9 results match your criteria: "Diabetes and Metabolism Research Institute and Beckman Research Institute[Affiliation]"
Sci Transl Med
May 2024
Department of Diabetes Complications and Metabolism, Arthur Riggs Diabetes and Metabolism Research Institute and Beckman Research Institute of City of Hope, Duarte, CA 91010, USA.
Variation in DNA methylation (DNAmet) in white blood cells and other cells/tissues has been implicated in the etiology of progressive diabetic kidney disease (DKD). However, the specific mechanisms linking DNAmet variation in blood cells with risk of kidney failure (KF) and utility of measuring blood cell DNAmet in personalized medicine are not clear. We measured blood cell DNAmet in 277 individuals with type 1 diabetes and DKD using Illumina EPIC arrays; 51% of the cohort developed KF during 7 to 20 years of follow-up.
View Article and Find Full Text PDFFront Bioeng Biotechnol
March 2023
Department of Translational Research and Cellular Therapeutics, Arthur Riggs Diabetes and Metabolism Research Institute and Beckman Research Institute of City of Hope, Duarte, CA, United States.
The transplantation of pancreatic endocrine islet cells from cadaveric donors is a promising treatment for type 1 diabetes (T1D), which is a chronic autoimmune disease that affects approximately nine million people worldwide. However, the demand for donor islets outstrips supply. This problem could be solved by differentiating stem and progenitor cells to islet cells.
View Article and Find Full Text PDFAm J Physiol Renal Physiol
December 2022
Department of Diabetes Complications and Metabolism, Arthur Riggs Diabetes and Metabolism Research Institute and Beckman Research Institute of City of Hope, Duarte, California.
Obesity is associated with increased risk for diabetes and damage to the kidneys. Evidence suggests that miR-379 plays a role in the pathogenesis of diabetic kidney disease. However, its involvement in obesity-induced kidney injury is not known and was therefore investigated in this study by comparing renal phenotypes of high-fat diet (HFD)-fed wild-type (WT) and miR-379 knockout (KO) mice.
View Article and Find Full Text PDFJCI Insight
June 2021
Department of Diabetes Complications and Metabolism, Arthur Riggs Diabetes and Metabolism Research Institute and Beckman Research Institute of City of Hope, Duarte, California, USA.
Long noncoding RNAs (lncRNAs) are increasingly implicated in the pathology of diabetic complications. Here, we examined the role of lncRNAs in monocyte dysfunction and inflammation associated with human type 2 diabetes mellitus (T2D). RNA sequencing analysis of CD14+ monocytes from patients with T2D versus healthy controls revealed downregulation of antiinflammatory and antiproliferative genes, along with several lncRNAs, including a potentially novel divergent lncRNA diabetes regulated antiinflammatory RNA (DRAIR) and its nearby gene CPEB2.
View Article and Find Full Text PDFMetabolism
February 2021
Department of Molecular and Cellular Endocrinology, Diabetes and Metabolism Research Institute and Beckman Research Institute at the City of Hope, Duarte, CA 91010, United States of America. Electronic address:
Objective: p21 (Cdc42/Rac1) activated Kinase 1 (PAK1) is a candidate susceptibility factor for type 2 diabetes (T2D). PAK1 is depleted in the islets from T2D donors, compared to control individuals. In addition, whole-body PAK1 knock out (PAK1-KO) in mice worsens the T2D-like effects of high-fat diet.
View Article and Find Full Text PDFStem Cells Dev
July 2018
1 Department of Translational Research and Cellular Therapeutics, and Diabetes and Metabolism Research Institute and Beckman Research Institute of City of Hope, Duarte, California.
Pluripotent stem cells may serve as an alternative source of beta-like cells for replacement therapy of type 1 diabetes; however, the beta-like cells generated in many differentiation protocols are immature. The maturation of endogenous beta cells involves an increase in insulin expression starting in late gestation and a gradual acquisition of the abilities to sense glucose and secrete insulin by week 2 after birth in mice; however, what molecules regulate these maturation processes are incompletely known. In this study, we aim to identify small molecules that affect immature beta cells.
View Article and Find Full Text PDFJ Biol Chem
November 2017
From the Departments of Biochemistry and Molecular Biology and
Defects in translocation of the glucose transporter GLUT4 are associated with peripheral insulin resistance, preclinical diabetes, and progression to type 2 diabetes. GLUT4 recruitment to the plasma membrane of skeletal muscle cells requires F-actin remodeling. Insulin signaling in muscle requires p21-activated kinase-1 (PAK1), whose downstream signaling triggers actin remodeling, which promotes GLUT4 vesicle translocation and glucose uptake into skeletal muscle cells.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2016
Diabetes and Metabolism Research Institute and Beckman Research Institute, City of Hope, Duarte, CA 91010;
We previously reported that long-term administration of a low dose of gastrin and epidermal growth factor (GE) augments β-cell neogenesis in late-stage diabetic autoimmune mice after eliminating insulitis by induction of mixed chimerism. However, the source of β-cell neogenesis is still unknown. SRY (sex-determining region Y)-box 9(+) (Sox9(+)) ductal cells in the adult pancreas are clonogenic and can give rise to insulin-producing β cells in an in vitro culture.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
December 2015
Diabetes and Metabolism Research Institute and Beckman Research Institute of City of Hope, Duarte, CA 91010;
Multiple sclerosis (MS) is an autoimmune inflammatory disease of the central nervous system with demyelination, axon damage, and paralysis. Induction of mixed chimerism with allogeneic donors has been shown to not cause graft-versus-host disease (GVHD) in animal models and humans. We have reported that induction of MHC-mismatched mixed chimerism can cure autoimmunity in autoimmune NOD mice, but this approach has not yet been tested in animal models of MS, such as experimental autoimmune encephalomyelitis (EAE).
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