ArticleJournal of obesity2012
Excessive Leucine-mTORC1-Signalling of Cow Milk-Based Infant Formula: The Missing Link to Understand Early Childhood Obesity.
Article in Journal of obesity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 56 citations in OpenAlex.
- Trial
- Lower Protein Intake Supports Normal Growth of Full-Term Infants Fed Formula: A Randomized Controlled Trial.Nutrients · 2018Trial
- Postprandial metabolic response of breast-fed infants and infants fed lactose-free vs regular infant formula: A randomized controlled trial.Scientific reports · 2017Trial
- Role of selected amino acids on plasma IGF-I concentration in infants.European journal of nutrition · 2017Trial
- Article
- White Adipocyte Stem Cell Expansion Through Infant Formula Feeding: New Insights into Epigenetic Programming Explaining the Early Protein Hypothesis of Obesity.International journal of molecular sciences · 2025Review
- Diabetes-preventive molecular mechanisms of breast versus formula feeding: new insights into the impact of milk on stem cell Wnt signaling.Frontiers in nutrition · 2025Review
- Risk of Fat Mass- and Obesity-Associated Gene-Dependent Obesogenic Programming by Formula Feeding Compared to Breastfeeding.Nutrients · 2024Review
- Bovine milk consumption affects the transcriptome of porcine adipose stem cells: Do exosomes play any role?PloS one · 2024Article
- Exosome-Derived MicroRNAs of Human Milk and Their Effects on Infant Health and Development.Biomolecules · 2021Review
- Long term follow-up of the dietary intake in propionic acidemia.Molecular genetics and metabolism reports · 2021Article
- Relationship between age at giving fortified powdered cow's milk and cessation of breastfeeding on the nutritional status of a Chilean child cohort followed from birth to 3 years of age.European journal of clinical nutrition · 2020Article
- Sexual dimorphism in hypothalamic inflammation in the offspring of dams exposed to a diet rich in high fat and branched-chain amino acids.American journal of physiology. Endocrinology and metabolism · 2019Article
- Introduction of fish and other foods during infancy and risk of asthma in the All Babies In Southeast Sweden cohort study.European journal of pediatrics · 2019Article
- Diseases of Civilization - Cancer, Diabetes, Obesity and Acne - the Implication of Milk, IGF-1 and mTORC1.Maedica · 2018Article
- Gender-Associated Impact of Early Leucine Supplementation on Adult Predisposition to Obesity in Rats.Nutrients · 2018Article
- Depurinized milk downregulates rat thymus MyD88/Akt/p38 function, NF-κB-mediated inflammation, caspase-1 activity but not the endonuclease pathway: in vitro/in vivo study.Scientific reports · 2017Article
- Milk: a postnatal imprinting system stabilizing FoxP3 expression and regulatory T cell differentiation.Clinical and translational allergy · 2016Review
- Milk--A Nutrient System of Mammalian Evolution Promoting mTORC1-Dependent Translation.International journal of molecular sciences · 2015Review
- Protective effect of breastfeeding against overweight can be detected as early as the second year of life: a study of children from one of the most socially-deprived areas of Brazil.Journal of health, population, and nutrition · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased protein supply by feeding cow-milk-based infant formula in comparison to lower protein content of human milk is a well-recognized major risk factor of childhood obesity. However, there is yet no conclusive biochemical concept explaining the mechanisms of formula-induced childhood obesity. It is the intention of this article to provide the biochemical link between leucine-mediated signalling of mammalian milk proteins and adipogenesis as well as early adipogenic programming. Leucine has been identified as the predominant signal transducer of mammalian milk, which stimulates the nutrient-sensitive kinase mammalian target of rapamycin complex 1 (mTORC1). Leucine thus functions as a maternal-neonatal relay for mTORC1-dependent neonatal β-cell proliferation and insulin secretion. The mTORC1 target S6K1 plays a pivotal role in stimulation of mesenchymal stem cells to differentiate into adipocytes and to induce insulin resistance. It is of most critical concern that infant formulas provide higher amounts of leucine in comparison to human milk. Exaggerated leucine-mediated mTORC1-S6K1 signalling induced by infant formulas may thus explain increased adipogenesis and generation of lifelong elevated adipocyte numbers. Attenuation of mTORC1 signalling of infant formula by leucine restriction to physiologic lower levels of human milk offers a great chance for the prevention of childhood obesity and obesity-related metabolic diseases.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.