Unraveling the Pathogenesis of Type 1 Diabetes with Proteomics: Present And Future Directions

Type 1 diabetes (T1D) is the result of selective destruction of the insulin-producing β-cells in the pancreatic islets of Langerhans. T1D is due to a complex interplay between the β-cell, the immune system, and the environment in genetically susceptible individuals. The initiating mechanism(s) beh...

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Published inMolecular & cellular proteomics Vol. 4; no. 4; pp. 441 - 457
Main Authors Sparre, Thomas, Larsen, Martin R, Heding, Peter E, Karlsen, Allan E, Jensen, Ole N, Pociot, Flemming
Format Journal Article
LanguageEnglish
Published United States American Society for Biochemistry and Molecular Biology 01.04.2005
Subjects
Animals
Cell Line
Diabetes Mellitus, Experimental
Diabetes Mellitus, Type 1 - etiology
Diabetes Mellitus, Type 1 - genetics
Diabetes Mellitus, Type 1 - metabolism
Forecasting
Humans
Proteomics - methods
Proteomics - trends
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Abstract Type 1 diabetes (T1D) is the result of selective destruction of the insulin-producing β-cells in the pancreatic islets of Langerhans. T1D is due to a complex interplay between the β-cell, the immune system, and the environment in genetically susceptible individuals. The initiating mechanism(s) behind the development of T1D are largely unknown, and no genes or proteins are specific for most T1D cases. Different pro-apoptotic cytokines, IL-1 β in particular, are present in the islets during β-cell destruction and are able to modulate β-cell function and induce β-cell death. In β-cells exposed to IL-1 β, a race between destructive and protective events are initiated and in susceptible individuals the deleterious events prevail. Proteins are involved in most cellular processes, and it is thus expected that their cumulative expression profile reflects the specific activity of cells. Proteomics may be useful in describing the protein expression profile and thus the diabetic phenotype. Relatively few studies using proteomics technologies to investigate the T1D pathogenesis have been published to date despite the defined target organ, the β-cell. Proteomics has been applied in studies of differentiating β-cells, cytokine exposed islets, dietary manipulated islets, and in transplanted islets. Although that the studies have revealed a complex and detailed picture of the protein expression profiles many functional implications remain to be answered. In conclusion, a rather detailed picture of protein expression in β-cell lines, islets, and transplanted islets both in vitro and in vivo have been described. The data indicate that the β-cell is an active participant in its own destruction during diabetes development. No single protein alone seems to be responsible for the development of diabetes. Rather the cumulative pattern of changes seems to be what favors a transition from dynamic stability in the unperturbed β-cell to dynamic instability and eventually to β-cell destruction.
AbstractList Type 1 diabetes (T1D) is the result of selective destruction of the insulin-producing β-cells in the pancreatic islets of Langerhans. T1D is due to a complex interplay between the β-cell, the immune system, and the environment in genetically susceptible individuals. The initiating mechanism(s) behind the development of T1D are largely unknown, and no genes or proteins are specific for most T1D cases. Different pro-apoptotic cytokines, IL-1 β in particular, are present in the islets during β-cell destruction and are able to modulate β-cell function and induce β-cell death. In β-cells exposed to IL-1 β, a race between destructive and protective events are initiated and in susceptible individuals the deleterious events prevail. Proteins are involved in most cellular processes, and it is thus expected that their cumulative expression profile reflects the specific activity of cells. Proteomics may be useful in describing the protein expression profile and thus the diabetic phenotype. Relatively few studies using proteomics technologies to investigate the T1D pathogenesis have been published to date despite the defined target organ, the β-cell. Proteomics has been applied in studies of differentiating β-cells, cytokine exposed islets, dietary manipulated islets, and in transplanted islets. Although that the studies have revealed a complex and detailed picture of the protein expression profiles many functional implications remain to be answered. In conclusion, a rather detailed picture of protein expression in β-cell lines, islets, and transplanted islets both in vitro and in vivo have been described. The data indicate that the β-cell is an active participant in its own destruction during diabetes development. No single protein alone seems to be responsible for the development of diabetes. Rather the cumulative pattern of changes seems to be what favors a transition from dynamic stability in the unperturbed β-cell to dynamic instability and eventually to β-cell destruction.
Type 1 diabetes (T1D) is the result of selective destruction of the insulin-producing beta-cells in the pancreatic islets of Langerhans. T1D is due to a complex interplay between the beta-cell, the immune system, and the environment in genetically susceptible individuals. The initiating mechanism(s) behind the development of T1D are largely unknown, and no genes or proteins are specific for most T1D cases. Different pro-apoptotic cytokines, IL-1 beta in particular, are present in the islets during beta-cell destruction and are able to modulate beta-cell function and induce beta-cell death. In beta-cells exposed to IL-1 beta, a race between destructive and protective events are initiated and in susceptible individuals the deleterious events prevail. Proteins are involved in most cellular processes, and it is thus expected that their cumulative expression profile reflects the specific activity of cells. Proteomics may be useful in describing the protein expression profile and thus the diabetic phenotype. Relatively few studies using proteomics technologies to investigate the T1D pathogenesis have been published to date despite the defined target organ, the beta-cell. Proteomics has been applied in studies of differentiating beta-cells, cytokine exposed islets, dietary manipulated islets, and in transplanted islets. Although that the studies have revealed a complex and detailed picture of the protein expression profiles many functional implications remain to be answered. In conclusion, a rather detailed picture of protein expression in beta-cell lines, islets, and transplanted islets both in vitro and in vivo have been described. The data indicate that the beta-cell is an active participant in its own destruction during diabetes development. No single protein alone seems to be responsible for the development of diabetes. Rather the cumulative pattern of changes seems to be what favors a transition from dynamic stability in the unperturbed beta-cell to dynamic instability and eventually to beta-cell destruction.
Author Peter E. Heding
Thomas Sparre
Ole N. Jensen
Allan E. Karlsen
Flemming Pociot
Martin R. Larsen
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  organization: Steno Diabetes Center, DK-2820 Gentofte, Denmark
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  givenname: Martin R
  surname: Larsen
  fullname: Larsen, Martin R
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  givenname: Peter E
  surname: Heding
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  givenname: Allan E
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  fullname: Karlsen, Allan E
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  givenname: Ole N
  surname: Jensen
  fullname: Jensen, Ole N
– sequence: 6
  givenname: Flemming
  surname: Pociot
  fullname: Pociot, Flemming
BackLink https://www.ncbi.nlm.nih.gov/pubmed/15699484$$D View this record in MEDLINE/PubMed
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Snippet Type 1 diabetes (T1D) is the result of selective destruction of the insulin-producing β-cells in the pancreatic islets of Langerhans. T1D is due to a complex...
Type 1 diabetes (T1D) is the result of selective destruction of the insulin-producing beta-cells in the pancreatic islets of Langerhans. T1D is due to a...
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StartPage 441
SubjectTerms Animals
Cell Line
Diabetes Mellitus, Experimental
Diabetes Mellitus, Type 1 - etiology
Diabetes Mellitus, Type 1 - genetics
Diabetes Mellitus, Type 1 - metabolism
Forecasting
Humans
Proteomics - methods
Proteomics - trends
Title Unraveling the Pathogenesis of Type 1 Diabetes with Proteomics: Present And Future Directions
URI http://www.mcponline.org/content/4/4/441.abstract
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