Background:: Many published studies attempted to elucidate the implication of glucokinase regulator gene (GCKR) polymorphisms in the susceptibility to nonalcoholic fatty liver disease (NAFLD), but the results among them were still with controversy. Objective:: This meta-analysis aims to precisely assess the relationship between the GCKR polymorphisms and the risk of NAFLD. Methods:: Systematic computerized searches in six databases were performed and updated to April 6, 2020. Meta-analyses were conducted by calling the R programs based on accumulated epidemiological data. Odds ratio (OR) and 95% confidential interval (CI) were calculated to summarize the effect estimates. Results:: In total, 25 studies involving 6,598 cases and 19,954 controls were included. The pooled estimates indicated that the T allele carrier of the GCKR rs780094 polymorphism has predisposition to NAFLD (allele model: OR: 1.20, 95% CI: 1.11~1.29; homozygote model: OR: 1.38, 95% CI: 1.15~1.67; heterozygote model: OR: 1.25, 95% CI: 1.12~1.39; dominant model: OR: 1.29, 95% CI: 1.13~1.47; recessive model: OR: 1.18, 95% CI: 1.06~1.31), and the same as the rs1260326 polymorphism (allele model: OR: 1.32, 95% CI: 1.22~1.42; homozygote model: OR: 1.65, 95% CI: 1.40~1.94; heterozygote model: OR: 1.24, 95% CI: 1.07~1.43; dominant model: OR: 1.39, 95% CI: 1.21~1.59; recessive model: OR: 1.44, 95% CI: 1.28~1.62). Further stratified analyses according to age and ethnicity confirmed the statistical existence in most subgroups. Conclusion:: This meta-analysis suggested that both of the GCKR rs780094 and rs1260326 polymorphisms are significantly associated with the increased risk of NAFLD.

The clinical presentation in Chinese patients with sporadic Creutzfeldt-Jakob disease (sCJD) may be unique due to the big difference in the codon 129 polymorphism of the prion protein gene (PRNP). This study retrospectively reviewed 26 cases of sCJD diagnosed in a single center in recent years. All 26 sCJD patients received brain magnetic resonance imaging scan, cerebrospinal fluid 14-3-3 protein detection, electroencephalogram, and PRNP gene screening. The codon 129 polymorphism were all homozygous MM in 26 sCJD patients. The main onset symptoms of sCJD patients were rapidly progressive dementia, visual impairment, and cerebellar ataxia. At the time of diagnosis, the incidence of myoclonus and akinetic mutism were relatively low (<50%). For auxiliary examinations, the positive rate of the typical magnetic resonance imaging (MRI) abnormalities, cerebrospinal fluid 14-3-3 protein, and electroencephalogram-periodic sharp wave complex was 96%, 64%, and 50%, respectively. As MM genotype is dominant and brain MRI is sensitive, brain MRI seems to play a major role in diagnosis of sCJD in Chinese.

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