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Mitsuyoshi Namba

Publications and source records attributed to Mitsuyoshi Namba.

12 recordsLinked to original sources
PubMed2006

Neogenesis and proliferation of beta-cells induced by human betacellulin gene transduction via retrograde pancreatic duct injection of an adenovirus vector.

Betacellulin (BTC) has been shown to have a role in the differentiation and proliferation of beta-cells both in vitro and in vivo. We administered a human betacellulin (hBTC) adenovirus vector to male ICR mice via retrograde pancreatic duct injection. As a control, we administered a beta-galactosidase adenovirus vector. In the mice, hBTC protein was mainly overexpressed by pancreatic duct cells. On immunohistochemical analysis, we observed features of beta-cell neogenesis as newly formed insulin-positive cells in the duct cell lining or islet-like cell clusters (ICCs) closely associated with the ducts. The BrdU labeling index of beta-cells was also increased by the betacellulin vector compared with that of control mice. These results indicate that hBTC gene transduction into adult pancreatic duct cells promoted beta-cell differentiation (mainly from duct cells) and proliferation of pre-existing beta-cells, resulting in an increase of the beta-cell mass that improved glucose tolerance in diabetic mice.

Adenoviridae↗
PubMed2006

[Glucagonoma].

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Biomarkers↗
PubMed2006

[Insulin treatment in elder patients with diabetes].

Diabetes is a highly expanding health problem in Japan, especially for older people. The prevalence of glucose intolerance and diabetes increases with age. A postprandial hyperglycemia is the primary clinical manifestation. In older diabetic patients, atherosclerotic complications (macroangiopathies), as well as microangiopathies, are significant problems, threatening their quality of life. Though insulin therapy requires some special considerations, insulin is indicated for any patients with a poor glycemic control with oral agents. Single or multiple dose (s) of insulin injection therapy is selected for each patient to prevent symptomatic hyperglycemia, or to achieve near-normal glycemic control. Also, to maintain the quality of life for these older patients, hypoglycemia, as well as hyperglycemia, should be avoided. Newly developed insulin analogue (s) may be more appropriate for preventing hypoglycemia. Another method of prevention and treatment of hypoglycemia are discussed in this article.

Aged↗
PubMed2004

Efficacy of glimepiride in type 2 diabetic patients treated with glibenclamide.

Multicentric study was conducted to evaluate the efficacy of glimepiride in the oral hypoglycemic agents therapy of type 2 diabetic patients treated with glibenclamide so far, and to claim an adequate use of this new generation sulfonylurea. In 66 diabetic outpatients, glibenclamide was switched to glimepiride. After 6 months' therapy, a significant reduction in fasting plasma IRI was observed in relatively hyperinsulinemic patients. In addition, weight reduction was achieved in patients with insulin resistance during this study. These findings suggest that glimepiride improves insulin resistance in hyperinsulinemic patients treated with glibenclamide. Also, glimepiride is favored especially for overweight, insulin-resistant patients inadequately controlled by glibenclamide.

Adult↗
PubMed2003

[Insulin therapy in diabetic patient with hypertension].

The advantage of insulin therapy for diabetic patient with hypertension is still controversial. Hyperinsulinemia, as well as insulin resistance have been known to be associated with hypertension and cardiovascular disease. Some mechanisms are reported in the conditions of hyperinsulinemia to induce hypertension and atherosclerosis. However, in many intervention studies, the intensive insulin therapy provided promising effects on preventing cardiovascular disease. Moreover, insulin have been shown to stimulate nitric oxide production by cultured endothelial cells, and to suppress the expression of intercellular adhesion molecule-1(ICAM-1), at least in vitro. In view of this anti-inflammatory effect, long-term insulin therapy may potentially have an anti-atherogenic effect.

Arteriosclerosis↗
PubMed2002

Enhancing effect of advanced glycation end products on serotonin-induced platelet aggregation in patients with diabetes mellitus.

