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Corn, a widely cultivated cereal, is a rich source of several antioxidant compounds, including phenolic compounds. Some of these compounds are bound within the components of the corn cell wall, requiring specific treatments to release them. Solid-state fermentation (SSF) using Rhizopus oryzae enhanced the antioxidant capacity and phenolic content in legumes and grains. However, there is limited information regarding its application in blue corn. This study aimed to evaluate the effect of R. oryzae growth on the phenolic content and antioxidant capacity of blue corn kernels. The results demonstrated that R. oryzae used blue corn kernels for growth, which led to an increase in free phenolic compounds, reaching their highest concentration at 60 h of culture. Compared to the unfermented control (0 h), SSF increased by up to 161% in total phenolic content and a 94% increase in antioxidant capacity. The main phenolic compounds identified in the blue corn extracts at 60 h using RP-HPLC-ESI-MS included caffeic acid 4-O-glucoside, rosmanol, p-coumaroyl tartaric acid glucosidic ester, 5-heptadecylresorcinol, and caffeoyl tartaric acid. The SSF represents an eco-friendly method for enhancing the antioxidant capacity and phenolic compounds of blue corn grain. Full article

Aging-associated hepatic fatty acid (FA) oxidation dysfunction contributes to impaired adaptive thermogenesis. 5-Heptadecylresorcinol (AR-C17) is a prominent functional component of whole wheat and rye, and has been demonstrated to improve the thermogenic capacity of aged mice via the regulation of Sirt3. However, the effect of AR-C17 on aging-associated hepatic FA oxidation dysfunction remains unclear. Here, 18-month-old C57BL/6J mice were orally administered with AR-C17 at a dose of 150 mg/kg/day for 8 weeks. Systemic glucose and lipid metabolism, hepatic FA oxidation, and the lipolysis of white adipose tissues (WAT) were measured. The results showed that AR-C17 improved the hepatic FA oxidation, and especially acylcarnitine metabolism, of aged mice during cold stimulation, with the enhancement of systemic glucose and lipid metabolism. Meanwhile, AR-C17 improved the WAT lipolysis of aged mice, promoting hepatic acylcarnitine production. Furthermore, the adipose-specific Sirt3 knockout mice were used to investigate and verify the regulation mechanism of AR-C17 on aging-associated hepatic FA oxidation dysfunction. The results showed that AR-C17 failed to improve the WAT lipolysis and hepatic FA oxidation of aged mice in the absence of adipose Sirt3, indicating that AR-C17 might indirectly influence hepatic FA oxidation via regulating WAT Sirt3. Our findings suggest that AR-C17 might improve aging-associated hepatic FA oxidation dysfunction via regulating adipose Sirt3. Full article

5-Heptadecylresorcinol (AR-C17), a primary biomarker of whole grain (WG) consumption, has been demonstrated to improve the thermogenic activity of aging mice. However, the intricate regulatory mechanism is not fully understood. This study conducted metabolomics analysis on young and aging mice with or without AR-C17 administration after cold exposure. The results showed that the aging mice displayed lower levels of acylcarnitine (ACar) in their plasma compared with the young mice during cold exposure, and 150 mg/kg/day of AR-C17 administration for 8 weeks could increase the plasma ACar levels of aging mice. ACar has been reported to be an essential metabolic fuel for the thermogenesis of brown adipose tissue (BAT). AR-C17 had similar effects on the ACar levels in the BAT as on the plasma of the aging mice during cold exposure. Furthermore, the aging mice had reduced ACar metabolism in the BAT, and AR-C17 could improve the ACar metabolism in the BAT of aging mice, thereby promoting the metabolic utilization of ACar by BAT. Moreover, the glucose and lipid levels of aging mice could be improved by AR-C17. This study revealed a deeper metabolic mechanism involved in the AR-C17-mediated thermogenic regulation of BAT, providing a new theoretical basis for the nutrition and health benefits of WG. Full article