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Objective To explore the association between insulin resistance （IR） and diabetic kidney disease （DKD） among adults with type 1 diabetes mellitus （T1DM） and compare multiple surrogate parameters of IR for their associations with DKD in this population. Methods For this cross-sectional study， 556 adults with classic T1DM admitted into Xijing Hospital between October 2008 and June 2021 were enrolled. Demographic， anthropometric and laboratory data were collected. IR-related parameters of estimated glucose disposal rate （eGDR）， metabolic score for insulin resistance （METS-IR） and triglyceride-glucose index （TyG） were calculated. They were categorized into two groups of DKD and non-DKD. The relationship between IR and DKD was explored by binary Logistic regression and restricted cubic spline （RCS） models. Receiver operating characteristic （ROC） curves were plotted for comparing the discriminatory performance of all parameters. Results Median age was 31.0（24.8，44.0） year and median disease duration 6.0（2.0，12.0） year. The prevalence of DKD was 20.14%. Lower eGDR was associated with a high prevalence of DKD. In multivariable analysis， as compared to quartile 1 （Q1）， odds ratios （OR， 95%CI） of DKD for participants in eGDR calculated with body mass index （eGDRBMI） Q2-Q4 were 1.08（0.40-2.92）， 0.13（0.03-0.45） and 0.26（0.07-0.83）， respectively. The corresponding risk in eGDR calculated with waist-to-hip ratio （eGDRWHR） Q2-Q4 was 0.68（0.20-2.23）， 0.51（0.15-1.66） and 0.16（0.03-0.72）， respectively. TyG， eGDR calculated with waist circumference （eGDRWC）， METS-IR， body mass index， waist-to-height ratio and waist-to-hip ratio were not significantly associated with the prevalence of DKD. Subgroup analyses indicated that the association between eGDRBMI and DKD was consistent with overall population in six subgroups of females， age 28-＜40 years and ≥40 years， disease duration ≥5 years， non-smokers and individuals with a family history of diabetes. RCS hinted at a linear and negative correlation between eGDRBMI， eGDRWHR and the prevalence of DKD. ROC analyses indicated that the cutoff values for identifying DKD were 8.23 mg·kg−1·min−1， 7.22 mg·kg−1·min−1 and 7.92 mg·kg−1·min−1 for eGDRBMI， eGDRWHR and eGDRWC， respectively. After adding into a basic model， all three eGDRs demonstrated incremental discriminatory performance. Conclusion IR， reflected by a declining eGDR， is associated with the prevalence of DKD among adults with classic T1DM. And eGDR has demonstrated some potential in identifying DKD in adult classic T1DM and its clinical implication should be validated by more studies.

Tea is a popular beverage with characteristic functional and flavor qualities, known to be rich in bioactive metabolites such as tea polyphenols and theanine. Recently, tea varieties with variations in leaf color have been widely used in agriculture production due to their potential advantages in terms of tea quality. Numerous studies have used genome, transcriptome, metabolome, proteome, and lipidome methods to uncover the causes of leaf color variations and investigate their impacts on the accumulation of crucial bioactive metabolites in tea plants. Through a comprehensive review of various omics investigations, we note that decreased expression levels of critical genes in the biosynthesis of chlorophyll and carotenoids, activated chlorophyll degradation, and an impaired photosynthetic chain function are related to the chlorina phenotype in tea plants. For purple-leaf tea, increased expression levels of late biosynthetic genes in the flavonoid synthesis pathway and anthocyanin transport genes are the major and common causes of purple coloration. We have also summarized the influence of leaf color variation on amino acid, polyphenol, and lipid contents and put forward possible causes of these metabolic changes. Finally, this review further proposes the research demands in this field in the future.

Multi-walled carbon nanotubes (MWCNTs) mainly induce oxidative stress through the overproduction of reactive oxygen species (ROS), which can lead to cytotoxicity. Celastrol, a plant-derived compound, can exert antioxidant effects by reducing ROS production. Our results indicated that exposure to MWCNTs decreased cell viability and increased ROS production. Nrf2 knockdown (kd) led to increased ROS production and enhanced MWCNT-induced cytotoxicity. Keap1-kd led to decreased ROS production and attenuated cytotoxicity. Treatment with celastrol significantly decreased ROS production and promoted Keap1 protein degradation through the lysosomal pathway, thereby enhancing the translocation of Nrf2 from the cytoplasm to the nucleus and increasing HO-1 expression. The in vivo results showed that celastrol could alleviate the inflammatory damage of lung tissues, increase the levels of the antioxidants, GSH and SOD, as well as promote the expression of the antioxidant protein, HO-1 in MWCNT-treated mice. Celastrol can alleviate MWCNT-induced oxidative stress through the Keap1/Nrf2/HO-1 signaling pathway.