Yun Ping Zhou

Summary

Affiliation: Merck Research Laboratories
Country: USA

Publications

  1. ncbi request reprint Chronic inhibition of dipeptidyl peptidase-4 with a sitagliptin analog preserves pancreatic beta-cell mass and function in a rodent model of type 2 diabetes
    James Mu
    Department of Metabolic Disorders, Merck Research Laboratories, P O Box 2000, Rahway, NJ 07065, USA
    Diabetes 55:1695-704. 2006
  2. pmc Selective small-molecule agonists of G protein-coupled receptor 40 promote glucose-dependent insulin secretion and reduce blood glucose in mice
    Carina P Tan
    Department of Metabolic Disorders Diabetes, Merck Research Laboratories, Rahway, New Jersey, USA
    Diabetes 57:2211-9. 2008
  3. ncbi request reprint Overexpression of repressive cAMP response element modulators in high glucose and fatty acid-treated rat islets. A common mechanism for glucose toxicity and lipotoxicity?
    Yun Ping Zhou
    Department of Insulin Secretion Genomics, Metabolex, Inc, Hayward, California 94545, USA
    J Biol Chem 278:51316-23. 2003
  4. ncbi request reprint Matrix metalloproteinases contribute to insulin insufficiency in Zucker diabetic fatty rats
    Yun Ping Zhou
    Metabolex, 3876 Bay Center Place, Hayward, CA 94583, USA
    Diabetes 54:2612-9. 2005
  5. doi request reprint Bombesin receptor subtype-3 (BRS-3) regulates glucose-stimulated insulin secretion in pancreatic islets across multiple species
    Yue Feng
    Department of Diabetes and Obesity, Merck Research Laboratories, Rahway, New Jersey 07065, USA
    Endocrinology 152:4106-15. 2011
  6. doi request reprint A small-molecule glucokinase activator lowers blood glucose in the sulfonylurea-desensitized rat
    Sumika Ohyama
    Tsukuba Research Institute, Banyu Pharmaceutical Co, Ltd, 3 Okubo, Tsukuba, Ibaraki 300 2611, Japan
    Eur J Pharmacol 640:250-6. 2010
  7. ncbi request reprint Blockers of the delayed-rectifier potassium current in pancreatic beta-cells enhance glucose-dependent insulin secretion
    James Herrington
    Department of Ion Channels, Merck Research Laboratories, RY80N C31, P O Box 2000, Rahway, NJ 07065 0900, USA
    Diabetes 55:1034-42. 2006
  8. doi request reprint Inhibition of DPP-4 with sitagliptin improves glycemic control and restores islet cell mass and function in a rodent model of type 2 diabetes
    James Mu
    Department of Metabolic Disorders, Merck Research Laboratories, Rahway, NJ 07065, USA
    Eur J Pharmacol 623:148-54. 2009
  9. doi request reprint Identification of glucose-dependant insulin secretion targets in pancreatic beta cells by combining defined-mechanism compound library screening and siRNA gene silencing
    Weizhen Wu
    Merck and Co Inc, Target Validation, Merck Research Laboratory, Rahway, NJ 07065, USA
    J Biomol Screen 13:128-34. 2008
  10. doi request reprint Phosphodiesterase 3 and 4 comprise the major cAMP metabolizing enzymes responsible for insulin secretion in INS-1 (832/13) cells and rat islets
    Deena Waddleton
    Department of Biochemistry and Molecular Biology, Merck Frosst Center for Therapeutic Research, Kirkland, Quebec, Canada
    Biochem Pharmacol 76:884-93. 2008

