Acrocomia aculeata (Jacq.) improves the antioxidant system but induces lipid accumulation in the liver of rats.

Acrocomia aculeata pulp (ACP) is a source of oleic acid, phenolic compounds, and flavonoids that protect against diseases and improve antioxidant capacity. We evaluated whether regular intake of ACP, in combination with a standard diet, improves the antioxidant system and physiological parameters. Male Wistar rats were divided into: control (C), 250 mg/kg ACP, and 500 mg/kg ACP groups. Rats received either water or the respective A. aculeata solution doses for 28 days. We observed increased food intake, lower carcass protein levels, and higher carcass lipid levels in the 500 mg/kg ACP group than in the other groups. Postprandial glucose, oral glucose tolerance test results, and the area under the curve were greater, while urea was lower in the 500 mg/kg ACP group. Total liver lipids were increased, and PPAR-α, PPARγ, and carbonylated protein levels were reduced in the 500 mg/kg ACP group. NRF2 contents and glutathione reductase, superoxide dismutase, and catalase activities were increased in the 500 mg/kg ACP group. In the 250 mg/kg ACP group, only glutathione system activity increased. Thus, ACP intake improved the enzymatic antioxidant system in the liver at the evaluated doses, although the 500 mg/kg dose induced alterations in lipid, protein, and carbohydrate metabolism.

Hyperphagia and hyperleptinemia induced by low-protein, high-carbohydrate diet is reversed at a later stage of development in rats.

This study investigated whether increased food intake after 15 days of low-protein, high-carbohydrate (LPHC) and its normalization in the later period of development change the content of key proteins related to leptin or adiponectin signaling in the hypothalamus. Male rats were divided into five groups: Control groups received a control diet (17% protein, 63% carbohydrate) for 15 (C15) or 45 (C45) days; LPHC groups received an LPHC diet (6% protein, 74% carbohydrate) for 15 (LPHC15) or 45 (LPHC45) days; and Reverse group (R): received LPHC diet for 15 days followed by control diet for another 30 days. The LPHC15 group showed increased adiposity index, leptin level, and adiponectin level, as well as decreased the leptin receptor (ObRb) and pro-opiomelanocortin (POMC) content in the hypothalamus compared with the C15 group. LPHC diet for 45 days or diet reversion (R group) rescued these alterations, except the adiponectin level in LPHC45 rats, which was higher. In summary, LPHC diet reduced hypothalamic leptin action by diminishing ObRb and POMC levels, leading to hyperphagia and adiposity body. Medium-term administration of LPHC diet or reverting to control diet restored the levels of these proteins, thereby improving body lipid mass rearrangement in adulthood.