ArticleEndocrinology2015
The role of hypothalamic mTORC1 signaling in insulin regulation of food intake, body weight, and sympathetic nerve activity in male mice.
Article in Endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- Glycation-lowering compounds inhibit ghrelin signaling to reduce food intake, lower insulin resistance, and extend lifespan.Cell reports · 2025Article
- Hippocampal Inhibitory Interneuron-Specific DREADDs Treatment Alters mTORC1-4E-BP Signaling and Impairs Memory Formation.Journal of neurochemistry · 2025Article
- Sex-dimorphic effects of glucose transporter-2 gene knockdown on hypothalamic primary astrocyte phosphoinositide-3-kinase (PI3K)/protein kinase B (PKB/Akt)/mammalian target of rapamycin (mTOR) cascade protein expression and phosphorylation.Molecular and cellular endocrinology · 2024Article
- Sex-specific molecular signature of mouse podocytes in homeostasis and in response to pharmacological challenge with rapamycin.Biology of sex differences · 2024Article
- Post-acute exercise cardiovagal modulation in older male adults with and without type 2 diabetes.European journal of applied physiology · 2024Article
- mTORC1 in energy expenditure: consequences for obesity.Nature reviews. Endocrinology · 2024Review
- Changes of Signaling Pathways in Hypothalamic Neurons with Aging.Current issues in molecular biology · 2023Review
- NeuronalCells · 2023Article
- Association of Maternal Metabolites and Metabolite Networks with Newborn Outcomes in a Multi-Ancestry Cohort.Metabolites · 2023Article
- Article
- Metformin acts as a dual glucose regulator in mouse brain.Frontiers in pharmacology · 2023Article
- Alpha-ketoglutarate partially alleviates effects of high-fat high-fructose diet in mouse muscle.EXCLI journal · 2023Article
- The Role of Insulin Signaling in Hippocampal-Related Diseases: A Focus on Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Exercise based assessment of cardiac autonomic function in type 1 versus type 2 diabetes mellitus.Cardiology journal · 2022Article
- Understanding the complex role of mTORC as an intracellular critical mediator of whole-body metabolism in anorexia nervosa: A mini review.Acta bio-medica : Atenei Parmensis · 2021Review
- Leucine Potentiates Glucose-mediatedBiomedicines · 2020Article
- Modulation of hypothalamic S6K1 and S6K2 alters feeding behavior and systemic glucose metabolism.The Journal of endocrinology · 2020Article
- DEPTOR at the Nexus of Cancer, Metabolism, and Immunity.Physiological reviews · 2018Review
- The gene expression of the neuronal protein, SLC38A9, changes in mouse brain after in vivo starvation and high-fat diet.PloS one · 2017Article
- Anorexic response to rapamycin does not appear to involve a central mechanism.Clinical and experimental pharmacology & physiology · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Insulin action in the brain particularly the hypothalamus is critically involved in the regulation of several physiological processes, including energy homeostasis and sympathetic nerve activity, but the underlying mechanisms are poorly understood. The mechanistic target of rapamycin complex 1 (mTORC1) is implicated in the control of diverse cellular functions, including sensing nutrients and energy status. Here, we examined the role of hypothalamic mTORC1 in mediating the anorectic, weight-reducing, and sympathetic effects of central insulin action. In a mouse hypothalamic cell line (GT1-7), insulin treatment increased mTORC1 activity in a time-dependent manner. In addition, intracerebroventricular (ICV) administration of insulin to mice activated mTORC1 pathway in the hypothalamic arcuate nucleus, a key site of central action of insulin. Interestingly, inhibition of hypothalamic mTORC1 with rapamycin reversed the food intake- and body weight-lowering effects of ICV insulin. Rapamycin also abolished the ability of ICV insulin to cause lumbar sympathetic nerve activation. In GT1-7 cells, we found that insulin activation of mTORC1 pathway requires phosphatidylinositol 3-kinase (PI3K). Consistent with this, genetic disruption of PI3K in mice abolished insulin stimulation of hypothalamic mTORC1 signaling as well as the lumbar sympathetic nerve activation evoked by insulin. These results demonstrate the importance of mTORC1 pathway in the hypothalamus in mediating the action of insulin to regulate energy homeostasis and sympathetic nerve traffic. Our data also highlight the key role of PI3K as a link between insulin receptor and mTORC1 signaling in the hypothalamus.
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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.