We investigated the difference in the inhibitory effect against a blood sugar level increase based on the fiber content of different types of vegetables. The subjects were 15 healthy subjects. There were 4 types of test diets: regular diet (1), 250 g of Kitsune noodles and 200 g of rice ("regular diet (1)"); fiber, a drink containing 4 g of indigestible dextrin ("test diet (2)"); radish salad ("test diet (3)"); and okra salad ("test diet (4)"). Regular diet (1) was ingested after finishing the dietary fiber for test diets (2) to (4). Blood glucose measurements were performed before meals and 15, 30, 60, and 120 minutes after meals. To compare the regular diet (1) group with each test diet, Wilcoxon's rank sum test was performed. A significant difference (Z= −2.075, p= 0.037) was observed 15 minutes after meals between the regular diet (1) group and the test diet (4) group. There were no significant differences at other times or between other diets tested. It was believed that viscous fiber had a better blood glucose suppression effect 15 minutes after meals than at other time points.

Since a serum level of alanine aminotransferase (ALT) exceeding that of aspartate aminotransferase (AST) suggests hyperalimentary fatty liver, we examined its prevalence among and the clinical characteristics of afflicted type 2 diabetic patients as well as the effect of antidiabetic agents on AST/ALT with the CoDiC-MS database prepared by the Japan Diabetes Clinical Data Management study group (JDDM). AST<ALT patients accounted for 37.5 % of 12,710 participants. These patients tended to be more frequently male, younger, and have higher values of body mass index, HbA1c, serum triglyceride, serum C peptide immunoreactivity, and HOMA-IR and lower values of FIB-4 index and rates of diabetic complications than AST≥ALT patients. Pioglitazone and sodium-glucose cotransporter 2 inhibitors remarkably reduced the ALT level, and 24.9 % of AST<ALT patients became AST≥ALT 1 year after starting these prescriptions. A multiple comparison test indicated that these patients tended to be more frequently female, older, and have a longer duration of diabetes mellitus, lower AST and HSI values and higher body mass index, γ-glutamyl transpeptidase, and FIB-4 index values than others.

We herein report an elderly patient on hemodialysis with persistent symptomatic hypoglycemia due to insulinoma. A 91-year-old woman without a history of diabetes mellitus was receiving hemodialysis. Since she demonstrated delirium and unconsciousness with a blood glucose level of <58 mg/dL, she required continuous infusion of glucose to avoid symptomatic hypoglycemia; however, due to the limited volume of liquid administration available for hemodialysis, high-calorie infusion was administered via a central venous port. Blood sampling during the hypoglycemic attacks revealed a blood glucose level of 5 mg/dL, serum insulin (IRI) level of 267 μU/mL, and serum C peptide level of 60.5 ng/mL, indicating hyperinsulinemic hypoglycemia. Insulioma was suspected as a differential diagnosis, but computed tomography did not detect hypervascular tumors in the pancreas. Selective arterial calcium injection (SACI) was not performed due to her age and dialysis status. Diazoxide was orally administered at treatment, and diazoxide at 100 mg in the morning and 150 mg in the evening on the day of hemodialysis ultimately resulted in the time in range (56 through 158 mg/dL) of her blood glucose level being 98 %, estimated flash glucose monitoring. The present case highlights the clinical utility of diazoxide for treating persistent hypoglycemia due to insulinoma with no indication of operation; however, dose titration is needed for patients on hemodialysis.

Introduction: Gain-of-function mutations in ATP-sensitive potassium channel (K_ATP channel) genes cause neonatal and juvenile-onset diabetes mellitus. Sulfonylureas are known to be effective for K_ATP channel diabetes. We herein report a case of poorly-controlled K_ATP channel diabetes that showed a marked response to high-dose glibenclamide. Case: A 17-year-old male had developed neonatal diabetes mellitus due to a c.124T>C (p.C42R) mutation in the KCNJ11 gene at 47 days old and then gone into remission around 1 year old. At 9 years old, his diabetes recurred, and he was treated with glimepiride 0.5 mg. From 15 years old, his glycemic control worsened, and he was treated with a combination of glimepiride 1 mg and saxagliptin 5 mg, but his HbA1c worsened to 11.1 %. After glibenclamide loading, good secretion of endogenous insulin was observed, and the treatment was changed to glibenclamide monotherapy. The HbA1c value quickly decreased to the 6 % range, and the patient has maintained good glycemic control without significant hypoglycemia. Conclusion: K_ATP-channel diabetes mellitus requires a different therapeutic strategy from ordinary type 2 diabetes mellitus. A correct diagnosis is key to successful treatment.

