Nutritional regulation of the insulin-like growth factors
Abstract
Nutrition is one of the main regulators of circulating IGF-I. In humans, serum IGF-I concentrations are markedly lowered by energy and/or protein deprivation. Both energy and proteins are critical in the regulation of serum IGF-I concentrations. Indeed, after fasting, optimal intake of both energy and protein is necessary for the rapid restoration of circulating IGF-I. We believe, however, that in adult humans energy may be somewhat more important than protein in this regard. While the lowest protein intake is able to increase IGF-I in the presence of adequate energy, there is a threshold energy requirement below which optimal protein intake fails to raise IGF-I after fasting. When energy intake is severely reduced, the carbohydrate content of the diet is a major determinant of responsiveness of IGF-I to GH. The essential amino acid content of the diet is also critical for the optimal restoration of IGF-I after fasting, when protein intake is reduced. The exquisite sensitivity of circulating IGF-I to nutrients, the nycthemeral stability of its concentrations and its relative short half-life constitute the basis for its use as a marker of both nutritional status and adequacy of nutritional rehabilitation. For these indications, IGF-I measurement is more sensitive and more specific than measurement of the other nutrient-related serum proteins (albumin, prealbumin, transferrin, retinol-binding protein). Animal models have been developed to investigate the mechanisms responsible for the nutritional regulation of IGF-I. There is no doubt that many mechanisms are involved (Fig. 12). Decline of serum IGF-I in dietary restriction is independent of the diet-induced alterations in pituitary GH secretion. The role of the liver GH receptors is dependent on the severity of the nutritional insult. In severe dietary restriction (fasting), a marked decrease of the number of somatogenic receptors supports the role of a receptor defect in the decline of circulating IGF-I. In contrast, in less severe forms of dietary restriction (protein restriction), the decline of IGF-I results from a postreceptor defect in the GH action at the hepatic level. Nutritional deprivation decreases hepatic IGF-I production by diminishing IGF-I gene expression. Decline in IGF-I gene expression is mainly caused by nutrient deficiency and less importantly by the nutritionally induced hormonal changes (insulin and T3). Diet restriction also increases the clearance and degradation of serum IGF-I through changes in the levels of circulating IGFBPs.(ABSTRACT TRUNCATED AT 400 WORDS)
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Free IGF-1 decreased by approximately 75% with fasting.
“whereas free IGF-1 decreased by approximately 75% with fasting (17, 18) (Table 2).”
From The role of falling leptin levels in the neuroendocrine and metabolic adaptation to short-term starvation in healthy men (2003) · cites this paper as [18]
Total IGF-1 levels declined significantly by over 50% with fasting.
“total IGF-1 levels declined significantly by over 50%”
From The role of falling leptin levels in the neuroendocrine and metabolic adaptation to short-term starvation in healthy men (2003) · cites this paper as [18]
Fasting decreases IGF-1 levels despite elevated GH levels, most likely because of changes in other determinants of its secretion, such as hormones (insulin) and nutritional status per se as well as GH resistance in the liver.
“fasting decreases IGF-1 levels despite elevated GH levels, most likely because of changes in other determinants of its secretion, such as hormones (insulin) and nutritional status per se as well as GH resistance in the liver (18, 45).”
From The role of falling leptin levels in the neuroendocrine and metabolic adaptation to short-term starvation in healthy men (2003) · cites this paper as [18]
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- Authors
- Thissen, J. P.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- ORCID
- Thissen, J. P.
- Venue
- Endocrine Reviews
- Publisher
- The Endocrine Society
- Published
- 1994-02-01
- Volume
- 15
- Issue
- 1
- Pages
- 80-101
- ISSN
- 0163-769X (ISSN-L)
- OpenAlex
- W1964652533
- Cited by
- 1,578
- References
- 0
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 18 · 2023: 14 · 2022: 19 · 2021: 29 · 2020: 32 · 2019: 25 · 2018: 28 · 2017: 24 · 2016: 34 · 2015: 37 · 2014: 38 · 2013: 47 · 2012: 45
- FWCI
- 41.61
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrine Reviews (publishedVersion)
- PubMed (publishedVersion)
- Digital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B)) (submittedVersion)
- Funders
- National Institutes of Health (5r01hd028081-05, 5r01hd026871-05)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-28081, HD 08299, HD 26871, R01HD008299)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Health Sciences › Medicine › Physiology › Dietary Effects on Health
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- insulin-like growth factor I, nutritional regulation, caloric restriction, protein restriction, fasting, growth hormone, IGF-I binding proteins, dietary biomarkers, nutritional rehabilitation, essential amino acids, carbohydrate intake, postreceptor defect
- MeSH terms
- Animals, Diet, Fasting, Gene Expression Regulation, Humans, Hypothalamus, Insulin, Insulin-Like Growth Factor I, Insulin-Like Growth Factor II, Nutritional Physiological Phenomena, Nutritional Status, Somatomedins, Thyroid Hormones, Exercise
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