The pathophysiology of cytokines released by infiltrating white blood cells upon pancreatic beta cells is not fully understood. Early growth response gene-1 (Egr-1) expression is specifically and transiently up regulated in pancreatic beta cells in response to glucose. We hypothesized that interleukin-1 beta (IL-1▀) induction of nitric oxide alters glucose induced Egr-1 transcription levels. Egr-1 levels were assessed via western blot, nitric oxide was measured with a Griess Reagent kit and insulin levels via ELISA. Glucose induced both insulin and Egr-1 production in INS-1 cells. IL-1▀ dose dependently increased nitric oxide production over time and significantly attenuated glucose induced Egr-1 expression. Sodium nitroprusside dose dependently reduced glucose induced Egr-1 production. The data suggest a strong relationship between IL-1▀ induced nitric oxide production and the reduction of glucose stimulated Egr-1 production. The pathways altered by this cytokine could provide a better understanding of the pathophysiology leading to pancreatic beta cell death.
","abstract_html":"<p>The pathophysiology of cytokines released by infiltrating white blood cells upon pancreatic beta cells is not fully understood. Early growth response gene-1 (Egr-1) expression is specifically and transiently up regulated in pancreatic beta cells in response to glucose. We hypothesized that interleukin-1 beta (IL-1▀) induction of nitric oxide alters glucose induced Egr-1 transcription levels. Egr-1 levels were assessed via western blot, nitric oxide was measured with a Griess Reagent kit and insulin levels via ELISA. Glucose induced both insulin and Egr-1 production in INS-1 cells. IL-1▀ dose dependently increased nitric oxide production over time and significantly attenuated glucose induced Egr-1 expression. Sodium nitroprusside dose dependently reduced glucose induced Egr-1 production. The data suggest a strong relationship between IL-1▀ induced nitric oxide production and the reduction of glucose stimulated Egr-1 production. The pathways altered by this cytokine could provide a better understanding of the pathophysiology leading to pancreatic beta cell death.</p>","abstract_has_math":false,"creators":["Young, Ada"],"institution":null,"degree_name":"MS (Master of Science)","degree_level":"Thesis - unrestricted","degree_discipline":"Biology","degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2012,"date_issued":"2012-08-15T07:00:00Z","date_published":"2012-08-15T07:00:00Z","updated_at":"2026-07-24T02:20:31Z","subjects":["interleukin- 1β","insulin dependent diabetes mellitus","egr-1","glucose stimulation","Biological Phenomena, Cell Phenomena, and Immunity","Medical Sciences","Medicine and Health Sciences"],"languages":[],"rights":["Copyright by the authors."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://dc.etsu.edu/etd/1463","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Young, Ada"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.issued","label":"Date","values":["2012-08-15T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis - unrestricted"]},{"key":"thesis:degree_name","label":"Degree Name","values":["MS (Master of Science)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["interleukin- 1β","insulin dependent diabetes mellitus","egr-1","glucose stimulation","Biological Phenomena, Cell Phenomena, and Immunity","Medical Sciences","Medicine and Health Sciences"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["Copyright by the authors."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://dc.etsu.edu/context/etd/article/2656/viewcontent/YoungA071112f.pdf","https://dc.etsu.edu/etd/1463"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["The pathophysiology of cytokines released by infiltrating white blood cells upon pancreatic beta cells is not fully understood. Early growth response gene-1 (Egr-1) expression is specifically and transiently up regulated in pancreatic beta cells in response to glucose. We hypothesized that interleukin-1 beta (IL-1▀) induction of nitric oxide alters glucose induced Egr-1 transcription levels. Egr-1 levels were assessed via western blot, nitric oxide was measured with a Griess Reagent kit and insulin levels via ELISA. Glucose induced both insulin and Egr-1 production in INS-1 cells. IL-1▀ dose dependently increased nitric oxide production over time and significantly attenuated glucose induced Egr-1 expression. Sodium nitroprusside dose dependently reduced glucose induced Egr-1 production. The data suggest a strong relationship between IL-1▀ induced nitric oxide production and the reduction of glucose stimulated Egr-1 production. The pathways altered by this cytokine could provide a better understanding of the pathophysiology leading to pancreatic beta cell death.
"]},{"key":"dc:title","label":"Title","values":["IL-1β Amplification of Nitric Oxide Production and Its Inhibitory Effects on Glucose Induced Early Growth Response-1 Expression in INS-1 Cells"]}]}],"canonical_facts":{"dc:creator":["Young, Ada"],"dc:date.issued":["2012-08-15T07:00:00Z"],"dc:description.abstract":["The pathophysiology of cytokines released by infiltrating white blood cells upon pancreatic beta cells is not fully understood. Early growth response gene-1 (Egr-1) expression is specifically and transiently up regulated in pancreatic beta cells in response to glucose. We hypothesized that interleukin-1 beta (IL-1▀) induction of nitric oxide alters glucose induced Egr-1 transcription levels. Egr-1 levels were assessed via western blot, nitric oxide was measured with a Griess Reagent kit and insulin levels via ELISA. Glucose induced both insulin and Egr-1 production in INS-1 cells. IL-1▀ dose dependently increased nitric oxide production over time and significantly attenuated glucose induced Egr-1 expression. Sodium nitroprusside dose dependently reduced glucose induced Egr-1 production. The data suggest a strong relationship between IL-1▀ induced nitric oxide production and the reduction of glucose stimulated Egr-1 production. The pathways altered by this cytokine could provide a better understanding of the pathophysiology leading to pancreatic beta cell death.
"],"dc:identifier":["https://dc.etsu.edu/context/etd/article/2656/viewcontent/YoungA071112f.pdf","https://dc.etsu.edu/etd/1463"],"dc:rights":["Copyright by the authors."],"dc:subject":["interleukin- 1β","insulin dependent diabetes mellitus","egr-1","glucose stimulation","Biological Phenomena, Cell Phenomena, and Immunity","Medical Sciences","Medicine and Health Sciences"],"dc:title":["IL-1β Amplification of Nitric Oxide Production and Its Inhibitory Effects on Glucose Induced Early Growth Response-1 Expression in INS-1 Cells"],"thesis:degree_discipline":["Biology"],"thesis:degree_level":["Thesis - unrestricted"],"thesis:degree_name":["MS (Master of Science)"]},"updated_at":"2026-07-24T02:20:31Z"}