevent their effects on biomolecules. Besides, ME and AE inhibit carbohydrate digestive enzymes. These properties may contribute to reduce postprandial hyperglycemia and regulate glycemia in diabetic patients.

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Cardiometabolic diseases are among the main leading causes of morbidity and mortality over the world. The coexistence of a bundle of metabolic risk factors in an individual has prompted Reaven to consider it as a syndrome, called “X syndrome”. The term has later evolved and the health condition is today called “cardiometabolics syndrome” (CMS). Significant progress in the understanding of the pathophysiology of the CMS has been made during the past years. Being able to adequately assess cardiometabolic risk (CMR) is crucial for proper diagnosis, prevention, and better management of CMS, as this could be helpful to slow down its progression and complications. This could also be useful in the preclinical and clinical evaluation of potential treatment strategies. Several methods have been developed to assess the risk of developing cardiometabolic diseases in chronic and clinical setting. However, these methods show limitations when applying to short and experimental settings involving rodents. Therefore, this commentary aims at redefining and highlighting the main risk factors to be reconsidered in cardiometabolic syndrome definition; and proposing a comprehensive estimation method for the evaluation of the CMR in rodents. This is relevant for an appropriate utilization of the term CMS and a deep evaluation of therapeutic targets in experimental settings.

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