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Axon Stretch Growth: The Mechanotransduction of Neuronal Growth

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Catch-Up Growth: Basic Mechanisms.

Ian J Griffin¹

¹UC Davis Children's Hospital, Sacramento, CA, USA.

Nestle Nutrition Institute Workshop Series

|June 27, 2015

Summary

This summary is machine-generated.

Catch-up growth involves increased ghrelin and growth hormone (GH) during malnutrition. Nutritionally responsive proteins block liver GH signaling, shifting effects to other tissues, then resume IGF-1 production post-malnutrition.

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Area of Science:

Neuroendocrinology
Growth regulation
Nutritional science

Background:

Nutritional inadequacy triggers neuroendocrine adaptations for catch-up growth.
Ghrelin and growth hormone (GH) increase during malnutrition.
Malnutrition induces sirtuin 1 (SIRT1) and fibroblast growth factor 21 (FGF21), inhibiting liver GH signaling.

Purpose of the Study:

To elucidate the neuroendocrine mechanisms regulating catch-up growth following nutritional inadequacy.
To investigate the role of ghrelin, GH, and specific inhibitory proteins in mediating catch-up growth.

Main Methods:

The study discusses a neuroendocrine model of catch-up growth.
It reviews findings from animal models of nutritional inadequacy.
Analysis focuses on the interplay between hormones (GH, ghrelin, IGF-1) and signaling pathways (JAK/STAT) influenced by SIRT1 and FGF21.

Main Results:

Malnutrition increases ghrelin and GH, while SIRT1 and FGF21 inhibit liver IGF-1 production via the JAK/STAT pathway.
GH's action shifts from liver to other tissues (muscle, adipose) and from IGF-1-mediated to GH-mediated effects.
Upon nutrient repletion, SIRT1 and FGF21 decrease, liver GH sensitivity recovers, and IGF-1 production resumes, driving catch-up growth.
Elevated ghrelin levels, potentially prolonged post-malnutrition, correlate with increased catch-up growth rates.

Conclusions:

The neuroendocrine model explains catch-up growth by shifting GH signaling from liver-centric IGF-1 production to GH-mediated effects in peripheral tissues during and after nutritional insufficiency.
Prolonged ghrelin and GH elevation combined with restored hepatic GH sensitivity provides a mechanism for accelerated growth post-malnutrition.