Somatomedin-C/Insulin-Like Growth Factor I and Vitamin D-Induced Growth*
- 1 October 1986
- journal article
- research article
- Published by The Endocrine Society in Endocrinology
- Vol. 119 (4) , 1660-1665
- https://doi.org/10.1210/endo-119-4-1660
Abstract
We measured serum somatomedin-C/insulin-like growth factor I (Sm-C/IGF-1) concentrations in vitamin D-deficient (-D) rat form 3-7 weeks of age to evaluate the role of Sm-C/IGF-I in the growth effects of vitamin D. To exclude effects of alterations in food intake, feeding patterns, and plasma minerals, controls included the following groups: pair fed (PFC; n = 10), low calcium diet (LCa; n = 10), meal fed (MFC; n = 10), and ad libitum fed (AdLC; n = 5). The -D, LCa, and PFC groups had similarly depressed growth rates and Sm-C/IGF-I concentrations. The growth and Sm-C/IGF-I concentrations of the MFC group were less than those in the AdLC group, but greater than those in the -D, PFC, and LCa groups. In all groups Sm-C/GF-I concentrations correlated well with food intake, indicating that calorie intake, and not vitamin D deficiency or hypocalcemia, was the primary factor in reducing Sm-C/IGF-L. In the final 4 days of the study, half of the -D rats were given 1,25-dihydroxyvitamin D3 (2 ng/g bW; -D/repleted), while half of the PFC rats were given excess food during the meal period (PFC/refed). The weight gain of -D/repleted rats surpassed that of the -D rats treated with vehicle (P < 0.050); similarly, the weight gain of PFC/refed rats exceeded that of the PFC rats (P < 0.01). In contrast, the food intake and Sm-C/IGF-I levels of PFC/refed rats were greater than those in PFC rats (P < 0.01), while the -D/repleted rats did not have significantly altered food intake or Sm-C/IGF-I levels. We conclude 1) that alterations in Sm-C/IGF-I concentrations of young growing -D rats are not directly related to lack of vitamin D, but, rather, to poor nutrition resulting from reduced food intake; and 2) that serum Sm-C/IGF-I is not a primary mediator of growth in -D/repleted rats since improved weight gain resulting from 1,25-dihydroxyvitamin D3 treatment can occur, acutely, without changes in serum Sm-C/IGF-I concentrations.This publication has 9 references indexed in Scilit:
- Time Course Study of Insulin Secretion after 1,25–Dihydroxyvitamin D3Administration*Endocrinology, 1985
- Relationship between Plasma Somatomedin-C and Liver Somatogenic Binding Sites in Neonatal Rats during Malnutrition and after Short and Long Term Refeeding*Endocrinology, 1984
- Tissue concentrations of somatomedin C: further evidence for multiple sites of synthesis and paracrine or autocrine mechanisms of action.Proceedings of the National Academy of Sciences, 1984
- Cellular Mechanisms of Insulin Release: The Effects of Vitamin D Deficiency and Repletion on Rat Insulin Secretion*Endocrinology, 1983
- Attenuation by Hypocalcemia of Pulsatile Growth Hormone Secretion in Conscious Male RatsNeuroendocrinology, 1982
- Hypocalcemic, Hypophosphatemic Rickets in Rat Pups Sucklinjg Vitamin D-Deprived Mothers*Endocrinology, 1981
- Intestinal and metabolic effect of 1,25-dihydroxyvitamin D3 in normal adult ratAmerican Journal of Physiology-Gastrointestinal and Liver Physiology, 1981
- Increased Growth after Long-Term Oral 1α,25-Vitamin D3in Childhood Renal OsteodystrophyNew England Journal of Medicine, 1978
- Vitamin D and Growth1Journal of Nutrition, 1955