Hiroki Mizukami

ORCID: 0000-0003-2920-582X
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About
Contact & Profiles
Research Areas
  • Pancreatic function and diabetes
  • Pain Mechanisms and Treatments
  • Diabetes and associated disorders
  • Botulinum Toxin and Related Neurological Disorders
  • Metabolism, Diabetes, and Cancer
  • Diabetes Management and Research
  • Diabetes Treatment and Management
  • Aldose Reductase and Taurine
  • Diet, Metabolism, and Disease
  • Mesenchymal stem cell research
  • Advanced Glycation End Products research
  • Neurological Disorders and Treatments
  • Nerve injury and regeneration
  • Pancreatic and Hepatic Oncology Research
  • Pancreatitis Pathology and Treatment
  • Lysosomal Storage Disorders Research
  • Cancer Diagnosis and Treatment
  • Alcohol Consumption and Health Effects
  • Gout, Hyperuricemia, Uric Acid
  • Liver Disease Diagnosis and Treatment
  • Parkinson's Disease Mechanisms and Treatments
  • Diabetic Foot Ulcer Assessment and Management
  • Acupuncture Treatment Research Studies
  • Endoplasmic Reticulum Stress and Disease
  • Glycosylation and Glycoproteins Research

Hirosaki University
2016-2025

Kushiro City General Hospital
2023

National Institutes of Health
2002-2006

National Institute of Diabetes and Digestive and Kidney Diseases
2002-2006

Justus-Liebig-Universität Gießen
2005

German Cancer Research Center
2005

Heidelberg University
2005

Universidad Nacional de Córdoba
2003

Research Centre in Biological Chemistry of Córdoba
2003

Ochanomizu University
2003

Gangliosides are sialic acid-containing glycosphingolipids that present on all mammalian plasma membranes where they participate in recognition and signaling activities. We have established mutant mice lack GM3 synthase (CMP-NeuAc:lactosylceramide α2,3-sialyltransferase; EC 2.4.99.-). These were unable to synthesize ganglioside, a simple widely distributed glycosphingolipid. The viable appeared without major abnormalities but showed heightened sensitivity insulin. A basis for the increased...

10.1073/pnas.0635898100 article EN Proceedings of the National Academy of Sciences 2003-03-10

Gangliosides, which are sialylated glycosphingolipids, the major class of glycoconjugates on neurons and carry majority sialic acid within central nervous system (CNS). To determine role ganglioside synthesis CNS, mice carrying null mutations in two critical ganglioside-specific glycosyltransferase genes, Siat9 (encoding GM3 synthase) Galgt1 GM2 synthase), were generated. These double-null unable to synthesize gangliosides ganglio-series CNS. Soon after weaning, viable developed a severe...

10.1073/pnas.0407785102 article EN Proceedings of the National Academy of Sciences 2005-02-14

Objectives ARID1A is a recently identified tumor suppressor participating in chromatin remodeling. Somatic inactivating mutations of and loss its expression occur frequently ovarian clear cell endometrioid carcinomas uterine carcinomas. Because endometriotic epithelium thought to be the origin most carcinomas, we undertook an analysis these tumors arising within cyst (endometrioma). Materials Methods Our immunohistochemical study set consisted 47 cysts containing carcinoma 24 cases,...

10.1097/igc.0b013e31826b5dcc article EN cc-by-nc-nd International Journal of Gynecological Cancer 2012-09-13

Deficits of β-cells characterize the islet pathology in type 2 diabetes. It is yet to be clear how β-cell loss develops We explored implication oxidative stress, endoplasmic reticulum (ER)-induced and autophagy deficit decline Japanese diabetic patients.Pancreases from recent autopsy cases 47 30 nondiabetic subjects were investigated on structure with morphometric analysis. Volume densities (Vi), (Vβ), α-cell (Vα) measured. To evaluate cell damage endocrine cells, immunohistochemical...

10.2337/dc13-2018 article EN cc-by-nc-nd Diabetes Care 2014-04-05

Gaucher disease, the most common lysosomal storage is caused by a deficiency of glucocerebrosidase resulting in impairment glucosylceramide degradation. The hallmark disease presence cell, macrophage containing much stored found tissues, which believed to cause many clinical manifestations disease. We have developed adult mice carrying L444P point mutation (Gba) gene and exhibiting partial enzyme deficiency. mutant demonstrate multisystem inflammation, including evidence B cell...

10.1172/jci14530 article EN Journal of Clinical Investigation 2002-05-01

Aims: Islet amyloid is a hallmark in type 2 diabetic subjects, but its implication clinical features and development of islet pathology still unclear.Methods: From 118 autopsy cases with diabetes, 26 deposition (DA+) were selected. Twenty subjects without obvious (DA−) matched for the age diabetes duration 20 non-diabetic (ND) served comparison. We examined severity relationships population endocrine cells, expression cell damage markers or macrophage infiltration. Correlation profile was...

