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Nonalcoholic fatty liver disease （NAFLD） is currently the main cause of chronic liver disease worldwide， and it can progress to hepatitis， liver fibrosis， liver cirrhosis， and even hepatocellular carcinoma. Although obesity plays a key role in the development of NAFLD， more and more studies have confirmed that NAFLD still exists in lean individuals， and lean NAFLD is associated with an increased risk of death and accelerated disease progression. Therefore， lean NAFLD also deserves careful evaluation and follow-up； however， we still know little about the pathophysiological mechanism of lean NAFLD. This article reviews the etiology， diagnosis， treatment， and prognosis of lean NAFLD.
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Background: The occurrence of gastrointestinal symptoms in cirrhotic patients with gastroesophageal varices (GOV) after endoscopic treatment is obvious, and the role of gastric myoelectrical activity (GMA) and autonomic nerve function imbalance in the development of gastrointestinal symptoms has not been clarified. Aims: To investigate the changes of GMA and autonomic nerve function in cirrhotic patients with GOV after endoscopic treatment. Methods: Twenty-five cirrhotic patients with GOV from May 2019 to October 2019 at the First Affiliated Hospital of Nanjing Medical University were enrolled, and 10 patients with gastric polyp were served as controls. Electrogastrogram (EGG) and heart rate variability (HRV) were detected before the operation, 1 day after the operation and 5 days after the operation in GOV group. For the gastric polyp group, EGG and HRV were detected before the operation and 1 day after the operation. Changes of GMA and autonomic nerve function were compared between the two groups. Results: No significant differences in GMA and autonomic nerve function were found between GOV group and gastric polyp group before and 1 day after the operation (P>0.05). LF, LF/HF were significantly increased 1 day after the operation in GOV group (P0.05). There were no significant differences in GMA and autonomic nerve function 1 day after the operation compared with pre-operation in gastric polyp group (P>0.05). Compared with Child-Pugh A group, Child-Pugh B group had more obvious GMA abnormalities, and the difference was statistically significant (P<0.05). Conclusions: In cirrhotic patients with GOV, the percentage of bradygastria and the sympathetic activity increased, and the vagal activity decreased 1 day after the operation. These results suggest that GMA and autonomic nerve dysfunction may be related to the gastrointestinal symptoms after endoscopic treatment.
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Background:Non-alcoholic fatty liver disease(NAFLD)is one of the most common chronic liver diseases worldwide and specific targeted therapy is still lacking up to now. Aims:To investigate the protective effect of berberine on high fat diet(HFD)-induced hepatic lipotoxicity in mice and its potential mechanisms. Methods:Thirty male C57BL/6J mice were randomly assigned to three groups,then fed either with standard diet or HFD or HFD plus berberine(200 mg/kg per day intragastrically)for 12 weeks. Serum biochemical indices including ALT,AST,TC,TG and glucose were measured at the end of the 12th week. HE staining was used to observe liver inflammation,and fatty infiltration was detected with oil red staining. Ileocecal feces was collected and the composition of gut microbiota was analyzed by 16S rRNA sequencing. Serum level of LPS and hepatic levels of TNF-α and IL-6 were detected by ELISA. In vitro,the primary hepatic macrophages of C57BL/6J mice were challenged with palmitic acid,LPS and/or berberine,respectively;the ultrastructure of macrophages was observed using electron microscope,and the proinflammatory cytokines were detected by real-time PCR. Results:In vivo,the treatment of berberine improved the liver dysfunction,hyperlipidemia and hyperglycemia in mice fed with HFD. Also,berberine significantly inhibited the HFD-induced hepatic lipid accumulation,and alleviated hepatocytes ballooning and lobular inflammatory cell infiltration;the levels of serum LPS and hepatic IL-6 were markedly decreased. 16S rRNA sequencing showed that berberine supplementation restored the abundance of Bacteroidaceae and Desulfovibrionaceae in ileocecus,which were disturbed by HFD. In vitro,berberine not only significantly reduced the palmitic acid-induced lipid accumulation in primary hepatic macrophages,but also decreased the expressions of TNF-α and IL-6 in macrophages stimulated with LPS. Conclusions:Berberine can ameliorate effectively the hepatic lipid accumulation and inflammation in mice with experimental NAFLD. The mechanism of its antiinflammatory effect might be related with regulating the gut microbiota,reducing the LPS production,and subsequently inhibiting the release of inflammatory cytokines by hepatic macrophages.