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Although nutritional health knowledge serves as the basis for the daily food guides, limited epidemiologic studies were conducted to verify whether adherence to the daily food guides reduced the prevalence of diseases. This study aims to examine whether adherence to the daily food guides relates to the lower risk of having metabolic syndrome, as well as to assess the association between levels of adherence to daily food guides and demographic characteristics. A cross-sectional study was conducted using data from the Nutrition and Health Survey in Taiwan (NAHSIT) 2013–2016. Face-to-face dietary assessments were conducted using a validated food-frequency questionnaire. Six food groups were defined according to the daily food guides in Taiwan. We constructed a daily food guide index to measure the levels of adherence to the daily food guides. Logistic regression was performed to assess the association between the levels of adherence to the daily food guides and the risk of having metabolic syndrome. A total of 2534 participants (51% of females) were included in the final analysis. After adjusting for age, sex, body mass index, education level, marital status, and family income, we found a negative correlation between the levels of adherence to daily food guides and the prevalence of metabolic syndrome. The odds ratios (ORs) for the highest versus lowest quartile of the adherence level was 0.65 (95% confidence interval (CI) = 0.48–0.88). In addition, males, younger age, lower education, divorced, separated, and widowed, and lower family income were associated with lower adherence to daily food guides. In conclusion, participants reporting better adherence to the daily food guides during the past month had a lower risk of having metabolic syndrome.

Voltage-gated ClC-2 channels are essential for chloride homeostasis. Complete knockout of mouse ClC-2 leads to testicular degeneration and neuronal myelin vacuolation. Gain-of-function and loss-of-function mutations in the ClC-2-encoding human CLCN2 gene are linked to the genetic diseases aldosteronism and leukodystrophy, respectively. The protein homeostasis (proteostasis) mechanism of ClC-2 is currently unclear. Here, we aimed to identify the molecular mechanism of endoplasmic reticulum-associated degradation of ClC-2, and to explore the pathophysiological significance of disease-associated anomalous ClC-2 proteostasis. In both heterologous expression system and native neuronal and testicular cells, ClC-2 is subject to significant regulation by cullin-RING E3 ligase-mediated polyubiquitination and proteasomal degradation. The cullin 4 (CUL4)-damage-specific DNA binding protein 1 (DDB1)-cereblon (CRBN) E3 ubiquitin ligase co-exists in the same complex with and promotes the degradation of ClC-2 channels. The CRBN-targeting immunomodulatory drug lenalidomide and the cullin E3 ligase inhibitor MLN4924 promotes and attenuates, respectively, proteasomal degradation of ClC-2. Analyses of disease-related ClC-2 mutants reveal that aldosteronism and leukodystrophy are associated with opposite alterations in ClC-2 proteostasis. Modifying CUL4 E3 ligase activity with lenalidomide and MLN4924 ameliorates disease-associated ClC-2 proteostasis abnormality. Our results highlight the significant role and therapeutic potential of CUL4 E3 ubiquitin ligase in regulating ClC-2 proteostasis.