Background
Caryocar brasiliense (pequi) oil is high in monounsaturated fat acids (MUFA), especially oleic, and in carotenoids, which have been associated with protection against cardiovascular disease. However, this food is poorly studied in this context, especially in the cardiac function. Therefore, we investigated the effects of a long-term intake of pequi oil in systemic cardiovascular risk factors and in the ex vivo cardiac function of rats.MethodsPreviously, we determined fatty acids and carotenoids in pequi oil. Next, male rats were divided in C – control group feed a standard diet, and PO – pequi oil group fed the same diet added pequi oil (+2.25 g.100 g−1). After 15 weeks, plasma lipids, glucose, insulin, blood pressure, heart rate, hepatic lipids were accessed and visceral fat pads were harvested. Hearts were used for the ex vivo cardiac function, histologic assays, SERCA2a and phospholanban (PLB) determinations.ResultsIn agreement with scientific data, pequi oil had expressive amounts MUFA, especially oleic acid, and carotenoids. Hepatic triglycerides (TG) were reduced by pequi oil intake (p < 0.05). All others cardiovascular risk factors were not changed. The intrinsic heart rate was lower in PO group (p < 0.05). SERCA2a content was higher in this group (p < 0.05), without affecting PLB. Also, SERCA2a/PLB ratio increased in PO group (p < 0.05).Conclusion
Pequi oil intake improved cardiac function ex vivo, despite no significant changes in systemic cardiovascular risk factors. The higher lipid offer in pequi oil diet, its composition in oleic acid and carotenoids could be related to those effects.
Caloric restriction (CR) reduces body weight and systemic inflammation, but effects on adipose tissue under dietary lipid overload are controversial. We evaluated the effects of CR-induced weight loss with a high-fat diet (HF) on adipose tissue inflammation of obese mice. Male mice were assigned into LF (low-fat diet) and HF. After 8-wk, HF was reassigned for another 7-wk into HF – kept at HF; LFAL - switched from HF to LF ad libitum; RHF - fed HF calorie-restricted to reach LFAL body weight. Serum markers, adipocytokines, morphology, and inflammatory infiltrates in retroperitoneal adipose tissue (RAT) were accessed. LFAL and RHF reduced body weights, equaling to LF. LFAL restored almost all inflammatory markers as LF, except tumor necrosis factor-alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and adiponectin. Compared to HF, RHF lowered visceral adiposity, retroperitoneal adipocyte sizes, RAT inflammatory cell infiltration as well as TNF-α, interleukin-6, hepatic and serum C-reactive protein, which were higher than LFAL; adiponectin and MCP-1 did not change. CR with high-fat diet reduced body weight and attenuated visceral adiposity, but did not fully recover visceral tissue inflammation.
Novelty bullets
• Caloric restriction in a high-fat diet ameliorated visceral adiposity.
• Caloric restriction in a high-fat diet did not recover visceral adipose tissue inflammation.
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