Abstract
Type 1 diabetes mellitus (T1D) arises from selective immunologically mediated destruction of the insulin-producing β-cells in the pancreatic islets of Langerhans with consequent insulin deficiency. This occurs in genetically susceptible individuals and is a cellular-mediated process, presumably a specific reaction to one or more β-cell proteins (autoantigens), although probably initiated by some environmental factor(s). There is consequent progressive impairment of β-cell function and decline in β-cell mass. A secondary humoral immune response is characterized by the appearance of autoantibodies that serve as markers of the immune damage to β-cells. This insidious T1D disease process evolves over a period of years. The decline in β-cell function and mass is evidenced metabolically by loss of first-phase insulin response to an intravenous glucose challenge, and later by the appearance of impairment in glycemic regulation, manifested as dysglycemia-usually as impaired glucose tolerance, but occasionally as impaired fasting glucose. Ultimately, the clinical syndrome of T1D becomes evident when the majority of β-cells have been destroyed and frank hyperglycemia supervenes. Given this sequence of events, for which it is possible to envision intervention to interdict the process, it is not surprising that much research effort has been expended to identify individuals at risk of the disease.
| Original language | English |
|---|---|
| Pages (from-to) | 768-771 |
| Number of pages | 4 |
| Journal | Clinical Pharmacology and Therapeutics |
| Volume | 81 |
| Issue number | 5 |
| DOIs | |
| State | Published - May 1 2007 |
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ASJC Scopus subject areas
- Pharmacology
Cite this
Prediction and prevention of type 1 diabetes : Progress, problems, and prospects. / Skyler, Jay S.
In: Clinical Pharmacology and Therapeutics, Vol. 81, No. 5, 01.05.2007, p. 768-771.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Prediction and prevention of type 1 diabetes
T2 - Progress, problems, and prospects
AU - Skyler, Jay S
PY - 2007/5/1
Y1 - 2007/5/1
N2 - Type 1 diabetes mellitus (T1D) arises from selective immunologically mediated destruction of the insulin-producing β-cells in the pancreatic islets of Langerhans with consequent insulin deficiency. This occurs in genetically susceptible individuals and is a cellular-mediated process, presumably a specific reaction to one or more β-cell proteins (autoantigens), although probably initiated by some environmental factor(s). There is consequent progressive impairment of β-cell function and decline in β-cell mass. A secondary humoral immune response is characterized by the appearance of autoantibodies that serve as markers of the immune damage to β-cells. This insidious T1D disease process evolves over a period of years. The decline in β-cell function and mass is evidenced metabolically by loss of first-phase insulin response to an intravenous glucose challenge, and later by the appearance of impairment in glycemic regulation, manifested as dysglycemia-usually as impaired glucose tolerance, but occasionally as impaired fasting glucose. Ultimately, the clinical syndrome of T1D becomes evident when the majority of β-cells have been destroyed and frank hyperglycemia supervenes. Given this sequence of events, for which it is possible to envision intervention to interdict the process, it is not surprising that much research effort has been expended to identify individuals at risk of the disease.
AB - Type 1 diabetes mellitus (T1D) arises from selective immunologically mediated destruction of the insulin-producing β-cells in the pancreatic islets of Langerhans with consequent insulin deficiency. This occurs in genetically susceptible individuals and is a cellular-mediated process, presumably a specific reaction to one or more β-cell proteins (autoantigens), although probably initiated by some environmental factor(s). There is consequent progressive impairment of β-cell function and decline in β-cell mass. A secondary humoral immune response is characterized by the appearance of autoantibodies that serve as markers of the immune damage to β-cells. This insidious T1D disease process evolves over a period of years. The decline in β-cell function and mass is evidenced metabolically by loss of first-phase insulin response to an intravenous glucose challenge, and later by the appearance of impairment in glycemic regulation, manifested as dysglycemia-usually as impaired glucose tolerance, but occasionally as impaired fasting glucose. Ultimately, the clinical syndrome of T1D becomes evident when the majority of β-cells have been destroyed and frank hyperglycemia supervenes. Given this sequence of events, for which it is possible to envision intervention to interdict the process, it is not surprising that much research effort has been expended to identify individuals at risk of the disease.
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U2 - 10.1038/sj.clpt.6100179
DO - 10.1038/sj.clpt.6100179
M3 - Article
VL - 81
SP - 768
EP - 771
JO - Clinical Pharmacology and Therapeutics
JF - Clinical Pharmacology and Therapeutics
SN - 0009-9236
IS - 5
ER -