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Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
Published on: May 6, 2013
Bone inflammation and altered gene expression with type I diabetes early onset
Katherine J Motyl1, Sergiu Botolin, Regina Irwin
1Department of Physiology, Biomedical Imaging Research Center, Michigan State University, East Lansing, Michigan 48824, USA.
Journal of Cellular Physiology
|November 14, 2008
Summary
Type I diabetes rapidly alters bone metabolism and increases inflammation in bone tissue. Early suppression of bone formation and resorption markers occurs, alongside changes in bone marrow adiposity.
Area of Science:
- Endocrinology
- Bone Biology
- Metabolic Diseases
Background:
- Type I diabetes is linked to bone loss and increased marrow fat.
- Understanding early diabetic bone pathology is crucial.
Purpose of the Study:
- To investigate early molecular and cellular events in diabetic bone loss.
- To examine the role of inflammation in the bone during diabetes onset.
Main Methods:
- Inducing diabetes in mice using streptozotocin.
- Analyzing serum markers of bone metabolism and inflammation.
- Examining tibial gene expression for bone and fat cell markers.
- Assessing the impact of Interferon-gamma deficiency.
Main Results:
- Elevated blood glucose and decreased body mass observed by 3 days post-injection.
- Suppressed bone formation and resorption markers by 5 days post-injection.
- Increased expression of inflammatory cytokines within bone tissue.
- Altered expression of osteogenic and adipogenic genes by 5 days post-injection.
- Interferon-gamma deficiency did not prevent diabetic bone pathology.
Conclusions:
- Bone inflammation is an early event in Type I diabetes induction.
- Altered bone cell gene expression and marrow adiposity accompany diabetes onset.
- While inflammation is implicated, Interferon-gamma alone is not the sole driver of rapid bone changes.
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