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Can thiazolidinediones delay disease progression in type 2 diabetes?
1Department of Medicine, University of Toronto, St. Michael's Hospital, Toronto, ON, Canada. leiterl@smh.toronto.on.ca
Background:
Type 2 diabetes results from increasing insulin resistance coupled with progressive loss of beta-cell function. Further deterioration of beta-cell function is associated with progression of diabetes and the potential development of microvascular and macrovascular complications.
Scope:
This review examines current knowledge of beta-cell function and uses this information to assess how the results of ongoing trials could increase our understanding of disease progression and potential interventions. Data were derived from a Medline search using the search terms 'beta-cell dysfunction', 'IGT', 'thiazolidinediones', 'metformin', and 'sulfonylurea'.
Results:
The mechanisms that underlie beta-cell dysfunction are complex and most likely involve the interplay of a range of factors that reduce both beta-cell mass and secretory function. These include detrimental effects associated with hyperglycemia itself, elevated free fatty acids, and inflammatory responses linked to adipocyte-derived cytokines, with apoptosis a key underlying mechanism. Early intervention with treatments that address these defects, and preserve beta-cell function while improving insulin sensitivity, may delay disease progression in patients with type 2 diabetes and also prevent the development of diabetes in 'at-risk' individuals. Two of the studies examining the effects of interventions on development and progression of diabetes that are due to report shortly are ADOPT (A Diabetes Outcome Progression Trial), comparing a thiazolidinedione, metformin and a sulfonylurea in patients with type 2 diabetes not previously treated with oral hypoglycemic agents, and DREAM (Diabetes REduction Assessment with ramipril and rosiglitazone Medication), assessing the effects of a thiazolidinedione and an angiotensin-converting enzyme inhibitor in subjects with impaired glucose tolerance and/or impaired fasting glucose.
Conclusions:
Although we do not have a full understanding of the mechanisms driving progression of type 2 diabetes, there is growing evidence that we may be able to modulate them and thereby improve patient outcomes.
Insights
Type 2 diabetes involves insulin resistance and beta-cell loss. Early interventions targeting these defects may slow disease progression and prevent diabetes in at-risk individuals.
Area of Science:
- Endocrinology and Metabolism
- Diabetes Research
Background:
- Type 2 diabetes stems from insulin resistance and declining beta-cell function.
- Deterioration of beta-cell function accelerates diabetes and risks micro/macrovascular complications.
Purpose of the Study:
- Review current knowledge on beta-cell function.
- Assess how ongoing trials can advance understanding of disease progression and interventions.
Main Methods:
- Medline search for 'beta-cell dysfunction', 'IGT', 'thiazolidinediones', 'metformin', 'sulfonylurea'.
- Review of existing literature and ongoing clinical trials.
Main Results:
- Beta-cell dysfunction involves complex factors reducing mass and function, including hyperglycemia, free fatty acids, and inflammation.
- Early interventions preserving beta-cell function and insulin sensitivity may delay type 2 diabetes progression.
- Ongoing trials like ADOPT and DREAM investigate interventions for diabetes development and progression.
Conclusions:
- Mechanisms of type 2 diabetes progression are not fully understood.
- Evidence suggests interventions can modulate disease progression and improve patient outcomes.
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