Serum syndecan-4 is associated with nonalcoholic fatty liver disease.

OBJECTIVES: The accelerated shedding of extracellular domains of syndecan-4 (SDC4) is associated with central obesity and insulin resistance, while the association between serum SDC4 and nonalcoholic fatty liver disease (NAFLD) is unknown. We aimed to examine the association between SDC4 and NAFLD. METHODS: Adults undergoing a health examination from 1 June 2019 to 31 December 2019 were enrolled. A diagnosis of NAFLD was made with an abdominal ultrasound. Logistic regression models and the receiver operating characteristic (ROC) curves were used to evaluate the role of SDC4 in predicting NAFLD. RESULTS: In total, 533 eligible participants were finally enrolled, among them 157 (29.46%) had NAFLD. The proportion of patients with NAFLD increased with the increasing quartiles of serum SDC4. With the increase of serum SDC4 levels, metabolic features including waist circumference, serum triglyceride, total cholesterol, fasting blood glucose, fasting insulin and homeostasis model assessment of insulin resistance were significantly increased. SDC4 was an independent factor for NAFLD (odds ratio 1.963, 95% confidence interval [CI] 1.628-2.367, P < 0.001). The area under the ROC curve of SDC4 for predicting NAFLD was 0.934 (95% CI 0.910-0.959). The optimal cut-off value was 6.575 ng/mL at Youden's index of 0.767. SDC4 had the highest diagnostic sensitivity (84.1%), positive predictive value (82.5%), negative predictive value (93.3%) and positive likelihood ratio (11.356) among all the variables. CONCLUSIONS: Elevated serum SDC4 level is associated with metabolic disorders and the prevalence of NAFLD among general population. Serum SDC4 may serve as a biomarker of NAFLD.

[Effect of MG-132 upon the expression of intercellular adhesion molecule-1 in cerulein-induced acute pancreatitis in mice].

OBJECTIVE: To investigate the effects of the proteasome inhibitor MG-132 upnon NF-kappaB and the expression of intercellular adhesion molecule-1 (ICAM-1) in cerulein-induced acute pancreatitis (AP) in mice. METHODS: Forty-five BalB/c mice were randomly allocated into nine groups: control 3, 6, 12 h group (n = 5); AP 3, 6, 12 h group (n = 5) and MG-132 3, 6, 12 h group (n = 5). AP group was induced by an ip injection of 100 microg/kg cerulein six times with a 1 h interval. Control group received physiological saline likewise. MG-132 group was injected ip with 10 mg/kg MG-132 at 30 min before induction of AP. The levels of serum amylase and soluble ICAM-1 (sICAM-1) were tested. The pathological changes of pancreas were observed. The expression of NF-kappaB proteins was examined by immunohistochemistry and the expression of ICAM-1 mRNA analyzed by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: In MG-132 group, the levels of serum amylase (U/L) and sICAM-1 (pg/ml) markedly decreased in comparison with AP group (1629 +/- 59, 1794 +/- 123, 2910 +/- 152 vs 1282 +/- 61, 1525 +/- 103, 1809 +/- 117, 133 +/- 10, 157 +/- 10, 217 +/- 43 vs 106 +/- 6, 135 +/- 4, 163 +/- 19, P < 0.05 or P < 0.01); the scores of pathological changes decreased in pancreas (5.7 +/- 1.0, 7.1 +/- 1.2, 9.6 +/- 2.1 vs 3.2 +/- 1.0, 5.3 +/- 1.0, 6.9 +/- 0.8, P < 0.05 or P < 0.01);the expression of NF-kappaB protein (3.8 +/- 1.1, 4.6 +/- 1.2, 6.7 +/- 0.4 vs 1.9 +/- 0.6, 3.1 +/- 1.0, 4.7 +/- 1.0, P < 0.05 or P < 0.01) were significantly lowered than those in AP group. ICAM-1 mRNA also decreased more than those in AP group (0.3 +/- 0.1, 1.0 +/- 0.2, 1.2 +/- 1.0 vs 0.3 +/- 0.2, 1.8 +/- 0.2, 2.1 +/- 0.2, P < 0.05 or P < 0.01). CONCLUSIONS: The proteasome inhibitor MG-132 can obviously improve the outcome of acute pancreatitis. And the mechanism may be related to the down-regulated expression of cytokines, including adhesion molecules, through the suppression of NF-kappaB activation.