Reduced prandial insulin secretion contributes to prandial hyperglycaemia in non-diabetic individuals with spinal cord injury
- PMID: 40605147
- PMCID: PMC12326903
- DOI: 10.1111/dom.16563
Reduced prandial insulin secretion contributes to prandial hyperglycaemia in non-diabetic individuals with spinal cord injury
Keywords: beta cell function; clinical physiology; glycaemic control; insulin secretion.
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References
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- Bauman WA, Spungen AM, Waters RL. The effect of residual neurological defecit on oral glucose tolerance in persons with chronic spinal cord injury. Spinal Cord. 1999;37:765‐771. - PubMed
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- Karlsson A. Insulin resistance and sympathetic function in high spinal cord injury. Spinal Cord. 1999;37:494‐500. - PubMed
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