Abstract
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.
Highlights
Metabolic syndrome (MetS) is an obesity-based condition characterized by the presence of insulin resistance (IR), high blood pressure and dyslipidemia
We isolated a trypsin inhibitor form tamarindo seeds (TTI), an endemic fruit in northeast Brazil, using steps previously determined by Ribeiro et al [20]
The current increase in overweight/obesity and the growing number of Metabolic Syndrome (MetS) cases is a worldwide public health problem [2]. This made the evaluation of new molecules with potential to promote satiety and modulate metabolic changes in the inflammatory context of MetS an important research field. Classically known by their antinutritional digestive effects, trypsin inhibitors have been studied as satiety inducers [15,18,20,21,22]
Summary
Metabolic syndrome (MetS) is an obesity-based condition characterized by the presence of insulin resistance (IR), high blood pressure and dyslipidemia. MetS clinical features include endothelial dysfunction and a pro-oxidant, pro-thrombotic, inflammatory condition [1,2]. The inflammatory process in MetS is due to the production of cytokines and chemokines by adipocytes. These inflammatory markers include TNF-α, IL-6, leptin, C-reactive protein (CRP), resistin, monocyte chemotactic protein (MCP-1), inducible nitric oxide synthase (iNOS), transforming growth factor-beta (TGF-β) and plasminogen activator inhibitor 1 (PAI-1). Among molecular mechanisms associated with inflammation in obesity, is the signaling pathway of nuclear factor kappa B (NF-κB), which induces expression of several genes related to inflammation [4]. NF-κB pathway can be triggered by TNF-α binding to its receptor or by lipopolysaccharide (LPS) and saturated fatty acids binding to toll-like receptor 4 (TLR4) [4]
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