Scope Adequate intake of whole grain foods is beneficial to type 2 diabetes mellitus (T2DM). Whether the preventive effects are related with metabolism of branched‐chain amino acids (BCAAs) is unclear. The study aims to evaluate the effects of germinated brown rice (GBR) intervention on BCAAs metabolism in T2DM patients. Methods and results In this randomized controlled trial, subjects with T2DM are instructed to consume 100 g day−1 GBR (GBR group, n=42) or equal staple food (Control group, n=25) for 3 months. Food frequency questionnaires (FFQ) and serum samples are collected before and after the intervention. In the GBR group, fasting blood glucose (FBG), fasting insulin (FINS), and serum BCAAs are decreased, and islet function is improved (p<0.05). Logistic regression analysis showed that FBG (odds ratios [OR]: 1.55, 95% confidence interval [CI]: 1.01–1.84) and energy (OR: 1.21, 95% CI: 1.09–1.30) are positively associated with serum total BCAAs level, while FINS is negatively associated (OR: 0.20, 95% CI: 0.04–0.88). Simultaneously, the key enzymes of BCAAs decomposition, which promotes glycolysis by activating pyruvate dehydrogenase (PDH), are significantly increased. Conclusion GBR improves the indicators of T2DM patients, and the underlying mechanisms include improving insulin resistance and accelerating catabolism of BCAAs.
Although sulforaphane (SFN) is reported to ameliorate the excessive accumulation of lipid droplets (LDs) in hepatocytes, its underlying mechanism remains unclear. This paper aims to investigate how SFN induces hepatic LD degradation via activating macroautophagy. High-fat diet and free fatty acids (FFAs) were used to induce excessive LD formation in hepatocytes in vivo and in vitro, respectively. SFN-induced macroautophagy was shown by the increased LC3 protein expression both (1.32 ± 0.18) in vivo and (2.43 ± 0.22) in vitro. The mRNA levels of Lc3 (1.99 ± 0.16), Atg4 (2.12 ± 0.23), Ulk1 (1.19 ± 0.12), Atg7 (1.25 ± 0.11), and Atg5 (0.81 ± 0.1) genes were elevated by SFN. SFN individually enhanced the localization of LC3 (0.41 ± 0.15), LAMP1 (0.66 ± 0.14), ATG7 (0.26 ± 0.08), and ATG5 (0.38 ± 0.09) with LDs, indicating the occurrence of lipophagy. In the components of LDs isolated from SFN treatment, the expressions of LC3, ATG7, and ATG5 protein were largely increased both in vivo and in vitro. LDs were visualized in autophagosomes which confirmed that the lipophagy was triggered by SFN. Moreover, SFN treatment improved the profile of FFAs which was characterized by increasing the FFAs in liver (total FFA: 261.51 ± 39.58 μM/g) and serum (total FFA: 967.59 ± 239.18 nM/mL). After silencing the nrf 2 gene, ATG7 and ATG5 protein expressions were decreased and attenuated this induction by SFN. Nrf2 gene silencing inversely increased TG contents. In summary, SFN enhanced the LD degradation via stimulating lipophagy in a Nrf2-dependent manner.
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