Plasma somatomedins, endogenous insulin secretion, and growth in transient neonatal diabetes mellitus
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Transient neonatal diabetes mellitus infants struggle to grow without insulin. This study found that insulin-like growth factor I (IGF-I) deficiency also contributes to impaired growth in these infants.
Area of Science:
- Endocrinology
- Pediatric Endocrinology
- Metabolic Disorders
Background:
- Transient neonatal diabetes mellitus (TNDM) is a rare condition characterized by intrauterine growth restriction and failure to thrive postnatally.
- Insulin therapy is crucial for managing TNDM, but the role of other growth factors in TNDM-related growth impairment is not fully understood.
Observation:
- A single infant with TNDM presented with low cord blood insulin and somatomedin C/insulin-like growth factor I (SMC/IGF-I) levels.
- Insulin-like growth factor II (IGF-II) levels were normal in the infant.
- Insulin therapy initiated on day four led to weight gain and a subsequent increase in SMC/IGF-I levels.
Findings:
- The study identified a potential dual etiology for growth failure in TNDM, involving both insulin deficiency and SMC/IGF-I deficiency.
- Insulin-like growth factor II (IGF-II) does not appear to play a significant role in the growth impairment observed in this TNDM case.
Implications:
- These findings suggest that addressing SMC/IGF-I deficiency alongside insulin therapy may be important for optimizing growth in infants with TNDM.
- Further research into the complex interplay between insulin and IGF-I in TNDM is warranted to improve patient outcomes.
Abstract:
Infants with transient neonatal diabetes mellitus are small for gestational age and fail to thrive postnatally unless insulin is administered. We have measured the concentrations of insulin-related growth factors in an infant girl with this condition to learn if deficiencies in one or more of these factors could be responsible for the impaired growth. Cord blood serum radioimmunoassayable insulin and somatomedin C/insulin-like growth factor I (SMC/IGF-I) were low, but insulin-like growth factor II (IGF-II) measured by a specific radioreceptor assay was normal. Insulin therapy begun on the fourth day of life resulted in a prompt increase in weight and a delayed rise in SMC/IFG-I. No significant changes in IGF-II were observed. After 2.5 months, insulin treatment was discontinued. At that time, endogenous insulin secretion was documented by increased urinary C-peptide. Normal growth and SMC/IFG-I levels persisted. We conclude that growth failure in this condition may be related not only to a lack of insulin but also to SMC/IGF-I deficiency. A deficiency in IGF-II is not involved.