Interleukin-6, a cytokine produced by various cell types, has a major role in inflammatory and immunological reactions. To define its potential role in inflammatory bowel disease, its concentrations in endoscopic biopsy samples from patients with ulcerative colitis and Crohn’s disease were measured. The involved colonic mucosa from active disease was found to contain significantly larger amounts of interleukin-6 than that from inactive disease or normal controls. Colonic mucosal interleukin-6 levels correlated well with the grade of macroscopic inflammation, especially in patients with ulcerative colitis. The levels of interleukin-6 decreased in parallel with clinical improvement following the start of therapy in patients with both forms of inflammatory bowel disease. Mucosal interleukin-6 is thus concluded to accurately reflect the degree of colonic inflammation and may be importantly associated with inflammatory and immunological phenomena seen in inflammatory bowel disease.

We demonstrated the altered expressions of GLP-1 and DPPIV in patients with HCV-associated glucose intolerance. Since hepatic glycogen synthesis, a GLP-1 action, was impaired, the altered expressions of GLP-1 and DPPIV may be involved in the development of HCV-associated glucose intolerance.

PNI and CONUT are potential tools for nutritional assessment in patients with chronic liver disease, especially for ordinary medical care, because of their simplicity.

This study looked at the intestinal permeability and the immune response to enteric bacterial antigens in patients with inflammatory bowel disease (IBD). They were evaluated by using a lactulose tolerance test and measuring blood anti-lipid A antibody concentrations, respectively.The lactulose tolerance tests were performed 22 times in 14 patients with Crohn's disease (CD), 19 times in 12 patients with ulcerative colitis (UC), and 12 times in 12 healthy controls. Blood lactulose concentrations were measured after oral administration every two hours for eight hours, also blood C reactive protein concentrations and anti-lipid A antibody concentrations were measured just before lactulose administration. Blood lactulose concentrations were significantly higher in patients with CD than in the controls from two to eight hours after administration, while in UC they were significantly higher than in the controls from six to eight hours. Maximum blood lactulose concentrations in each tolerance test in patients with the active phase significantly exceeded those in the inactive phase of either CD or UC. A significant correlation was also seen between the maximum blood lactulose concentrations and the C reactive protein concentrations. Blood anti-lipid A antibody concentrations in patients with CD were significantly higher than in the controls as well as in patients with UC in immunoglobulin (Ig) A class and IgG class. In UC they were significantly higher than in the controls in IgA class. But, they were not related to the severity of the disease of either CD or UC, and not correlated significantly with the maximum blood lactulose concentrations in either CD or UC. The intestinal permeability and the immune response to enteric bacterial antigens in patients with inactive CD were significantly increased over those in the controls as well as in patients with inactive UC. These findings suggest that an increase of the intestinal permeability and that of producing antibodies to enteric bacterial antigens are both important for the pathogenesis of IBD, and that the characteristics of CD and UC differ.

Hepatitis C virus (HCV) infection causes insulin resistance. Because increased insulin resistance is a risk factor for development of hepatocellular carcinoma and reduced long-term survival, insulin resistance is a therapeutic target in patients with HCV infection. Branched-chain amino acids (BCAAs) are not only structural constituents of proteins but they are also considered as regulators of insulin signalling. We first describe two cases suggesting that administration of BCAAs improves insulin resistance associated with HCV-related liver disease. Although there were no changes in body weight, plasma glucose concentration and haemoglobin A1c (HbA1c) value were decreased. Moreover, BCAAs caused a decrease in both fasting insulin concentration and the value of homeostasis model assessment for insulin resistance. Thus, BCAAs are a potential therapeutic agent for improving insulin resistance in patients with HCV-related liver disease.

Abstract. Body cell mass (BCM) is a nutritional parameter, however, changes in BCM in patients with non-ascitic liver cirrhosis (LC) in comparison to patients with other malnutritional diseases remains unclear. We investigated the difference in BCM between patients with LC and malnourished gastrointestinal disease controls (M.CON), and examined the relationship between BCM and the severity of LC. Results demonstrated that serum nutritional parameters were not significantly different between the LC (n=56) and M.CON groups (n=25), whereas BCM%BW was significantly lower in the LC group than in the M.CON group (50.9±4.6 vs. 54.4±7.1%, P=0.018). Furthermore, BCM%BW negatively correlated with the model for end-stage liver disease (MELD) score (P=0.04). In concluson, BCM showed a significant decrease and a negative correlation with the MELD score in the LC group. BCM may be a useful parameter for assessing malnutrition and severity of

A 67-year-old Asian woman was referred to Kurume University Hospital due to abnormal liver function tests. She was diagnosed with nonalcoholic fatty liver disease (NAFLD). NAFLD was treated by diet therapy with medication of metformin and pioglitazone; however, NAFLD did not improve. Subsequently, the patient was administered sitagliptin. Although her energy intake and physical activity did not change, her hemoglobin A1c level was decreased from 7.8 to 6.4% 3 months after treatment. Moreover, her serum insulin level and homeostasis model assessment-insulin resistance value were also improved, as was the severity of hepatic steatosis. These findings indicate that sitagliptin may improve insulin resistance and steatosis in patients with refractory NAFLD.

No abstract