Nobumasa Ohara

Quantitative relationship between body weight gain in adulthood and incident type 2 diabetes: a meta-analysis.

This meta‐analysis quantified the risk of type 2 diabetes mellitus (T2DM) preceded by body weight (BW) gain in the general population. Systematic literature searches retrieved 15 eligible studies. The BW gain was divided into early weight‐gain, which was defined as BW gain from early adulthood (18–24 years of age) to cohort entry (≥25 years of age), and late weight‐gain, which was defined as BW gain from cohort entry. The pooled relative risk (RR; 95% confidence interval [CI]) of T2DM for an increment of BW gain standardized into a 5‐kg m−2 increment in the body mass index (BMI) was 3.07 (2.49–2.79) for early weight‐gain and 2.12 (1.74–2.58) for late weight‐gain. When limiting analysis to studies that concurrently examined T2DM risk for current BMI (defined in both groups as BMI at cohort entry), a larger magnitude of T2DM risk was revealed for early weight‐gain compared with current BMI (RR [95% CI], 3.38 [2.20–5.18] vs. 2.39 [1.58–3.62]), while there was little difference between late weight‐gain (RR [95% CI], 2.21 [1.91–2.56]) and current BMI (RR [95% CI], 2.47 [1.97–3.30]). The meta‐analysis suggested that BW gain was a quantifiable predictor of T2DM, as well as current obesity in adults. Particularly, BW gain in early rather than middle‐to‐late adulthood played an important role in developing T2DM.

Risk of the development of Type 2 diabetes in relation to overall obesity, abdominal obesity and the clustering of metabolic abnormalities in Japanese individuals: does metabolically healthy overweight really exist? The Niigata Wellness Study

We investigated the risk of developing diabetes across various metabolic phenotypes by considering the presence of overall adiposity or abdominal adiposity and the number of metabolic abnormalities and aimed to clarify whether a ‘healthy overweight’ phenotype, that is, overweight with no metabolic abnormalities, was protective of the development of diabetes.

Hypertension increases urinary excretion of immunoglobulin G, ceruloplasmin and transferrin in normoalbuminuric patients with type 2 diabetes mellitus.

Objective: Increased urinary excretion of certain plasma proteins, such as immunoglobulin G (IgG), ceruloplasmin and transferrin, with different molecular radii of 55 Å or less and different isoelectric points have been reported to precede development of microalbuminuria in patients who have diabetes mellitus with hypertension. We examined how hypertension affects these urinary proteins in a diabetic state. Methods: Excretion of IgG, ceruloplasmin, transferrin, albumin, &agr;2-macroglobulin with a large molecular radius of 88 Å and N-acetylglucosaminidase in first-morning urine samples were measured in normoalbuminuric patients (urinary albumin-to-creatinine ratio < 15 mg/g) with hypertension and nondiabetes mellitus (group hypertension, n = 32), type 2 diabetes mellitus and normotension (group diabetes mellitus, n = 52) and type 2 diabetes mellitus and hypertension (group Both, n = 45), and in age-matched controls (n = 72). Results: Urinary IgG, ceruloplasmin, transferrin, albumin and N-acetylglucosaminidase and estimated glomerular filtration rate (eGFR) were significantly elevated in groups diabetes mellitus and Both compared with controls. Furthermore, urinary IgG, ceruloplasmin and transferrin in group Both were significantly higher than those in group diabetes mellitus. These exhibited a positive and relatively strong association with eGFR compared with controls. No significant difference in urinary albumin or N-acetylglucosaminidase was found between the two diabetic groups. In contrast, group hypertension had elevated urinary transferrin without any changes in the other compounds. Urinary &agr;2-macroglobulin did not differ among the four groups. Conclusion: These findings suggest that normoalbuminuric diabetic patients without hypertension have both glomerular hemodynamic changes such as increased intraglomerular hydraulic pressure and altered proximal tubules, and that hypertension increases intraglomerular hydraulic pressure. Increased urinary IgG, ceruloplasmin and transferrin may reflect an increase in intraglomerular hydraulic pressure.

Normal Response of Active GLP-1 Level like Substances to Test Meal in Non-Obese Type 2 Diabetic Japanese Patients with Complications and Receiving Treatments

Background: Study has shown no significant differences in basal and postprandial plasma active glucagon-like peptide-1 (p-active GLP-1) levels following test meal (TM) between complication- and treatment-naive non-obese Japanese patients with type 2 diabetes (T2DM) and controls. Methods: In non-obese Japanese patients with T2DM (n=23, group 1) and healthy individuals as control (n=13, group 2), blood levels of plasma glucose (PG), serum insulin (s-IRI), serum C-peptide (s-CPR) and p-active GLP-1 like substances (p-active GLP-1-S) were measured 0, 30, and 60 min after TM (520-560 kcal. 23% fat, 60% carbohydrate and 17% protein). HbA1c levels were also measured in the groups. Patients with mean of 9.2 years disease had various complications and treatment with diet, exercise and/or oral medical drugs except incretin-related drugs for hyperglycemia. Results: There was no significant difference in mean of sex, age, or BMI between groups. Means of HbA1c and basal and postprandial PG with area under curve (AUC), and HOMA-R were significantly higher in group 1 than in group 2. Means of HOMA-β and insulinogenic index after ingestion of TM were significantly lower in group 1 than in group 2. However, there were no significant differences in means of basal and postprandial with AUC levels of s-IRI, s-CPR and p-active GLP-1-S levels between groups. Conclusion: These results indicated that a response of p-active GLP-1-S to TM in non-obese Japanese patients with T2DM associated with a long duration of disease, various complications and various treatments with except incretin-related drugs was similar to those in non-obese healthy individuals.

