Type 2 diabetes mellitus (T2DM) is characterized by hyperglycemia. Proteins in plant sources that enable the maintenance of the glycemic profile may be of interest in the context of T2DM. However, their mechanisms of action are unclear, unlike other bioactive compounds. This systematic review identified and described the mechanisms of action of isolated and purified proteins and peptides extracted from vegetables on the reduction of blood glucose in T2DM in experimental studies. The research was done in PubMed, ScienceDirect, Scopus, Web of Science, Embase and Virtual Health Library (VHL) databases in March 2019. The initial search retrieved 916 articles, and, after reading the title, abstract and keywords, 24 articles were eligible for full reading. Then, five articles were eligible to build this systematic review. The evaluation of the evidence and the strength of the recommendations of the studies was evaluated with the SYstematic Review Center for Laboratory animal Experimentation - SYRCLE. Studies with proteins or peptides extracted from soybean (Glycine max), corn (Zea mays), peas (Pisum sativum), costus (Costus igneus) and ginseng (Panax ginseng) were found, and all of them decreased glycemia but not by the same mechanisms. The mechanism of action of proteins extracted from Glycine max, Pisum sativum, Costus igneus were similar, acting in the insulin-mediated pathways. The peptide derived from Zea mays increased GLP-1 expression, and the peptide from Panax ginseng reduced NF-kB signaling, both resulting in stimulating the release of insulin. Therefore, bioactive proteins and peptides of plant sources act through biochemical pathways, in the modulation of insulin resistance and the hyperglycemic state. These compounds are promising in scientific research on T2DM, because there is a probable similarity of these proteins with insulin, which enables them to act as insulin-like molecules.
OBJECTIVE: This study evaluated the effect of a protein, the isolated Trypsin Inhibitor (TTI) from Tamarindus indica L. seed, as a CCK secretagogue and its action upon food intake and leptin in obese Wistar rats. METHODS: Three groups of obese rats were fed 10 days one of the following diets: Standard diet (Labina®) + water; High Glycemic Index and Load (HGLI) diet + water or HGLI diet + TTI. Lean animals were fed the standard diet for the 10 days. Food intake, zoometric measurements, plasma CCK, plasma leptin, relative mRNA expression of intestinal CCK-related genes, and expression of the ob gene in subcutaneous adipose tissue were assessed. RESULTS: TTI decreased food intake but did not increase plasma CCK in obese animals. On the other hand, TTI treatment decreased CCK-1R gene expression in obese animals compared with the obese group with no treatment (p = 0.027). Obese animals treated with TTI presented lower plasma leptin than the non-treated obese animals. CONCLUSION: We suggest that TTI by decreasing plasma leptin may improve CCK action, regardless of its increase in plasma from obese rats, since food intake was lowest.
Appetite Depressants/pharmacology , Eating/drug effects , Leptin/blood , Obesity , Plant Proteins, Dietary/pharmacology , Receptors, Cholecystokinin/genetics , Tamarindus/chemistry , Animals , Appetite Depressants/isolation & purification , Appetite Depressants/therapeutic use , Down-Regulation/drug effects , Gene Expression/drug effects , Male , Obesity/blood , Obesity/drug therapy , Obesity/genetics , Plant Proteins, Dietary/isolation & purification , Rats , Rats, Wistar , Receptors, Cholecystokinin/metabolism , Satiety Response/drug effects , Seeds/chemistry
Trypsin inhibitors are studied in a variety of models for their anti-obesity and anti-inflammatory bioactive properties. Our group has previously demonstrated the satietogenic effect of tamarind seed trypsin inhibitors (TTI) in eutrophic mouse models and anti-inflammatory effects of other trypsin inhibitors. In this study, we evaluated TTI effect upon satiety, biochemical and inflammatory parameters in an experimental model of metabolic syndrome (MetS). Three groups of n = 5 male Wistar rats with obesity-based MetS received for 10 days one of the following: (1) Cafeteria diet; (2) Cafeteria diet + TTI (25 mg/kg); and (3) Standard diet. TTI reduced food intake in animals with MetS. Nevertheless, weight gain was not different between studied groups. Dyslipidemia parameters were not different with the use of TTI, only the group receiving standard diet showed lower very low density lipoprotein (VLDL) and triglycerides (TG) (Kruskal-Wallis, p < 0.05). Interleukin-6 (IL-6) production did not differ between groups. Interestingly, tumor necrosis factor-alpha (TNF-α) was lower in animals receiving TTI. Our results corroborate the satietogenic effect of TTI in a MetS model. Furthermore, we showed that TTI added to a cafeteria diet may decrease inflammation regardless of weight loss. This puts TTI as a candidate for studies to test its effectiveness as an adjuvant in MetS treatment.
