Dataset Information

The Morbidity and Comorbidity of Nonalcoholic Fatty Liver Disease and Different Glucose Intolerance Strata in a Community-Based Chinese Population.

ABSTRACT: Objective: To investigate the morbidity and comorbidity of nonalcoholic fatty liver disease (NAFLD) and different glucose intolerance strata in a community-based population and to explore the association between glucose tolerance levels and NAFLD. Methods: A community-based cohort established for Pinggu Metabolic Disease Study in a suburb of Beijing, China, was established from September 2013 to July 2014 using a random sampling method. Participants were eligible if they were born in Pinggu and had been living there for at least 5 years within the age range of 26-76 years. A 75 grams oral glucose tolerance test was used to determine the strata of glucose tolerance. Unenhanced abdominal computed tomography scan was performed to identify NAFLD. Results: A total of 3122 subjects were included in this analysis. The prevalence of NAFLD was 22.68% (27.58% vs. 19.97% among men and women). The prevalence of type 2 diabetes (T2D) was 18.03% (20.83% vs. 16.22% among men and women). Up to 7.21% of residents had both T2D and NAFLD. 39.96% of diabetic patients and 28.77% of prediabetic patients combined with NAFLD. Compared with adults with normal glucose tolerance, the incidence of NAFLD in T2D patients was more than three times higher after adjusting for sex, age, body mass index (BMI), sedentary time, and dietary habit [odds ratio (OR) = 3.58, confidence interval (95% CI) 2.80-4.58, P < 0.001]. NAFLD was also more common in individuals with prediabetes, especially patients with impaired glucose tolerance (IGT) (OR = 2.27, 1.75-2.95) or impaired fasting glucose+IGT (OR = 2.78, 1.92-4.03). Conclusions: The morbidity and comorbidity of NAFLD and glucose intolerance are high in the Pinggu population in northern China, highlighting the importance of early prevention and treatment of these two diseases at the same time.

SUBMITTER: Zhang X

PROVIDER: S-EPMC7407000 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Nonalcoholic fatty liver disease (NAFLD) contributes to the pathogenesis of type 2 diabetes and cardiovascular disease, and patients with nonalcoholic steatohepatitis (NASH) are also at risk of developing cirrhosis, liver failure, and hepatocellular carcinoma. To date, no specific therapy exists for NAFLD/NASH, which has been recognized as one of the major unmet medical needs of the twenty-first century. We recently identified serine/threonine protein kinase (STK)25 as a critical regulator of energy homeostasis and NAFLD progression. Here, we investigated the effect of antisense oligonucleotides (ASOs) targeting Stk25 on the metabolic and molecular phenotype of mice after chronic exposure to dietary lipids. We found that Stk25 ASOs efficiently reversed high-fat diet-induced systemic hyperglycemia and hyperinsulinemia, improved whole-body glucose tolerance and insulin sensitivity, and ameliorated liver steatosis, inflammatory infiltration, apoptosis, hepatic stellate cell activation, and nutritional fibrosis in obese mice. Moreover, Stk25 ASOs suppressed the abundance of liver acetyl-coenzyme A carboxylase (ACC) protein, a key regulator of both lipid oxidation and synthesis, revealing the likely mechanism underlying repression of hepatic fat accumulation by ASO treatment. We also found that STK25 protein levels correlate significantly and positively with NASH development in human liver biopsies, and several common nonlinked single-nucleotide polymorphisms in the human STK25 gene are associated with altered liver fat, supporting a critical role of STK25 in the pathogenesis of NAFLD in humans. Conclusion: Preclinical validation for the metabolic benefit of pharmacologically inhibiting STK25 in the context of obesity is provided. Therapeutic intervention aimed at reducing STK25 function may provide a new strategy for the treatment of patients with NAFLD, type 2 diabetes, and related complex metabolic diseases. (Hepatology Communications 2018;2:69-83).

Project description:Clozapine is widely employed in the treatment of schizophrenia. Compared with that of atypical first-generation antipsychotics, atypical second-generation antipsychotics such as clozapine have less severe side effects and may positively affect obesity and blood glucose level. However, no systematic study of clozapine's adverse metabolic effects-such as changes in kidney and liver function, body weight, glucose and triglyceride levels, and retinopathy-was conducted. This research investigated how clozapine affects weight, the bodily distribution of chromium, liver damage, fatty liver scores, glucose homeostasis, renal impairment, and retinopathy in mice fed a high fat diet (HFD). We discovered that obese mice treated with clozapine gained more weight and had greater kidney, liver, and retroperitoneal and epididymal fat pad masses; higher daily food efficiency; higher serum or hepatic triglyceride, aspartate aminotransferase, alanine aminotransferase, blood urea nitrogen, and creatinine levels; and higher hepatic lipid regulation marker expression than did the HFD-fed control mice. Furthermore, the clozapine group mice exhibited insulin resistance, poorer insulin sensitivity, greater glucose intolerance, and less Akt phosphorylation; their GLUT4 expression was lower, they had renal damage, more reactive oxygen species, and IL-1 expression, and, finally, their levels of antioxidative enzymes (superoxide dismutase, glutathione peroxidase, and catalase) were lower. Moreover, clozapine reduced the thickness of retinal cell layers and increased iNOS and NF-κB expression; a net negative chromium balance occurred because more chromium was excreted through urine, and this influenced chromium mobilization, which did not help overcome the hyperglycemia. Our clozapine group had considerably higher fatty liver scores, which was supported by the findings of lowered adiponectin protein levels and increased FASN protein, PNPLA3 protein, FABP4 mRNA, and SREBP1 mRNA levels. We conclude that clozapine can worsen nonalcoholic fatty liver disease, diabetes, and kidney and retinal injury. Therefore, long-term administration of clozapine warrants higher attention.

Dataset Information

The Morbidity and Comorbidity of Nonalcoholic Fatty Liver Disease and Different Glucose Intolerance Strata in a Community-Based Chinese Population.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure