TYK2 Promoter Variant Is Associated with Impaired Insulin Secretion and Lower Insulin Resistance in Japanese Type 2 Diabetes Patients.

Accumulating evidence has suggested that viral infection causes type 1 diabetes due to direct ß-cell damage and the triggering of autoimmune reactivity to ß cells. Here, we elucidated that the tyrosine kinase 2 (Tyk2) gene, encoding an interferon receptor signaling molecule, is responsible for virus-induced diabetes in mice, and its promoter variant confers a risk of type 1 diabetes in humans. This study investigated the relationship between a TYK2 promoter variant (TYK2PV) and insulin secretion in type 2 diabetes patients. TYK2PV status was determined using direct DNA sequencing and its associations with fasting insulin, C-peptide, and homeostatic model assessment of insulin resistance (HOMA-IR) were evaluated in type 2 diabetes patients without sulfonylurea or insulin medication. Of the 172 patients assessed, 18 (10.5%) showed TYK2PV-positivity. Their body mass index (BMI) was significantly lower than in those without the variant (23.4 vs. 25.4 kg/m2, p = 0.025). Fasting insulin (3.9 vs. 6.2 µIU/mL, p = 0.007), C-peptide (1.37 vs. 1.76 ng/mL, p = 0.008), and HOMA-IR (1.39 vs. 2.05, p = 0.006) were lower in those with than in those without the variant. Multivariable analysis identified that TYK2PV was associated with fasting insulin ≤ 5 µIU/mL (odds ratio (OR) 3.63, p = 0.025) and C-peptide ≤ 1.0 ng/mL (OR 3.61, p = 0.028), and also lower insulin resistance (HOMA-IR ≤ 2.5; OR 8.60, p = 0.042). TYK2PV is associated with impaired insulin secretion and low insulin resistance in type 2 diabetes. Type 2 diabetes patients with TYK2PV should be carefully followed in order to receive the appropriate treatment including insulin injections.

Knowledge of Vibrio vulnificus infection among Japanese patients with liver diseases: a prospective multicenter study.

BACKGROUND: Vibrio vulnificus (V. vulnificus) is a seafood-borne infectious pathogen that can be lethal to humans. The infection has been correlated with pre-existing liver disease, particularly liver cirrhosis. Awareness of V. vulnificus infection among Japanese citizens is low, despite the increasing number of patients with hepatocellular carcinoma (HCC). The present study was conducted to assess the level of knowledge of patients with liver disease regarding V. vulnificus infection. MATERIAL/METHODS: Questionnaires were sent to patients with chronic liver disease who had been treated by liver specialists at 14 medical institutes. RESULTS: Of 1,336 patients, 304 (22.8%) had liver cirrhosis, and 732 (54.8%) had comorbidities of this disease. Only 14.5% (194/1,336) of patients had knowledge of V. vulnificus infection. Of 304 patients with liver cirrhosis, 17.4% (53/304) of the patients had knowledge of V. vulnificus infection. Of 60 patients with liver cirrhosis and diabetes mellitus, 11 (18.3%) patients had knowledge of V. vulnificus infections. Even when the patients with high risk factors such as liver cirrhosis and diabetes mellitus had knowledge of V. vulnificus infections, most ate raw seafood without regard to season. CONCLUSIONS: Patients with chronic liver diseases and their physicians need to be better educated about V. vulnificus infection and its prevention.

A patient with hyperlipidemia who had a gallbladder stone caused by administration of fenofibrate.

Fibrates are widely used for treatment of hyperlipidemia. It has been reported that gallbladder stones are formed by administration of clofibrate. It is thought that fenofibrate can cause the formation of gallbladder stone as a side effect. We encountered a patient with hyperlipidemia in whom a gallbladder stone was detected by computed tomographic scanning 3 months after the start of administration of fenofibrate during follow-up observation by blood biochemical examination and computed tomographic scanning. This case report will be of great value and importance.