The association of triglyceride-glucose-waist circumference with metabolic associated fatty liver disease and the severity of liver steatosis and fibrosis in American adults: a population-based study.

BACKGROUND: The global obesity pandemic has led to an alarming rise in the prevalence of metabolic-associated fatty liver disease (MAFLD), making it a substantial clinical and economic burden on society. Early detection and effective treatment of MAFLD are imperative to mitigate its impact. METHODS: This cross-sectional study was conducted involving 4634 adults from the National Health and Nutrition Examination Surveys (NHANES) 2017-2018 cycle. Transient elastography (TE) was used to diagnose MAFLD and assess the extent of liver steatosis and fibrosis. Multivariate logistic regression models were utilized to examine the association between the triglyceride and glucose index-waist circumference (TyG-WC) and the risk of MAFLD, liver fibrosis, and steatosis. RESULTS: A positive association between TyG-WC and MAFLD persisted across all three models: model1: OR = 8.44, 95% CI: 6.85-10.38 (unadjusted), model2: OR = 8.28, 95% CI: 6.53-10.50 (partially adjusted), and model3: OR = 7.98, 95% CI: 4.11-15.46 (fully adjusted). Further investigation through interaction and stratified analysis revealed that this association was more pronounced in the non-obese and Non-Hispanic White persons groups. Moreover, a non-linear relationship analysis unveiled threshold and saturation effects between TyG-WC and MAFLD. Specifically, a TyG-WC value of approximately 600 may represent the threshold effect for MAFLD risk, while 1200 may signify the saturation effect of MAFLD risk. Finally, a robust correlation between TyG-WC and the severity of liver steatosis and fibrosis was found. CONCLUSIONS: The findings suggest that the TyG-WC index exhibits excellent predictive value for MAFLD in the general American population.

Association of glycated hemoglobin with non-alcoholic fatty liver disease patients and the severity of liver steatosis and fibrosis measured by transient elastography in adults without diabetes.

BACKGROUND: Type 2 diabetes mellitus (T2DM) is a well-known independent risk factor for non-alcoholic fatty liver disease (NAFLD). However, research exploring the association between blood glucose management and the risk of NAFLD status in subjects without diabetes was insufficient. This study aimed to explore the association of glycated hemoglobin (HbA1c) with NAFLD status and the severity of liver steatosis and fibrosis in non-diabetic people. METHODS: A cross-sectional analysis was conducted on 2998 non-diabetic American adults using data from the National Health and Nutrition Examination Survey (NHANES) 2017-2018 cycle. We used multivariable logistic regression models to evaluate the association between HbA1c and NAFLD status and the severity of liver steatosis and fibrosis. Interaction and stratified analyses were additionally performed. RESULTS: The multivariate regression analyses showed that HbA1c was associated independently with NAFLD status in all the models (model1: OR = 2.834, 95%CI: 2.321, 3.461; model 2: OR = 2.900, 95%CI: 2.312, 3.637 and model 3: OR = 1.664, 95%CI: 1.284, 2.156). We further performed the interaction and stratified analyses and discovered a significant interaction between HbA1c and BMI (Pinteraction < 0.05). Finally, a robust link was shown between HbA1c level and the severity of liver steatosis, which was mainly significant in the prediabetes group, while the correlation was not significant in HbA1c level and severity of liver fibrosis after controlling for all the potential confounders. CONCLUSIONS: We concluded that HbA1c level was positively correlated to the risk of developing NAFLD in a large non-diabetic American population. Moreover, HbA1c level was associated with the severity of liver steatosis in subjects with prediabetes, suggesting that routine screening for HbA1c among individuals with prediabetes is necessary.

Association of serum uric acid-to-high-density lipoprotein cholesterol ratio with non-alcoholic fatty liver disease in American adults: a population-based analysis.

Objective: Non-invasive disease indicators are currently limited and need further research due to the increased non-alcoholic fatty liver disease (NAFLD) prevalence worldwide. The serum uric acid-to-high-density lipoprotein cholesterol ratio (UHR) has been recognized as a novel inflammatory and metabolic marker. Herein, we explored the correlation between UHR and the risk of NAFLD in-depth. Methods: A total of 3,766 participants were included in our survey, and the National Health and Nutrition Examination Survey (NHANES) 2017-2018 cycle provided the cross-sectional study population. Weighted multivariable logistic regression and multivariate linear regression analyses were performed to assess the association between the UHR and the odds of NAFLD and liver steatosis and fibrosis severity, respectively. Moreover, we explored the non-linear relationship between the UHR and NAFLD by the generalized additive model. Results: NAFLD probabilities were statistically demonstrated to be positively correlated with the UHR (OR = 1.331 per SD increase, 95% CI: 1.100, 1.611). The positive connection of the UHR with NAFLD risk persisted significantly in female subjects but not in male subjects in subgroup analyses stratified by gender. The non-linear relationship analysis demonstrated that a UHR between ~20 and 30% suggested a saturation effect of NAFLD risk. Furthermore, a dramatically positive correlation was found between the UHR and hepatic steatosis severity but not fibrosis. Finally, the receiver operating characteristic analysis suggested that UHR had a better predictive value for NAFLD than either serum uric acid (sUA) or high-density lipoprotein cholesterol (HDL) alone [UHR (area under curve): 0.6910; 95% CI: 0.6737-0.7083; P < 0.0001]. Conclusion: Our investigation revealed that the elevated UHR level was independently related to an increased NAFLD risk and the severity of liver steatosis in American individuals. The correlation differed according to sex. This non-invasive indicator may enhance the capacity to predict the onset of NAFLD and may uncover alternative therapeutic interventional targets.

The high frequency oscillation in orbitofrontal cortex is susceptible to phenethylamine psychedelic 25C-NBOMe in male rats.

Serotoninergic psychedelics induced extensive alterations in perception and cognition, which has been attributable to its disruptive effect on oscillatory rhythms of prefrontal cortex. However, there is a lack of information how serotoninergic psychedelics affect the intra-prefrontal network, which intrinsically interact to accomplish perceptual processing. Uncovering the altered neural network caused by psychedelics helps to understand the mechanisms of their psychoactive effects and contribute to develop biological markers of psychedelic effects. In present study, we investigated the effects of substituted phenethylamine psychedelic 25C-NBOMe on neural oscillations in the intra-prefrontal and hippocampal-prefrontal network. The effective dose of 25C-NBOMe (0.1 mg/kg) disrupting sensorimotor gating in male Sprague-Dawley rats was used to observe its effects on neural oscillations in the prelimbic cortex, anterior cingulate cortex, orbitofrontal cortex (OFC) and hippocampus CA1. The power of high frequency oscillation (HFO, 120-150 Hz) was potentiated by 25C-NBOMe selectively in the OFC, with peaking at 20-30 min after treatment. 25C-NBOMe strengthened HFO coherence within the intra-prefrontal, rather than hippocampal-prefrontal network. Potentiated HFO in the OFC had a strong positive correlation with the strengthened inter-prefrontal HFO coherence by 25C-NBOMe. The 25C-NBOMe-induced alterations of rhythmic patterns were prevented by pre-treatment with selective serotonin 2A receptor antagonist MDL100,907. These results demonstrate that OFC rhythmic activity in HFO is relatively susceptible to substituted phenethylamine and potentially drives drug-induced rhythmic coherence within intra-prefrontal regions. Our findings provide additional insight into the neuropathophysiology of the psychoactive effects of psychedelics and indicate that the altered HFO might be applied as a potential biological marker of psychedelic effect.