Fulminant Type 1 Diabetes Mellitus Associated with Coxsackie Virus Type A2 Infection: A Case Report and Literature Review

A 65-year-old Japanese man presented to our hospital in June 2013 with a 6-day history of fever and fatigue, a 24-h history of thirst, and polyuria. His temperature was 37.8°C and he was alert. However, laboratory tests revealed severe hyperglycemia, undetectable C-peptide levels, and diabetic ketoacidosis. Serum antibody testing confirmed a Coxsackie virus A2 infection. A variety of viral infections are reported to be involved in the development of fulminant type 1 diabetes mellitus (FT1D). Our patient is the first reported case of FT1D associated with Coxsackie virus A2 infection and supports the etiological role of common viral infections in FT1D.

Fulminant type 1 diabetes mellitus and fulminant viral myocarditis. A case report and literature review.

A 35-year-old Japanese woman was admitted with coma following flu-like symptoms. She was diagnosed with diabetic ketoacidosis and fulminant type 1 diabetes (FT1D) and received intravenous infusion of insulin and saline. The next day, the ketoacidosis disappeared, and she recovered consciousness. However, extensive ST-segment elevations in the electrocardiogram appeared with a positive troponin test, and the patient developed pulmonary edema on day 3. An echocardiogram showed globally reduced wall motion of the left ventricle and mild pericardial effusion. Despite medical therapy with intravenous furosemide, carperitide, and catecholamines, her cardiac function deteriorated rapidly, with the left ventricular ejection fraction decreasing to 26% within 7 hours, and progressed to cardiogenic shock that afternoon. The patient received mechanical circulatory support for 4 days with intra-aortic balloon pumping and percutaneous cardiopulmonary support, and recovered fully from circulatory failure. A paired serum antibody test showed a significantly elevated titer against parainfluenza-3 virus, indicating a diagnosis of fulminant viral myocarditis. She was discharged on multiple daily insulin injection therapy, and her subsequent clinical course has been uneventful. In summary, we present a case of concurrent FT1D and fulminant viral myocarditis. Parainfluenza-3 viral infection was confirmed serologically and was considered to be a cause of both the FT1D and fulminant myocarditis.

Vildagliptin-induced acute lung injury: a case report.

BackgroundDipeptidyl peptidase-4 inhibitors are a class of oral hypoglycemic drugs and are used widely to treat type 2 diabetes mellitus in many countries. Adverse effects include nasopharyngitis, headache, elevated serum pancreatic enzymes, and gastrointestinal symptoms. In addition, a few cases of interstitial pneumonia associated with their use have been reported in the Japanese literature. Here we describe a patient who developed drug-induced acute lung injury shortly after the administration of the dipeptidyl peptidase-4 inhibitor vildagliptin.Case presentationA 38-year-old Japanese woman with diabetes mellitus developed acute respiratory failure 1 day after administration of vildagliptin. Chest computed tomography revealed nonsegmental ground-glass opacities in her lungs. There was no evidence of bacterial pneumonia or any other cause of her respiratory manifestations. After discontinuation of vildagliptin, she recovered fully from her respiratory disorder. She received insulin therapy for her diabetes mellitus, and her subsequent clinical course has been uneventful.ConclusionsThe period of drug exposure in previously reported cases of patients with drug-induced interstitial pneumonia caused by dipeptidyl peptidase-4 inhibitor varied from several days to over 6 months. In the present case, our patient developed interstitial pneumonia only 1 day after the administration of vildagliptin. The precise mechanism of her vildagliptin-induced lung injury remains uncertain, but physicians should consider that dipeptidyl peptidase-4 inhibitor-induced lung injury, although rare, may appear acutely, even within days after administration of this drug.

Meta‐analytic research on the relationship between cumulative risk alleles and risk of type 2 diabetes mellitus

Our aim is to examine the dose–response association between cumulative genetic risk and actual risk of type 2 diabetes mellitus (T2DM) and the influence of adjustment for covariates on T2DM risk through a comprehensive meta‐analysis of observational studies.

Type 1 diabetes mellitus and isolated adrenocorticotropin deficiency manifested by parkinsonism: a case report and literature review.

A 67-year-old woman developed isolated adrenocorticotropin deficiency (IAD), which manifested as lethargy, a 20-kg body weight loss, hypoglycemia, and parkinsonism, and began corticosteroid replacement. Her symptoms resolved rapidly, and her weight returned to normal within six months. However, she then developed slowly progressive type 1 diabetes mellitus (T1D) with co-existing Hashimoto thyroiditis, and commenced insulin therapy. To our knowledge, this is the first reported case of parkinsonism associated with IAD. In addition, because diabetes mellitus, including T1D, could be latent in patients with untreated IAD, careful assessment of glucose metabolism is needed after commencing corticosteroid replacement until weight regain is achieved.

Unstable bodyweight and incident type 2 diabetes mellitus: A meta-analysis

The present meta‐analysis aimed to clarify the association of unstable bodyweight with the risk of type 2 diabetes mellitus, an association that has been controversial among longitudinal studies.