Abstract
Obesity is associated with modern diets that are rich in saturated fatty acids. These dietary patterns are linked to low-grade proinflammatory mechanisms, such as the toll-like receptor 4/nuclear factor kappa-B (NF-κB) pathway rapidly activated through high-fat diets. Juçara is a berry rich in anthocyanins and unsaturated fatty acids, which prevents obesity and associated comorbidities. We evaluated the effect of different doses of freeze-dried juçara pulp on NF-κB pathway after the consumption of short-term high-fat diet. Male Wistar rats with ad libitum access to food and water were divided into four groups: Control diet (C), high-fat diet (HFC), high-fat diet with 0.25% juçara (HFJ 0.25%), and high-fat diet with 0.5% juçara (HFJ 0.5%). Energy intake and body weight gain were increased in HFC and HFJ 0.5% groups compared to C group. The hypothalamus weight reduced in the HFC group compared to C and HFJ 0.25% groups. Cytokines, MYD88, TRAF6, and pNF-κBp50 levels in the hypothalamus, serum triacylglycerol, LDL-cholesterol (LDL-C), and free fatty acid levels were improved in the HFJ 0.25% group. In summary, the HFJ 0.25% group had better protective effects than those in the HFJ 0.5%. Therefore, 0.25% juçara can be used to protect against central inflammation through the high-fat diet-induced NF-κB pathway.
Highlights
In obesity, deleterious mechanisms are activated early, even before significant weight gain occurs [1]
Considering the lack of research in this field, the present study aimed to evaluate the effectiveness of different doses of juçara pulp in preventing the deleterious effects of a short-term high-fat diet on the modulation of the NF-κB pathway
We elucidated the effects of supplementation of different doses of juçara pulp (0.5% and 0.25%)
Summary
Deleterious mechanisms are activated early, even before significant weight gain occurs [1]. The convenience of obtaining processed foods has promoted the increased consumption of high-fat diets, which are rich in saturated fatty acids (SFAs) and sugars and poor in dietary fibers [1,3]. This unhealthy dietary practice can rapidly induce asymptomatic and deleterious. TLR4 recognizes lipid ligands from pathogens, such as bacteria, and SFAs, which results in the activation of the nuclear factor kappa-B (NF-κB), promoting an increase in chronic subclinical inflammation and playing an important signaling role in the pathogenesis of noninfectious inflammatory and chronic noncommunicable diseases [5]
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