Trypsin inhibitors: promising candidate satietogenic proteins as complementary treatment for obesity and metabolic disorders?

The increase in non-communicable chronic diseases has aroused interest in the research of adjuvants to the classic forms of treatments. Obesity and metabolic syndrome are the main targets of confrontation because they relate directly to other chronic diseases. In this context, trypsin inhibitors, molecules with wide heterologous application, appear as possibilities in the treatment of overweight and obesity due to the action on satiety related mechanisms, mainly in the modulation of satiety hormones, such as cholecystokinin. In addition, trypsin inhibitors have the ability to also act on some biochemical parameters related to these diseases, thus, emerging as potential candidates and promising molecules in the treatment of the obesity and metabolic syndrome. Thus, the present article proposes to approach, through a systematic literature review, the advantages, disadvantages and viabilities for the use of trypsin inhibitors directed to the treatment of overweight and obesity.

Gastroprotective and antielastase effects of protein inhibitors from Erythrina velutina seeds in an experimental ulcer model.

Trypsin and chymotrypsin inhibitors from Erythrina velutina seeds have been previously isolated by our group. In previous studies using a sepsis model, we demonstrated the antitumor and anti-inflammatory action of these compounds. This study aimed to evaluate the gastroprotective and antielastase effects of protein inhibitors from E. velutina seeds in an experimental stress-induced ulcer model. Two protein isolates from E. velutina seeds, with antitrypsin (PIAT) and antichymotrypsin (PIAQ) activities, were tested. Both protein isolates showed a high affinity and inhibitory effect against human neutrophil elastase, with 84% and 85% inhibition, respectively. Gastric ulcer was induced using ethanol (99%) in 6 groups of animals (female Wistar rats, n = 6). Before ulcer induction, these animals were treated for 5 days with one of the following: (1) PIAT (0.2 mg·kg-1), (2) PIAT (0.4 mg·kg-1), (3) PIAQ (0.035 mg·kg-1), (4) ranitidine hydrochloride (50 mg·kg-1), (5) saline solution (0.9%), or (6) no intervention (sham). Both PIAT and PIAQ protected gastric mucosa, preventing hemorrhagic lesions, edema, and mucus loss. No histologic toxic effects of PIAT or PIAQ were seen in liver and pancreatic cells. Our results show that protein isolates from E. velutina seeds have potential gastroprotective effects, placing these compounds as natural candidates for gastric ulcer prevention.