Patients with spinal cord injury (SCI) develop type 2 diabetes earlier and at 2-3 times higher frequency compared to the matched able-bodied persons (AB) . The difference in glucose abnormalities among SCI and AB cohorts remains after adjusting for known risk factors for DM, such as decreased physical activity, or lower body lean mass, or larger visceral fat mass. The mechanism for this dramatic effect of SCI on glucose metabolism is unknown but is consistent with endocrine-neurological alterations after injury. We hypothesized that SCI is associated with abnormalities in prandial glucose metabolism and β-cell function. To test this hypothesis glucose, insulin, and C-peptide levels were measured during 3-hr mixed meal tolerance test in 4 non-diabetic SCI (3M/1F, ages 33-61 years) and 6 age-matched AB with normal glucose tolerance test (2M/4F, ages 37-57 years) . SCI subjects had lower BMI (p=0.05) and A1C (p<0.05) than AB (SCI vs. AB; BMI range: 19-29 vs. 25-39 kg/m2; A1C range: 5.0-5.3 vs. 5.3-5.9%) . Fasting values of glucose, insulin, C-peptide, insulin sensitivity (HOMA-IR) , and insulin clearance (CP/insulin) were similar between SCI and AB. Prandial glucose (AUCGlucose3h) and insulin (AUCInsulin3h) responses, however, were greater in SCI than AB (p<0.01) . Despite larger prandial insulinemia β-cell output (AUCC-peptide3h) did not differ among 2 groups. This was consistent with a diminished insulin clearance (Total AUCC-peptide3h / Total AUCInsulin3h) in SCI compared to AB by 3-fold (p<0.05) . Oral glucose insulin sensitivity (OGIS) was similar between 2 groups while β-cell glucose sensitivity and disposition index were smaller in SCI than AB by 2-fold (p=0.08) . These findings indicate that among subjects with normal glucose tolerance, those with SCI have larger prandial glycemic concentration despite lower BMI and A1C. This glycemic effect of SCI is associated with impaired β-cell function as well as insulin clearance.


M.Trbovich: None. R.Dimas: None. M.Salehi: None.

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