10.3109/13506129.2014.937857 article EN Amyloid 2014-07-09

Gaucher disease, the most common lysosomal storage is caused by a deficiency of glucocerebrosidase resulting in impairment glucosylceramide degradation. The hallmark disease presence cell, macrophage containing much stored found tissues, which believed to cause many clinical manifestations disease. We have developed adult mice carrying L444P point mutation (Gba) gene and exhibiting partial enzyme deficiency. mutant demonstrate multisystem inflammation, including evidence B cell...

10.1172/jci0214530 article EN Journal of Clinical Investigation 2002-05-01

Abstract Pioglitazone, one of thiazolidinediones, a peroxisome proliferator‐activated receptor (PPAR)‐γ ligand, is known to have beneficial effects on macrovascular complications in diabetes, but the effect diabetic neuropathy not well addressed. We demonstrated expression PPAR‐γ Schwann cells and vascular walls peripheral nerve then evaluated pioglitazone treatment for 12 weeks (10 mg/kg/day, orally) streptozotocin‐diabetic rats. At end, improved conduction delay rats without affecting...

10.1111/j.1471-4159.2007.05050.x article EN Journal of Neurochemistry 2007-10-10

Autophagy is cellular machinery for maintenance of β-cell function and mass. The implication autophagy failure in β-cells on the pathophysiology type 2 diabetes its relation to effect treatment remains elusive. Here, we found increased expression p62 islets db/db mice patients with mellitus. Treatment exendin-4, a glucagon like peptide-1 receptor agonist, improved glucose tolerance without significant changes β-cells. Also β-cell-specific Atg7-deficient mice, exendin-4 efficiently blood...

10.1210/en.2013-1578 article EN Endocrinology 2013-10-09

A sufficient β-cell mass is crucial for preventing diabetes, and perinatal proliferation important in determining the adult mass. However, it not yet known how regulated. Here, we report that serotonin regulates through receptor 2B (HTR2B) an autocrine/paracrine manner during period. In β-cell–specific Tph1 knockout (Tph1 βKO) mice, was reduced along with loss of production β-cells. Adult βKO mice exhibited glucose intolerance decreased Disruption Htr2b β-cells also resulted adulthood....

10.2337/db19-0546 article EN Diabetes 2019-12-05

Background Systemic inflammatory response syndrome is a fatal disease because of multiple organ failure. Acute kidney injury serious complication systemic and its genesis still unclear posing difficulty for an effective treatment. Aldose reductase (AR) inhibitor recently found to suppress lipopolysaccharide (LPS)-induced cardiac failure lethality. We studied the effects AR on LPS-induced acute mechanism. Methods Mice were injected with LPS (Fidarestat 32 mg/kg) before or after injection...

10.1371/journal.pone.0030134 article EN cc-by PLoS ONE 2012-01-12

Abstract Aims/Introduction Impaired growth and premature death of β‐cells are implicated in the progression islet pathology type 2 diabetes. It remains unclear, however, how aging affects cells, or whether change diabetes is an augmented process aging. We studied age‐related changes structure J apanese non‐diabetic subjects explored underlying mechanism changes. Materials Methods A total 115 autopsy cases were subjected to morphometric analysis for volume densities islets, β‐ non‐β‐cells, as...

10.1111/jdi.12118 article EN cc-by-nc Journal of Diabetes Investigation 2013-08-04

It is suggested that activation of receptor for advanced glycation end products (RAGE) induces proinflammatory response in diabetic nerve tissues. Macrophage infiltration invoked the pathogenesis polyneuropathy (DPN), while association between macrophage and RAGE downstream effects macrophages remain to be fully clarified DPN. This study explored role DPN through modified macrophages. Infiltrating impaired insulin sensitivity, atrophied neurons dorsal root ganglion, slowed retrograde axonal...

10.1172/jci.insight.160555 article EN cc-by JCI Insight 2022-12-07

Insulin-dependent diabetes in patients with Wolfram syndrome (WS; OMIM 222300) has been linked to endoplasmic reticulum (ER) stress caused by WFS1 gene mutations. However, the pathological process of ER stress–associated β cell failure remains be fully elucidated. Our results indicate loss lineage and subsequent dedifferentiation as mechanisms underlying functional mass deficits WS. An immunohistochemical analysis human pancreatic sections from deceased individuals WS revealed a...

10.1126/scitranslmed.adp2332 article EN Science Translational Medicine 2025-02-19
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