Advanced glycation end products (AGEs) are thought to be responsible for some complications of diabetes mellitus (DM), including microangiopathy. Plasma serotonin is increased in diabetes mellitus patients, and this increase is related, at least in part, to platelet hyperfunction. In order to clarify the relationship between advanced glycation end products, serotonin, and thrombotic complications in diabetes mellitus patients, we examined the effect of advanced glycation end products on serotonin-induced platelet aggregation. In diabetic patients, although serotonin-induced platelet aggregation was enhanced with an increase in serum-advanced glycation end products, there was no correlation between platelet aggregation and either hemoglobin A1c or fasting blood sugar. To examine the direct effect of advanced glycation end products on platelet aggregation, we prepared advanced glycation end products by in vitro incubation of human albumin with glucose (250 mM) at 37 degrees C for 8 weeks. Serotonin-induced platelet aggregation was dose-dependently increased by advanced glycation end products. Adenosine diphosphate-induced platelet aggregation also was increased by advanced glycation end products, but this increment was diminished by addition of sarpogrelate, a selective serotonin receptor antagonist. These results suggest that advanced glycation end products enhance platelet aggregation through the serotonin receptor, and perhaps influencing the development of thrombotic complications in diabetic patients.

Diabetes Mellitus, Type 2↗
PubMed2002

Metabolic consequence of long-term exposure of pancreatic beta cells to free fatty acid with special reference to glucose insensitivity.

Long-term exposure of the pancreatic beta cells to free fatty acid (FFA) reportedly inhibits glucose-stimulated insulin secretion. We here studied the impact of FFA on glucose and lipid metabolism in pancreatic beta cells with special reference to insulin secretion. Pancreatic beta-cell line MIN6 was exposed to various concentrations of palmitate for 3 days. Glucose-stimulated insulin secretion and insulin content were decreased corresponding to the concentration of the palmitate exposed. Glycolytic flux and ATP synthesis was unchanged, but pyruvate-stimulated change in NAD(P)H concentration was decreased. Pyruvate carboxylase was decreased at the protein level, which was restored by the removal of palmitate or the inhibition of beta-oxidation. Intracellular content of triglyceride and FFA were elevated, beta-oxidation was increased, and de novo lipogenesis from glucose was decreased. NADPH content and citrate output into the medium, which reflected pyruvate malate shuttle flux, were decreased, but malic enzyme activity was unaffected. The malic enzyme inhibitor alone inhibited insulin response to glucose. In conclusion, long-term exposure of FFA to beta cells inhibits glucose-stimulated insulin secretion via the decreased NADPH contents due to the inhibition of pyruvate carboxylase and malate pyruvate shuttle flux.

Animals↗
PubMed2002

Thyroid hormone receptor interacting protein 3 (trip3) is a novel coactivator of hepatocyte nuclear factor-4alpha.

Mutations of the hepatocyte nuclear factor-4alpha (HNF-4alpha) gene are associated with a subtype of maturity-onset diabetes of the young (MODY1) that is characterized by impaired insulin secretion in response to a glucose load. HNF-4alpha, which is a transcription factor expressed in pancreatic beta-cells, plays an important role in regulating the expression of genes involved in glucose metabolism. Thus, cofactors that interact with HNF-4alpha and modify its transcriptional activity might also play an important role in regulating the metabolic pathways in pancreatic beta-cells, and the genes of such cofactors are plausible candidate genes for MODY. In the present study, we showed, using a yeast two-hybrid screening assay, that thyroid hormone receptor interacting protein 3 (Trip3) interacted with HNF-4alpha, and their interaction was confirmed by the glutathione S-transferase pull-down assay. Human Trip3 cDNA contained an open reading frame for a protein of 155 amino acids, and the gene was expressed in both pancreatic islets and MIN6 cells. Cotransfection experiments indicated that Trip3 could enhance (two- to threefold) the transcription activity of HNF-4alpha in COS-7 cells and MIN6 cells. These results suggest that Trip3 is a coactivator of HNF-4alpha. Mutation screening revealed that variation of the Trip3 gene is not a common cause of MODY/early-onset type 2 diabetes in Japanese individuals. Trip3 may play an important role in glucose metabolism by regulating the transcription activity of HNF-4alpha.

Animals↗
PubMed2002

[Insulin aspart].

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Blood Glucose↗