title: Nutritionally-induced catch-up growth.
abstract: Malnutrition is considered a leading cause of growth attenuation in children. When food is replenished, spontaneous catch-up (CU) growth usually occurs, bringing the child back to its original growth trajectory. However, in some cases, the CU growth is not complete, leading to a permanent growth deficit. This review summarizes our current knowledge regarding the mechanism regulating nutrition and growth, including systemic factors, such as insulin, growth hormone, insulin- like growth factor-1, vitamin D, fibroblast growth factor-21, etc., and local mechanisms, including autophagy, as well as regulators of transcription, protein synthesis, miRNAs and epigenetics. Studying the molecular mechanisms regulating CU growth may lead to the establishment of better nutritional and therapeutic regimens for more effective CU growth in children with malnutrition and growth abnormalities. It will be fascinating to follow this research in the coming years and to translate the knowledge gained to clinical benefit.
authors.affiliation: The Jesse Z and Sara Lea Shafer Institute for Endocrinology and Diabetes, National Center for Children's Diabetes, Schneider Children's Medical Center of Israel, and Felsenstein Medical Research Center, Petach Tikva 49100, and Sackler School of Medicine, Tel Aviv University, Tel Aviv, 69978, Israel. galiagy@post.tau.ac.il.
authors.forename: Galia
authors.initials: G
authors.lastname: Gat-Yablonski
authors.affiliation: The Jesse Z and Sara Lea Shafer Institute for Endocrinology and Diabetes, National Center for Children's Diabetes, Schneider Children's Medical Center of Israel, and Felsenstein Medical Research Center, Petach Tikva 49100, and Sackler School of Medicine, Tel Aviv University, Tel Aviv, 69978, Israel. mosheph@post.tau.ac.il.
authors.forename: Moshe
authors.initials: M
authors.lastname: Phillip
mesh_terms: D001343:Autophagy / Q000502:physiology; D002648:Child; D057890:Epigenomics; D005346:Fibroblast Growth Factors / Q000097:blood; D005938:Glucocorticoids / Q000097:blood; D006130:Growth Disorders / Q000178:diet therapy / Q000209:etiology / Q000503:physiopathology*; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000235:genetics / Q000378:metabolism; D007223:Infant; D007328:Insulin / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D020738:Leptin / Q000097:blood; D044342:Malnutrition / Q000150:complications / Q000178:diet therapy / Q000503:physiopathology*; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism; D009752:Nutritional Status; D058570:TOR Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D013963:Thyroid Hormones / Q000097:blood; D014807:Vitamin D / Q000097:blood
chemical_list: D005938:Glucocorticoids; C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D007328:Insulin; D020738:Leptin; D035683:MicroRNAs; D013963:Thyroid Hormones; C414620:fibroblast growth factor 21; D014807:Vitamin D; D005346:Fibroblast Growth Factors; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; C546842:MTOR protein, human; D058570:TOR Serine-Threonine Kinases