Metabolic syndrome as a risk factor for gallstone disease

AIM: To establish an association between the presence of metabolic syndrome and the development of gallstone disease.METHOIDS: We carried out a cross-sectional study in a check-up unit in a university hospital in Mexico City. We enrolled 245 subjects, comprising 65 subjects with gallstones (36 women, 29 men) and 180 controls (79women and 101 men without gallstones). Body mass index, waist circumference, blood pressure, plasma insulin, and serum lipids and lipoproteins levels were measured. Insulin resistance was calculated by homeostasis model assessment. Unconditional logistic regressionanalysis (univariate and multivariate) was used to calculate the risk of gallstone disease associated with the presence of at least three of the criteria (Adult Treatment Panel Ⅲ). Analyses were adjusted for age and sex.RESULTS: Among 245 subjects, metabolic syndrome was present in 40% of gallstone disease subjects, compared with 17.2% of the controls, adjusted by age and gender (odds ratio (OR) = 2.79; 95%CI, 1.46-5.33; P = 0.002),a dose-dependent effect was observed with each component of metabolic syndrome (OR = 2.36, 95%CI, 0.72-7.71;P = 0.16 with one component and OR = 5.54, 95%CI,1.35-22.74; P = 0.02 with four components of metabolic syndrome). Homeostasis model assessment was significantly associated with gallstone disease (adjusted OR = 2.25;95%CI, 1.08-4.69; P = 0.03).CONCLUSION: We conclude that as for cardiovascular disease and diabetes mellitus, gallstone disease appears to be strongly associated with metabolic syndrome.

Serum leptin levels and insulin resistance are associated with gallstone disease in overweight subjects

AIM: To establish an association between the serum leptin levels and the development of gallstone disease (GD).METHODS: We carried out a non-matched case-controlled study in a university hospital in Mexico City. Two hundred and eighty-seven subjects were included: 97 cases with gallstones and 190 controls. Body mass index (BMI), fasting plasma leptin, insulin, serum lipid, and lipoprotein levels were measured. Insulin resistance was calculated by homeostasis model assessment (HOMA-IR). Unconditional logistic regression analysis (univariate and multivariate)stratified by BMI was used to calculate the risk of GD.RESULTS: The multivariate conditional regression analysis revealed a model for those patients with BMI ＜30. The selected variables in the model were HOMA-IR index with OR = 1.31, P= 0.02 and leptin higher than median with OR = 2.11, P= 0.05. In the stratum of BMI ≥30, we did not find a useful model.CONCLUSION: We concluded that insulin resistance and the development of GD appears to be associated with serum leptin levels in subjects with overweight, but not in obese subjects with similar metabolic profiles.

Low serum levels of ghrelin are associated with gallstone disease

瞄准：在胆石疾病探索 ghrelin 的角色。方法：我们在 150 个题目，执行了代表性的研究 38 与胆石(盒子) 和 112 控制。我们也各在二十件胆囊样品做了即时 PCR-RT 研究。身体集体索引(BMI ) ，浆液胰岛素， ghrelin，和浆液类脂化合物被测量。逻辑回归分析(univariate 并且多变量) 被进行估计与浆液 ghrelin 集中联系的胆石疾病的概率。结果：盒子与在性分发的控制统计上不同(P = 0.01 ) ，年龄(53 对 44 年， P = 0.002 ) ， BMI (28 对 25；P = 0.004 ) ，并且葡萄糖(5.26 对 4.98 mmol/L；P = 0.05 ) 。没有新陈代谢的症候群，在第三 tercile 上面的 ghrelin 浆液层次的流行在题目是更低的(P 【 0.05 ) 。在里面一多，变量当模特儿，当 ghrelin 价值比中部的价值高时，我们发现了保护的效果(或 = 0.27， 95%CI 0.09-0.82， P = 0.02 ) 。二十(20%) 胆囊标本表示了 ghrelin mRNA。结论：浆液 ghrelin 集中与 GD 的保护的效果被联系。

The mechanism of dysbiosis in alcoholic liver disease leading to liver cancer

Currently, alcoholic liver disease (ALD) is one of the most prevalent chronic liver diseases worldwide, representing one of the main etiologies of cirrhosis and hepatocellular carcinoma (HCC). Although we do not know the exact mechanisms by which only a selected group of patients with ALD progress to the final stage of HCC, the role of the gut microbiota within the progression to HCC has been intensively studied in recent years. To date, we know that alcohol-induced gut dysbiosis is an important feature of ALD with important repercussions on the severity of this disease. In essence, an increased metabolism of ethanol in the gut induced by an excessive alcohol consumption promotes gut dysfunction and bacterial overgrowth, setting a leaky gut. This causes the translocation of bacteria, endotoxins, and ethanol metabolites across the enterohepatic circulation reaching the liver, where the recognition of the pathogen-associated molecular patterns via specific Toll-like receptors of liver cells will induce the activation of the nuclear factor kappa-B pathway, which releases pro-inflammatory cytokines and chemokines. In addition, the mitogenic activity of hepatocytes will be promoted and cellular apoptosis will be inhibited, resulting in the development of HCC. In this context, it is not surprising that microbiota-regulating drugs have proven effectiveness in prolonging the overall survival of patients with HCC, making attractive the implementation of these drugs as co-adjuvant for HCC treatment.