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"Type 2 Diabetes Mellitus"[MeSH Terms] AND "Insulin Resistance"[MeSH Terms]
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NIDDK insulin resistance type 2 diabetes beta cells obesity
The diagram shows the usual progression from obesity to type 2 diabetes mellitus:
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Obesity expands adipose tissue
- Enlarged fat cells and their blood supply release:
- Adipokines: signaling substances from fat tissue
- FFAs: free fatty acids
- Inflammatory mediators
- Enlarged fat cells and their blood supply release:
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These cause insulin resistance
- Muscle, liver, and fat cells become less responsive to insulin.
- Therefore, glucose is not taken up or controlled as effectively.
- The upper part of the page refers to impaired insulin signaling and reduced GLUT-4-mediated glucose uptake in insulin-sensitive tissues, especially muscle and fat.
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Initially, pancreatic beta cells compensate
- Beta cells in the pancreatic islets sense the higher glucose/insulin demand.
- They enlarge/increase functional activity and secrete more insulin.
- This produces hyperinsulinemia, which may keep blood glucose normal at first, or lead only to impaired glucose tolerance.
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Eventually beta-cell failure develops
- Persistent demand, together with glucotoxicity, lipotoxicity, and inflammation, progressively damages or exhausts beta-cell function.
- Insulin secretion then falls.
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Diabetes occurs
- With insulin resistance plus inadequate insulin secretion, blood glucose rises and type 2 diabetes mellitus appears.
| Stage | Beta-cell insulin secretion | Blood glucose |
|---|---|---|
| Normal | Normal | Normal |
| Insulin resistance with compensation | Increased | Normal or impaired glucose tolerance/prediabetes |
| Beta-cell failure | Decreased relative to need | Diabetes mellitus |
Key concept: insulin resistance alone does not always cause diabetes. Diabetes develops when pancreatic beta cells can no longer make enough insulin to compensate. This matches the description in Robbins, Cotran & Kumar Pathologic Basis of Disease, where beta cells eventually fail to meet the sustained demand imposed by insulin resistance. The NIDDK explanation similarly notes that obesity-associated insulin resistance can precede impaired glucose tolerance and diabetes, once beta cells can no longer keep up.
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