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Relationship between inflammation, insulin resistance and type 2 diabetes: 'cause or effect'?
Jerry R Greenfield1, Lesley V Campbell
1Diabetes and Obesity Research Program, Garvan Institute of Medical Research, Sydney, Australia.
Current Diabetes Reviews
|January 29, 2008
Summary
Mildly elevated inflammatory markers like C-reactive protein (CRP) and interleukin-6 in obesity are a consequence, not cause, of insulin resistance. Body fatness, not inflammation, primarily determines these marker levels.
Area of Science:
- Metabolic disease research
- Immunology
- Endocrinology
Background:
- Inflammation is linked to insulin resistance and type 2 diabetes.
- Elevated C-reactive protein (CRP) and interleukin-6 (IL-6) are associated with these conditions.
- The role of obesity in mediating these associations is debated.
Purpose of the Study:
- To investigate whether elevated inflammatory markers are a cause or consequence of insulin resistance.
- To clarify the relationship between body fat, inflammation, and insulin resistance.
Main Methods:
- Review of existing studies on inflammation, obesity, and insulin resistance.
- Emphasis on studies using gold-standard methods for body fat measurement (DXA, CT, MRI).
Main Results:
- Body fatness is the primary determinant of basal inflammatory marker levels.
- Elevated IL-6 and CRP in obesity are consequences, not causes, of insulin resistance.
- Genetic factors influence both body fat and CRP levels.
Conclusions:
- Obesity-related inflammation is a consequence, not a cause, of insulin resistance.
- Body fat is the main driver of circulating inflammatory markers.
- Further research into mechanisms linking body fat, insulin resistance, and inflammation is warranted.
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