Diabetic gastroparesis (DG) is a serious yet underdiagnosed and undertreated condition, posing a challenge to the management of diabetes patients. The symptoms are non-specific, diagnostic standards are unestablished, and pharmacological approaches often fail. We herein report a 65-year-old female type 1 diabetic patient who suffered from severe malnutrition. She was diagnosed with DG by gastric emptying scintigraphy with egg white labeled with 99mTc-sulfur colloid. The condition was refractory to pharmacological treatments, and the patient kept losing weight. Laparoscopic subtotal gastrectomy was ultimately performed, and the symptoms were relieved, allowing the patient to regain weight. At three years after surgery, she was able to return to her social activities.

A 53-year-old man visited our hospital because of severe appetite loss, thirst, and nausea. He had been receiving treatment for type 2 diabetes mellitus for the past nine years and had also been receiving pembrolizumab therapy as second-line treatment for ureter cancer for the past three months. Severe hyperglycemia, insulin secretion deficiency (fasting plasma C-peptide, 0.3 ng/mL), and ketosis after pembrolizumab administration led to the diagnosis of pembrolizumab-induced type 1 diabetes mellitus. Even two years after the onset of type 1 diabetes mellitus, his insulin secretion remained decreased. Several cases of programmed death receptor-1 (PD-1) antibody-induced type 1 diabetes mellitus in patients with type 2 diabetes mellitus have been reported. Previous case reports revealed that the HbA1c value at the diagnosis in PD-1 antibody-induced type 1 diabetes mellitus that developed from type 2 diabetes mellitus was higher than X, and all reported cases were in men. Immune checkpoint inhibitors, including PD-1 antibody, are widely used for advanced malignancy treatment in patients with type 2 diabetes mellitus. Clinicians should thus carefully monitor patients for ketosis or ketoacidosis-related symptoms, glycemic control, and endogenous insulin secretion when administering PD-1 antibody therapy, even in those who already have type 2 diabetes mellitus.

A woman in her 50s had suffered repeated hypoglycemic episodes since her 20s and been diagnosed with reactive hypoglycemia 7 years ago. She was found to have diabetes (HbA1c: 9.3 %) with 15 kg of weight gain (body mass index: 26.0 kg/m²) and was admitted to our hospital 1 year ago. Although her glycemic control improved, hypoglycemia (30-40 mg/dL) began to occur from two months before her most recent admission, and she was referred to our hospital again. She was not taking any causative medication for the hypoglycemia. Insulin autoantibody was negative, and adrenal insufficiency was not found. No tumor lesions were detected in her pancreas. The 75 g-OGTT demonstrated remarkable hyperinsulinemia after glucose loading (Before: plasma glucose [PG] level, 94 mg/dL and immunoreactive insulin (IRI), 9.1 μU/mL; 120 min: PG, 209 mg/dL and IRI, 545.0 μU/mL), and the PG level decreased to 46 mg/dL at 5 h. A fasting test was negative (PG: 50 mg/dL, IRI: 2.1 μU/mL at 72 h), and the PG value increased after glucagon loading (ΔPG 17 mg/dL). The Selective Arterial Calcium Injection (SACI) test revealed that the serum IRI level more than doubled (8.6 to 17.7 μU/mL) after calcium injection into the superior mesenteric artery. Based on these observations, the pathophysiology of her hypoglycemia was considered to be non-insulinoma pancreatogenous hypoglycemia syndrome (NIPHS). After dulaglutide was started, her PG profile promptly flattened, and her symptomatic hypoglycemia disappeared.