Impact of serum levels of lipoprotein lipase, hepatic lipase, and endothelial lipase on the progression of coronary artery disease

Purpose: The purpose of this study was to investigate the relationship between serum levels of lipoprotein lipase(LPL), hepatic lipase(HL), and endothelial lipase(EL) and the progression of coronary artery disease(CAD).Materials and methods: According to the inclusion criteria, exclusion criteria, diagnostic criteria, angiography results, and the random matching scheme, the enrolled patients were divided into the following two groups: the progression-free group(n ? 47) and the progression group(n ? 15). The baseline characteristics and various biochemical parameters were obtained from the medical records and medical history. Serum LPL, HL, and EL levels were detected by ELISA. The correlation between serum LPL, HL, and EL levels and coronary lesions was statistically analyzed with SPSS software.Results: Significant differences were observed in serum levels of HL and EL between the progression-free group and the progression group(HL, 75.5 ? 39.2 ng/mL vs. 125.1 ? 42.1 ng/mL, P < 0.05;EL, 139.2 ? 59.6 pg/mL vs.175.1 ? 40.1 pg/mL, P < 0.05), while the difference in the LPL level was not significant(P > 0.05). Receiver operating characteristic curve(ROC) analysis showed that the area under the curve(AUC) values of LPL, HL, and EL were 0.506(95% CI: 0.369–0.642, P ? 0.9470), 0.792(95% CI: 0.664–0.888, P < 0.0001), and 0.693(95% CI:0.553–0.811, P ? 0.0095), respectively. Additionally, logistic regression analysis showed that the serum level of HL was an independent risk factor for coronary artery lesion progression.Conclusion: Serum levels of EL and HL, but not the serum level of LPL, were positively correlated with the progression of CAD. The serum level of HL was an independent risk factor for the progression of CAD, while the serum level of EL or LPL was not an independent risk factor for the progression of CAD. For the diagnosis of CAD progression, the serum level of HL was better than the serum level of EL or LPL.

Intestinal Barrier Function in the Pathogenesis of Nonalcoholic Fatty Liver Disease

Nonalcoholic fatty liver disease(NAFLD)is the most common chronic liver disease worldwide.The mechanisms involved in NAFLD onset are complicated and multifactorial.Recent literature has indicated that altered intestinal barrier function is related to the occurrence and progression of liver disease.The intestinal barrier is important for absorbing nutrients and electrolytes and for defending against toxins and antigens in the enteric environment.Major mechanisms by which the intestinal barrier influences the development of NAFLD involve the altered epithelial layer,decreased intracellular junction integrity,and increased intestinal barrier permeability.Increased intestinal permeability leads to luminal dysbiosis and allows the translocation of pathogenic bacteria and metabolites into the liver,inducing inflammation,immune response,and hepatocyte injury in NAFLD.Although research has been directed to NAFLD in recent decades,the pathophysiological changes in NAFLD initiation and progression are still not completely understood,and the therapeutic targets remain limited.A deeper understanding on the correlation between NAFLD pathogenesis and intestinal barrier regulation must be attained.Therefore,in this review,the components of the intestinal barrier and their respective functions and disruptions during the progression of NAFLD are discussed.