Although somatomedin levels may be low in animals with experimental diabetes, values in humans have generally been normal. Because humans with severely decompensated diabetes have not been studied, we characterized somatomedin C responses during metabolic restoration in 21 patients with diabetic ketoacidosis. Somatomedin C values were compared with those of 25 outpatient controls. Somatomedin C in controls (mean ± SE) was 0.72 ± 0.09 U/ml, 69% of the mean sex-adjusted normal level; 28% of patients had values below the lower limit of normal. In ketoacidotic subjects, initial somatomedin C was 0.43 ± .06 U/ml, 33% of the mean normal level; 52% of subjects had somatomedin C below the lower limit of normal. Initial levels in ketoacidotic subjects were unrelated to presenting levels of glucose, bicarbonate, ketones, or blood urea nitrogen but were significantly lower in patients of less than ideal body weight (0.30 vs. 0.58 U/ml, P < .03). Presenting levels of somatomedin C in ketoacidotic subjects were significantly lower than in controls (P <.02). During insulin-infusion therapy, somatomedin C rose to a peak of 1.16 ± 0.21 U/ml after 28 h, significantlyhigher than initial levels (P <.05). With continued subcutaneous insulin, somatomedin C fell to a nadir after an additional 22 h then rose more slowly to a final value of 0.75 ± 0.12 U/ml, significantly higher than the nadir (P <.05) but lower than peak values; final values in the ketoacidotic subjects were comparable to outpatient somatomedin C levels. Although final somatomedin C exhibited no apparent relationship to percent ideal body weight or final metabolic indices, values were lower in patients who had higher initial glucose (r = .43, P <.05). During the rapid rise of somatomedin C from initial to peak levels, somatomedin C values were correlated with levels of both bicarbonate (r = .37, P <.001) and ketones (r = −.31 , P <.005). Altered somatomedin C could not be attributed to changes in serum somatomedinbinding activity. Although improvement in somatomedin C levels over several days may be due to gradual intracellular normalization in response to subcutaneous insulin, the acute rise during the 1st day of intravenous therapy probably reflects rapid anabolic flux conferred by high levels of insulin and metabolic fuels. These findings establish a strong relationship between levels of somatomedin C and metabolic status in diabetic humans.
Nutrition and Somatomedin: XVII. Circulating Somatomedin C During Treatment of Diabetic Ketoacidosis
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Elyse W Glaser, Steven Goldstein, Lawrence S Phillips; Nutrition and Somatomedin: XVII. Circulating Somatomedin C During Treatment of Diabetic Ketoacidosis. Diabetes 1 October 1987; 36 (10): 1152–1160. https://doi.org/10.2337/diab.36.10.1152
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