Literature DB >> 3115852

Nutrition and somatomedin. XVII. Circulating somatomedin C during treatment of diabetic ketoacidosis.

E W Glaser1, S Goldstein, L S Phillips.   

Abstract

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 less than .03). Presenting levels of somatomedin C in ketoacidotic subjects were significantly lower than in controls (P less than .02). During insulin-infusion therapy, somatomedin C rose to a peak of 1.16 +/- 0.21 U/ml after 28 h, significantly higher than initial levels (P less than .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 less than .05) but lower than peak values; final values in the ketoacidotic subjects were comparable to outpatient somatomedin C levels.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1987        PMID: 3115852     DOI: 10.2337/diab.36.10.1152

Source DB:  PubMed          Journal:  Diabetes        ISSN: 0012-1797            Impact factor:   9.461


  3 in total

1.  Inability to stimulate skeletal muscle or whole body protein synthesis in type 1 (insulin-dependent) diabetic patients by insulin-plus-glucose during amino acid infusion: studies of incorporation and turnover of tracer L-[1-13C]leucine.

Authors:  W M Bennet; A A Connacher; K Smith; R T Jung; M J Rennie
Journal:  Diabetologia       Date:  1990-01       Impact factor: 10.122

2.  Symptomatic cerebral oedema during treatment of diabetic ketoacidosis: effect of adjuvant octreotide infusion.

Authors:  Ora Seewi; Anne Vierzig; Bernhard Roth; Eckhard Schönau
Journal:  Diabetol Metab Syndr       Date:  2010-08-19       Impact factor: 3.320

3.  Evidence that upregulation of serum IGF-1 concentration can trigger acceleration of diabetic retinopathy.

Authors:  E Chantelau
Journal:  Br J Ophthalmol       Date:  1998-07       Impact factor: 4.638

  3 in total

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