Clinical research results of vitamin D supplementation in the improvement of prediabetes remain controversial. Accordingly, a literature search was conducted of PubMed, Embase (Ovid), and Web of Science prior to 9 November 2021. Randomized controlled studies reported that the following indicators were included: body mass index (BMI), fasting blood glucose (FBG), 2 h oral glucose tolerance test plasma glucose (2h-PG), hemoglobin A1c (HbA1c), insulin resistance by homeostasis model assessment (HOMA-IR), homeostasis model assessment of β-cell function (HOMA-B), and fasting insulin (FINS). Twenty-nine articles (N = 3792) were included in the present meta-analysis. Intriguingly, vitamin D supplementation resulted in a vast improvement in FBG (standardized mean difference (SMD) = −0.38; 95%CI: −0.59, −0.16), HbA1c (SMD = −0.14; 95%CI: −0.22, −0.06) and FINS (SMD = 0.18; 95%CI: −0.26, −0.09), but not in other outcomes. However, preferred changes were observed in subgroups, as follows: Asia (SMD_2h-PG = −0.25, 95%CI: −0.45, −0.04), study duration ≥1 year (SMD_HOMA-IR = −0.44, 95%CI: −0.81, −0.06) (SMD_HOMA-B = 0.34, 95%CI: 0.01, 0.66), baseline 25(OH)D < 50 nmol/L (SMD_2h-PG = −0.23, 95%CI: −0.39, −0.06), and baseline 25(OH)D ≥ 50 nmol/L (SMD_HOMA-IR = −0.50, 95%CI: −0.96, −0.03). In conclusion, oral supplementation of vitamin D has shown better effects in improving FBG, HbA1c, and FINS compared with controls among prediabetics; long-term vitamin D supplementation could have additional effects in participants with vitamin D deficiency for 2h-PG, HOMA-IR, and HOMA-B.

Alzheimer’s disease (AD) is characterized by the deposition of senile plaques (SPs) and the formation of neurofibrillary tangles (NTFs), as well as neuronal dysfunctions in the brain, but in fact, patients have shown a sustained disease progression for at least 10 to 15 years before these pathologic biomarkers can be detected. Consequently, as the most common chronic neurological disease in the elderly, the challenge of AD treatment is that it is short of effective biomarkers for early diagnosis. The protein quality control system is a collection of cellular pathways that can recognize damaged proteins and thereby modulate their turnover. Abundant evidence indicates that the accumulation of abnormal proteins in AD is closely related to the dysfunction of the protein quality control system. In particular, it is the synthesis, degradation, and removal of essential biological components that have already changed in the early stage of AD, which further encourages us to pay more attention to the protein quality control system. The review mainly focuses on the endoplasmic reticulum system (ERS), autophagy–lysosome system (ALS) and the ubiquitin–proteasome system (UPS), and deeply discusses the relationship between the protein quality control system and the abnormal proteins of AD, which can not only help us to understand how and why the complex regulatory system becomes malfunctional during AD progression, but also provide more novel therapeutic strategies to prevent the development of AD.