Cited by 183Regulation of Appetite and ObesityHypothalamic control of reproductive hormonesBiochemical Analysis and Sensing Techniques

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Amino acids inhibit Agrp gene expression via an mTOR-dependent mechanism

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Morrison, Christopher D., Xi, Xiaochun, White, Christy L., Ye, Jianping, Martin, Roy J.·2007·American Journal of Physiology-Endocrinology and Metabolism

DOI 10.1152/ajpendo.00675.2006PMC PMC2596875

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Abstract

Metabolic fuels act on hypothalamic neurons to regulate feeding behavior and energy homeostasis, but the signaling mechanisms mediating these effects are not fully clear. Rats placed on a low-protein diet (10% of calories) exhibited increased food intake (P < 0.05) and hypothalamic Agouti-related protein (Agrp) gene expression (P = 0.002). Direct intracerebroventricular injection of either an amino acid mixture (RPMI 1640) or leucine alone (1 mug) suppressed 24-h food intake (P < 0.05), indicating that increasing amino acid concentrations within the brain is sufficient to suppress food intake. To define a cellular mechanism for these direct effects, GT1-7 hypothalamic cells were exposed to low amino acids for 16 h. Decreasing amino acid availability increased Agrp mRNA levels in GT1-7 cells (P < 0.01), and this effect was attenuated by replacement of the amino acid leucine (P < 0.05). Acute exposure to elevated amino acid concentrations increased ribosomal protein S6 kinase phosphorylation via a rapamycin-sensitive mechanism, suggesting that amino acids directly stimulated mammalian target of rapamycin (mTOR) signaling. To test whether mTOR signaling contributes to amino acid inhibition of Agrp gene expression, GT1-7 cells cultured in either low or high amino acids for 16 h and were also treated with rapamcyin (50 nM). Rapamycin treatment increased Agrp mRNA levels in cells exposed to high amino acids (P = 0.01). Taken together, these observations indicate that amino acids can act within the brain to inhibit food intake and that a direct, mTOR-dependent inhibition of Agrp gene expression may contribute to this effect.

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Authors: Morrison, C. D., Xi, X., White, C. L., Ye, J., & Martin, R. J.
Affiliations: Pennington Biomedical Research Center (US)
ORCID: Morrison, Christopher D.
Ye, Jianping
Martin, Roy J.
Venue: American Journal of Physiology-Endocrinology and Metabolism
Publisher: American Physiological Society
Published: 2007-07
Volume: 293
Issue: 1
Pages: E165-E171
ISSN: 0193-1849 (ISSN-L)
1522-1555
DOI: 10.1152/ajpendo.00675.2006
PMC: PMC2596875
OpenAlex: W2015145490
Cited by: 183
References: 36
Citations by year: 2026: 5 · 2025: 5 · 2024: 4 · 2023: 5 · 2022: 6 · 2021: 4 · 2020: 15 · 2019: 7 · 2018: 9 · 2017: 10 · 2016: 13 · 2015: 7 · 2014: 7 · 2013: 11 · 2012: 16
FWCI: 6.53
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute of General Medical Sciences (P20GM103528, P30GM118430)
National Institute of Diabetes and Digestive and Kidney Diseases (P30DK072476)
National Institute of Neurological Disorders and Stroke (NS-051570, R03NS051570)
National Center for Research Resources (RR 021945, P20RR021945)
Topics: Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
Health Sciences › Nursing › Nutrition and Dietetics › Biochemical Analysis and Sensing Techniques
Keywords: amino acids, agouti-related protein, mTOR signaling, leucine, food intake regulation, hypothalamic neurons, GT1-7 cells, S6K, rapamycin, low-protein diet, energy homeostasis
MeSH terms: Amino Acids, Animals, Cells, Cultured, Eating, Gene Expression Regulation, Hypothalamus, Male, Protein Kinases, Signal Transduction, Rats, Sprague-Dawley, Diet, Protein-Restricted, Intercellular Signaling Peptides and Proteins, Rats, Agouti-Related Protein, TOR Serine-Threonine Kinases

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Amino acids inhibit Agrp gene expression via an mTOR-dependent mechanism

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