The effect of residual neurological deficit on oral glucose tolerance in persons with chronic spinal cord injury

Study design: Oral glucose tolerance testing was performed prospectively in 201 subjects with spinal cord injury (SCI). The dependent variables includ ed the values from the oral glucose tolerance test (glucose and insulin) an d diagnostic classification (i.e., diabetes mellitus, impaired glucose tole rance, normal glucose tolerance); the independent variables consisted of st udy group, gender, ethnic group, age, age at onset of SCI, duration of inju ry, and anthropometric measurements. Objective: To determine the potential effects of level and completeness of SCI on oral glucose tolerance testing. In addition, the effects of gender e thnicity, age, age at onset of SCI, duration of injury, and anthropometric measurements on glucose tolerance were investigated. Setting: Subjects with chronic SCI were recruited during their annual physi cal examination at the Comarr Spinal Injury Clinic at Rancho Los Amigos Med ical Center, Downey, California. Methods: An oral 75 g glucose load was administered after an overnight fast . Serum glucose was determined by autoanalyzer and plasma insulin levels, b y radioimmunoassay. The results are reported as mean plus or minus standard error of the mean (mean +/- SEM). Analysis of variance (ANOVA) applying a Scheffe' post hoc F ratio was used for the continuous variables. Chi-square d analyses were performed to determine differences between the groups and a mong the subgroups for per cent distribution. Linear regression analyses we re performed between variables of interest. Stepwise regression analyses we re used to predict peak serum glucose concentration and peak plasma insulin level from potential determinants. Results: The total group consisted of 169 men with a mean age of 38 +/- 0.8 0 (range = 20 - 73) years and 32 women with a mean age of 44 +/- 2.13 (rang e = 20 - 72) years. The distribution by ethnicity for the total group with SCI consisted of 114(57%) Latino, 54 (27%) white, and 28) 14%) African Amer ican individuals. There was no significant difference in ethnic distributio n among the subgroups for neurological deficit. Subjects were grouped by te traplegia (Tetra; n=81) or paraplegia (Para; n=120) and by subgroup for deg ree of neurological deficit: complete Tetra (n=56), incomplete Tetra (n=25) , complete Para (n=84), and incomplete Para (n=36). Of the total group, 27 subjects (13.4%) had diabetes mellitus and 56 (28.8%) had impaired glucose tolerance. Significantly more subjects in the complete Tetra group were cla ssified with a disorder of carbohydrate metabolism than in the other neurol ogical deficit subgroups (73 vs 44%, 24% and 31%, respectively for level of decreasing neurological deficit; X-2=36.9, P<0.0001). The complete Tetra g roup had significantly higher serum glucose concentrations at 60 min, 90 mi n, and 120 min and serum insulin concentration at 90 and 120 min compared w ith the other neurological subgroups (P<0.05 for each time point). No diffe rences for plasma glucose were evident between men and women, however, plas ma insulin levels were significantly higher for men at the intermediate tim e points (30 min, 60 min and 90 min), suggesting a relative state of insuli n resistance in men. By stepwise regression analyses, higher peak serum glu cose concentrations were associated with increased total body %fat, highest level of lesion (complete Tetra vs other neurological subgroups), older ag e at time of injury, and male gender; higher peak plasma insulin was associ ated with increased total body %fat and male gender. Conclusions: This study is the first to report that those individuals with the greatest levels of neurological deficit have increased risk of developi ng disorders of carbohydrate metabolism. Males with SCI are more insulin re sistant than females. Glucose tolerance appears to be independent of the ef fects of ethnicity. Sponsorship: Funded in part by the National Institute on Disability and Reh abilitation Research (NIDRR) Grant # H133B30029. This work, would not have been possible without the gracious support of Quest Diagnostics, Inc.