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Key Clinical Message: Atezolizumab and bevacizumab combination therapy might be one of the treatment options for hepatocellular carcinoma concurrent with gastric adenocarcinoma. [ABSTRACT FROM AUTHOR]

Three Japanese adolescents with chronic hepatitis C were treated by direct‐acting antivirals (DAAs). No adverse events or laboratory abnormalities were observed during and after DAA therapy, and a sustained virological response was achieved in all cases. The emotional functioning of the patients and their mothers were improved after DAA therapy. Key Clinical Message: The efficacy/safety of therapy with direct‐acting antivirals for chronic hepatitis C in Japanese adolescents were favorable and the improvement of emotional functioning of them and their mothers by viral eradication was observed in all cases. [ABSTRACT FROM AUTHOR]

Noonan syndrome is a genetic multisystem disorder and is associated with mutation of genes encoding the proteins in the RAS‐MAPK pathway. We reported the first case of Noonan syndrome complicated with hepatocellular carcinoma. [ABSTRACT FROM AUTHOR]

Dysregulation of glucagon is associated with the pathophysiology of type 2 diabetes. We previously reported that postprandial hyperglucagonemia is more obvious than fasting hyperglucagonemia in type 2 diabetes patients. However, which nutrient stimulates glucagon secretion in the diabetic state and the underlying mechanism after nutrient intake are unclear. To answer these questions, we measured plasma glucagon levels in diabetic mice after oral administration of various nutrients. The effects of nutrients on glucagon secretion were assessed using islets isolated from diabetic mice and palmitate-treated islets. In addition, we analyzed the expression levels of branched chain amino acid (BCAA) catabolism-related enzymes and their metabolites in diabetic islets. We found that protein, but not carbohydrate or lipid, increased plasma glucagon levels in diabetic mice. Among amino acids, BCAAs, but not the other essential or nonessential amino acids, increased plasma glucagon levels. BCAAs also directly increased the intracellular calcium concentration in α cells. When BCAAs transport was suppressed by an inhibitor of system L-amino acid transporters, glucagon secretion was reduced even in the presence of BCAAs. We also found that the expression levels of BCAA catabolism-related enzymes and their metabolite contents were altered in diabetic islets and palmitate-treated islets compared to control islets, indicating disordered BCAA catabolism in diabetic islets. Furthermore, BCKDK inhibitor BT2 suppressed BCAA-induced hypersecretion of glucagon in diabetic islets and palmitate-treated islets. Taken together, postprandial hypersecretion of glucagon in the diabetic state is attributable to disordered BCAA catabolism in pancreatic islet cells. [ABSTRACT FROM AUTHOR]