| Type 1 | Type 2 | |
| Pathology | Insulin deficiency | Insulin resistance |
| Hyperinsulinemia | ||
| Raised IGF-1 | ||
| Raised blood glucose | Raised blood glucose | |
| Age of onset | Younger | Older |
| May affect peak bone mass | Usually maturity onset | |
| BMI | May be low | Usually high |
| Increased load on skeleton | ||
| May protect against impact | ||
| Increased estrogen, leptin, and adiponectin production in adipose tissue | ||
| Mechanism | Hyperglycemia may cause increased urine calcium loss and inhibit bone formation | Hyperglycemia may cause increased urine calcium loss and inhibit bone formation |
| Bone turnover is usually low | Bone turnover is usually low | |
| Advanced glycosylation end products may affect bone fragility | Advanced glycosylation end products may affect bone fragility | |
| Anabolic effect of insulin resistance | ||
| BMD | May be low | May be increased |
| Fracture risk | Increased | Increased |
| Treatment | Insulin has anabolic effect | Different effects of drugs on fracture risk (reduction with metformin, increase with thiazolidinediones and SGLT2 inhibitors) |
| Insulin has anabolic effect but use marks longstanding or severe diabetes | ||
| Complications | Micro- and macrovascular complications may increase fracture risk by effects on bone (eg, by metabolic effects of nephropathy) or by association with an increased risk of falling (eg, secondary to visual loss, cerebrovascular disease, or neuropathy). Neuropathy-related local bone loss may increase fracture risk at the foot and ankle. | |
