Randomized Controlled Trial of Two Forms of Self-Management Group Education in Japanese People with Impaired Glucose Tolerance

The aim of this study was to determine the effectiveness of education on diabetes prevention in subjects with impaired glucose tolerance. A total of 100 subjects of impaired glucose tolerance with hemoglobin A1c (HbA1c) levels ≥5.5 to <6.1% were assigned randomly to either support or control groups. All subjects received education in 8 sessions over a 6-month period. The support group consisted of 10 members collaborating with a dietitian or a nurse who learned coping skills by employing a participant-centered approach. Participants in the support group were required to keep a diary that monitored weight, food intake and blood glucose levels, while the control group attended several lectures. Subjects assigned to the support group had a reduction in mean HbA1c levels from 5.77 ± 0.36% at baseline to 5.39 ± 0.24% at the endpoint (p<0.01). Weight, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG) levels also decreased (p<0.01) in the support group, whereas subjects in the control group had no observable reduction in these indices. After intervention, participants of the support group had improvements in their 2-h post-meal blood glucose levels. Support group education can be effective for improving glycemic control in participants when carried out in collaboration with educators and other team members

Pancreatic insulin release in vitamin C-deficient senescence marker protein-30/gluconolactonase knockout mice

We recently identified senescence marker protein-30 as the lactone-hydrolyzing enzyme gluconolactonase, which is involved in vitamin C biosynthesis. In this study, we investigated the effects of vitamin C on insulin secretion from pancreatic β-cells using senescence marker protein-30/gluconolactonase knockout mice. In intraperitoneal glucose tolerance tests, vitamin C-deficient senescence marker protein-30/gluconolactonase knockout mice demonstrated impaired glucose tolerance with significantly lower blood insulin levels at 30 and 120 min post-challenge than in wild type mice (p<0.01–0.05). In contrast, vitamin C-sufficient senescence marker protein-30/gluconolactonase knockout mice demonstrated significantly higher blood glucose and lower insulin only at the 30 min post-challenge time point (p<0.05). Senescence marker protein-30/gluconolactonase knockout mice showed enhanced insulin sensitivity regardless of vitamin C status. Static incubation of islets revealed that 20 mM glucose-stimulated insulin secretion and islet ATP production were significantly decreased at 60 min only in vitamin C-deficient SMP30/GNL knockout mice relative to wild type mice (p<0.05). These results indicate that the site of vitamin C action lies between glycolysis and mitochondrial oxidative phosphorylation, while SMP30 deficiency itself impairs the distal portion of insulin secretion pathway

Possible role of tumor necrosis factor and interleukin-1 in the development of diabetic nephropathy

Possible role of tumor necrosis factor and interleukin-1 in the development of diabetic nephropathy. The possibility that tumor necrosis factor (TNF) and interleukin-1 (IL-1) could participate in the development of diabetic nephropathy was evaluated in streptozocin (STZ)-treated diabetic rats. Diabetic rats were divided into two groups: aminoguanidine treated group (25 mg/kg body wt, daily i.p. injection; DM-AG group) and untreated group (DM group). Non-diabetic age-matched rats were also divided into two groups with the same manner and used as controls. After twelve weeks of treatment, glomerular basement membranes (GBM) were isolated from rats of each experimental group. When thioglycollate-elicited peritoneal macrophages (Mø) from normal rats were incubated with these GBM materials, GBM from DM group induced significantly greater levels of TNF and IL-1 production than did GBM from other three groups with at doses of 2.5 to 10 mg. The TNF and IL-1 production by stimulation of GBM from the DM-AG group were similar to those from each control group. Aminoguanidine treatment significantly decreased the accumulation of advanced glycation end-products (AGEs) in GBM of diabetic rats. These findings suggest that AGE-proteins may be involved in the production of TNF and IL-1 from Mø AGE-induced cytokines may be implicated in the development of diabetic nephropathy