Collaborators

Detail Information

Publications12

  1. ncbi request reprint Chronic inhibition of dipeptidyl peptidase-4 with a sitagliptin analog preserves pancreatic beta-cell mass and function in a rodent model of type 2 diabetes
    James Mu
    Department of Metabolic Disorders, Merck Research Laboratories, P O Box 2000, Rahway, NJ 07065, USA
    Diabetes 55:1695-704. 2006
    ..These findings suggest that DPP-4 inhibitors may offer long-lasting efficacy in the treatment of type 2 diabetes by modifying the courses of the disease...
  2. pmc Selective small-molecule agonists of G protein-coupled receptor 40 promote glucose-dependent insulin secretion and reduce blood glucose in mice
    Carina P Tan
    Department of Metabolic Disorders Diabetes, Merck Research Laboratories, Rahway, New Jersey, USA
    Diabetes 57:2211-9. 2008
    ..We sought to evaluate the specific role of GPR40 in islets and its potential as a therapeutic target using compounds that specifically activate GPR40...
  3. ncbi request reprint Overexpression of repressive cAMP response element modulators in high glucose and fatty acid-treated rat islets. A common mechanism for glucose toxicity and lipotoxicity?
    Yun Ping Zhou
    Department of Insulin Secretion Genomics, Metabolex, Inc, Hayward, California 94545, USA
    J Biol Chem 278:51316-23. 2003
    ..Taken together, these data suggest that up-regulation of CREM repressors by either FFA or high glucose exacerbates beta-cell failure in type 2 diabetes by suppressing insulin gene transcription...
  4. ncbi request reprint Matrix metalloproteinases contribute to insulin insufficiency in Zucker diabetic fatty rats
    Yun Ping Zhou
    Metabolex, 3876 Bay Center Place, Hayward, CA 94583, USA
    Diabetes 54:2612-9. 2005
    ..Class-targeted protease inhibitors should be explored for their potential therapeutic utility in preservation of beta-cell mass in type 2 diabetes...
  5. doi request reprint Bombesin receptor subtype-3 (BRS-3) regulates glucose-stimulated insulin secretion in pancreatic islets across multiple species
    Yue Feng
    Department of Diabetes and Obesity, Merck Research Laboratories, Rahway, New Jersey 07065, USA
    Endocrinology 152:4106-15. 2011
    ..Thus, in addition to its potential role in the treatment of obesity, BRS-3 may also regulate blood glucose levels and have a role in the treatment of diabetes mellitus...
  6. doi request reprint A small-molecule glucokinase activator lowers blood glucose in the sulfonylurea-desensitized rat
    Sumika Ohyama
    Tsukuba Research Institute, Banyu Pharmaceutical Co, Ltd, 3 Okubo, Tsukuba, Ibaraki 300 2611, Japan
    Eur J Pharmacol 640:250-6. 2010
    ..Compound B also significantly increased pancreatic insulin content, compared with controls. These findings suggest that Compound B has sustained glucose-lowering effects in a rat model of sulfonylurea failure...
  7. ncbi request reprint Blockers of the delayed-rectifier potassium current in pancreatic beta-cells enhance glucose-dependent insulin secretion
    James Herrington
    Department of Ion Channels, Merck Research Laboratories, RY80N C31, P O Box 2000, Rahway, NJ 07065 0900, USA
    Diabetes 55:1034-42. 2006
    ..These data point to a mechanism for specific enhancement of glucose-dependent insulin secretion by applying blockers of the beta-cell I(DR), which may provide advantages over currently used therapies for the treatment of type 2 diabetes...
  8. doi request reprint Inhibition of DPP-4 with sitagliptin improves glycemic control and restores islet cell mass and function in a rodent model of type 2 diabetes
    James Mu
    Department of Metabolic Disorders, Merck Research Laboratories, Rahway, NJ 07065, USA
    Eur J Pharmacol 623:148-54. 2009
    ..The ability of sitagliptin to enhance islet cell function may offer insight into the potential for disease modification...
  9. doi request reprint Identification of glucose-dependant insulin secretion targets in pancreatic beta cells by combining defined-mechanism compound library screening and siRNA gene silencing
    Weizhen Wu
    Merck and Co Inc, Target Validation, Merck Research Laboratory, Rahway, NJ 07065, USA
    J Biomol Screen 13:128-34. 2008
    ..The data support that the approach described here offers a rapid and effective way for target identification and validation...
  10. doi request reprint Phosphodiesterase 3 and 4 comprise the major cAMP metabolizing enzymes responsible for insulin secretion in INS-1 (832/13) cells and rat islets
    Deena Waddleton
    Department of Biochemistry and Molecular Biology, Merck Frosst Center for Therapeutic Research, Kirkland, Quebec, Canada
    Biochem Pharmacol 76:884-93. 2008
    ..The combination of PDE3 and PDE4 selective inhibitors demonstrate that these enzymes comprise a significant proportion of the cAMP metabolizing activity in INS-1 cells and rat islets...
  11. ncbi request reprint A 48-hour exposure of pancreatic islets to calpain inhibitors impairs mitochondrial fuel metabolism and the exocytosis of insulin
    Yun Ping Zhou
    Departments of Medicine, Neurobiology, Pharmacology and Physiology, Biochemistry and Molecular Biology, Human Genetics, and the Howard Hughes Medical Institute, University of Chicago, Chicago, IL, USA
    Metabolism 52:528-34. 2003
    ....
  12. ncbi request reprint Antidiabetic effects of Panax ginseng berry extract and the identification of an effective component
    Anoja S Attele
    Tang Center for Herbal Medicine Research, The Pritzker School of Medicine, University of Chicago, Chicago, Illinois 60637, USA
    Diabetes 51:1851-8. 2002
    ..This antidiabetic effect of ginsenoside Re was not associated with body weight changes, suggesting that other constituents in the extract have distinct pharmacological mechanisms on energy metabolism...