Association of diet quality with the risk of Sarcopenia based on the Chinese diet balance index 2016: a cross-sectional study among Chinese adults in Henan Province.

BACKGROUND: Sarcopenia can lead to a series of unfavourable health outcomes. Diet is an important factor influencing sarcopenia. In this study, we aimed to evaluate the association of sarcopenia with diet quality assessed by the Chinese Diet Balance Index 2016 (DBI-16). METHODS: A cross-sectional study was conducted to collect information on nutrition and health in Henan Province, China, and a total of 644 individuals were studied. Sarcopenia was defined according to the Asian Working Group for Sarcopenia (AWGS) criteria updated in 2019. Diet quality was assessed by using the Chinese Diet Balance Index 2016 (DBI-16), which includes three indicators: the lower bound score (LBS), higher bound score (HBS) and diet quality distance (DQD). Binary logistic regression analysis was used to estimate the risk of sarcopenia associated with diet quality. RESULTS: A total of 49 of the 644 participants were diagnosed with sarcopenia. Excessive intake (score > 0) of cereals, meat, eggs and salt, inadequate intake (score < 0) of vegetables, fruits, dairy products, soybeans and low diet variety were commonly seen in both groups of participants. The participants with sarcopenia had a more serious inadequate intake of fruit than those without sarcopenia (p < 0.05). The overall LBS, HBS and DQD in both groups were in the interval of low-level problems. Compared with participants with a suitable LBS, those with an unsuitable LBS were more likely to have a low gait speed (OR: 2.58; 95%CI: 1.13-7.04) after multiple adjustments. However, the other two DBI-16 indicators, the HBS and DQD, were not associated with sarcopenia or its related diagnostic variables. CONCLUSION: Unfavourable diet quality, mainly referring to inadequate dietary intake in this study, may be a risk factor for low gait speed.

A novel dammarane triterpenoid alleviates atherosclerosis by activating the LXRα pathway.

BACKGROUND: We have previously demonstrated that ginsenoside compound K can attenuate the formation of atherosclerotic lesions. Therefore, ginsenoside compound K has potential for atherosclerosis therapy. How to improve the druggability and enhance the antiatherosclerotic activity of ginsenoside compound K are the core problems in the prevention and treatment of atherosclerosis. CKN is a ginsenoside compound K derivative that was previously reported to have excellent antiatherosclerotic activity in vitro, and we have applied for international patents for it. METHODS: Male C57BL/6 ApoE-/- mice were fed a high-fat and high-choline diet to induce atherosclerosis and were subjected to in vivo studies. In vitro, the CCK-8 method was applied to evaluate cytotoxicity in macrophages. Foam cells were utilized, and cellular lipid determination was performed for in vitro studies. The area of atherosclerotic plaque and fatty infiltration of the liver were measured by image analysis. Serum lipid and liver function were determined by a seralyzer. Immunofluorescence and western blot analysis were conducted to explore the alterations in the expression levels of lipid efflux-related proteins. Molecular docking, reporter gene experiments and cellular thermal shift assays were used to verify the interaction between CKN and LXRα. RESULTS: After confirming the therapeutic effects of CKN, molecular docking, reporter gene experiments and cellular thermal shift assays were used to predict and investigate the antiatherosclerotic mechanisms of CKN. CKN exhibited the greatest potency, with a 60.9% and 48.1% reduction in en face atherosclerotic lesions on the thoracic aorta and brachiocephalic trunk, reduced plasma lipid levels and decreased foam cell levels in the vascular plaque content in HHD-fed ApoE-/- mice. Moreover, CKN in the present study may exert its antiatherosclerotic effects through activated ABCA1 by promoting LXRα nuclear translocation and reducing the adverse effects of LXRα activation. CONCLUSIONS: Our results revealed that CKN prevented the formation of atherosclerosis in ApoE-/- mice by activating the LXRα pathway.