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Recently the common adiponutrin (PNPLA3) polymorphism p.I148M has been identified as a genetic determinant of severe forms of non-alcoholic fatty liver disease and alcoholic liver disease. Additionally, insulin resistance - linked to the development of non-alcoholic steatohepatitis - increases the risk of developing gallstones. Here we assessed whether the PNPLA3 p.I148M (c.444 C>G) polymorphism affects glucose and lipid levels and increases gallstone risk. We analysed 229 individuals with gallstones from 108 families (age 24-80 years, BMI 17-55 kg/m2) and 258 gallstone-free controls (age 20-70 years, BMI 14-43 kg/m2). Fasting glucose, triglyceride and cholesterol serum levels were determined. The p.I148M polymorphism was genotyped using a PCR-based assay with 5'-nuclease and fluorescence detection. Case-control association tests and nonparametric linkage (NPL) analysis in sib-pairs were performed. Individuals carrying the [GG] genotype had significantly (P<0.0001) higher median fasting glucose levels as compared to [GC] and [CC] carriers. After adjustment for multiple testing, we detected a trend for an association between triglyceride levels and variant adiponutrin in gallstone patients (P=0.032), and gallstone cases carrying the genotype [CC] presented with significantly higher triglyceride levels than the corresponding controls (P<0.003). No significant effects on cholesterol metabolism were detected. Neither genotype distributions nor NPL scores provided evidence for association or linkage between the PNPLA3 variant and gallstones. In conclusion, homozygous carriers of the PNPLA3 risk allele display higher fasting glucose. Although this adiponutrin variant may affect triglyceride homeostasis, it does not increase the risk of cholelithiasis.
In recent years there have been remarkable developments in the prevention of diseases, especially with regards to the role of free radicals and antioxidants. Ethanol-induced oxidative stress appears to be one mechanism by which ethanol causes liver injury. The protective effect of aqueous plant extract of Aframomum melegueta on ethanol-induced toxicity was investigated in male Wistar rats. The rats were treated with 45 % ethanol (4.8 g/kg b.w.t.) for 16 days to induce alcoholic diseases in the liver. The activities of alanine aminotransferase, aspartate aminotransferase and triglyceride were monitored and the histological changes in liver examined in order to evaluate the protective effects of the plant extract. Hepatic malondialdehyde and reduced glutathione, as well as superoxide dismutase and glutathione-S-transferase activities were determined for the antioxidant status. Chronic ethanol administration resulted in a statistically significant elevation of serum alanine aminotransferases and triglyceride levels, as well as a decrease in reduced glutathione and superoxide dismutase which was dramatically attenuated by the co-administration of the plant extract. Histological changes were related to these indices. Co-administration of the plant extract suppressed the elevation of lipid peroxidation, restored the reduced glutathion, and enhanced the superoxide dismutase activity. These results highlight the ability of Aframomum melegueta to ameliorate oxidative damage in the liver and the observed effects are associated with its antioxidant activities.
Alcoholic liver disease (ALD) is one of the most common diseases in modern society. A large number of studies are in progress aiming to identify natural substances that would be effective in reducing the severity of ALD. Although there are currently a number of drugs on the market, their long-term use can have numerous side effects. Hemidesmus indicus is an indigenous Ayurvedic medicinal plant used in soft drinks in India. In this study, we examined the effects of its ethanolic root extract on experimental liver damage in order to evaluate its hepatoprotective effects against hepatotoxicity induced in rats by ethanol at a dosage of 5 g/kg body weight for 60 days. The H. indicus root extract was given at a dose of 500 mg/kg body weight for the last 30 days of the experiment. The animals were monitored for food intake and weight gain. The liver was analysed for the degree of lipid peroxidation using thiobarbituric acid reactive substances (TBARS) and antioxidant status using the activities of glutathione-depedendant enzymes. The degree of liver damage was analysed using serum marker enzyme activities, the total protein, albumin, globulin, ceruloplasmin and liver glycogen contents, and the A/G ratio. The Fourier transform infrared spectra (FT-IR) of the liver tissues were recorded in the region of 4000–400 cm−1. The ethanol-fed rats showed significantly elevated liver marker enzyme activities, lipid peroxidation levels and reduced antioxidant levels as compared to the control rats. Oral administration of H. indicus for the latter 30 days resulted in an increased food intake and weight gain, decreased TBARS levels, near normal levels of glutathione-dependent enzymes, increased total protein, albumin, globulin and liver glycogen contents, an increased A/G ratio, and decreased liver marker enzyme activities and ceruloplasmin levels. The relative intensity of the liver FT-IR bands for the experimental groups were found to be altered significantly (p < 0.05) compared to the control samples. For the group that had H. indicus co-administered with ethanol, the intensity of the bands was near normal. Moreover, the results of the FT-IR study correlated with our biochemical results.
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