ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2016
Early postnatal amylin treatment enhances hypothalamic leptin signaling and neural development in the selectively bred diet-induced obese rat.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- Hypothalamic obesity in pediatric vs. adult craniopharyngioma: mechanisms, management, and cardiometabolic outcomes.Pituitary · 2026Review
- Amylin: A Multi-Functional Pancreatic Hormone-A Review.Diabetes, obesity & metabolism · 2026Review
- Neurodevelopmental Programming of Adiposity: Contributions to Obesity Risk.Endocrine reviews · 2024Review
- Neurofibromatosis type 1-dependent alterations in mouse microglia function are not cell-intrinsic.Acta neuropathologica communications · 2023Article
- Mediators of Amylin Action in Metabolic Control.Journal of clinical medicine · 2022Review
- Developmental programming of hypothalamic melanocortin circuits.Experimental & molecular medicine · 2022Review
- Mouse Microglial Calcitonin Receptor Knockout Impairs Hypothalamic Amylin Neuronal pSTAT3 Signaling but Lacks Major Metabolic Consequences.Metabolites · 2022Article
- A spontaneous leptin receptor point mutation causes obesity and differentially affects leptin signaling in hypothalamic nuclei resulting in metabolic dysfunctions distinct from db/db mice.Molecular metabolism · 2019Article
- Amylin Selectively Signals Onto POMC Neurons in the Arcuate Nucleus of the Hypothalamus.Diabetes · 2018Article
- Maternal metabolic adaptations are necessary for normal offspring growth and brain development.Physiological reports · 2018Article
- Amylin - Its role in the homeostatic and hedonic control of eating and recent developments of amylin analogs to treat obesity.Molecular metabolism · 2018Review
- 10 lessons learned by a misguided physician.Physiology & behavior · 2017Review
- Involvement of Amylin and Leptin in the Development of Projections from the Area Postrema to the Nucleus of the Solitary Tract.Frontiers in endocrinology · 2017Article
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Authors and funding
6 authors at 5 institutions in 3 countries.
Funding
Abstract
Selectively bred diet-induced obese (DIO) rats become obese on a high-fat diet and are leptin resistant before becoming obese. Compared with diet-resistant (DR) neonates, DIO neonates have impaired leptin-dependent arcuate (ARC) neuropeptide Y/agouti-related peptide (NPY/AgRP) and α-melanocyte-stimulating hormone (α-MSH; from proopiomelanocortin (POMC) neurons) axon outgrowth to the paraventricular nucleus (PVN). Using phosphorylation of STAT3 (pSTAT3) as a surrogate, we show that reduced DIO ARC leptin signaling develops by postnatal day 7 (P7) and is reduced within POMC but not NPY/AgRP neurons. Since amylin increases leptin signaling in adult rats, we treated DIO neonates with amylin during postnatal hypothalamic development and assessed leptin signaling, leptin-dependent ARC-PVN pathway development, and metabolic changes. DIO neonates treated with amylin from P0-6 and from P0-16 increased ARC leptin signaling and both AgRP and α-MSH ARC-PVN pathway development, but increased only POMC neuron number. Despite ARC-PVN pathway correction, P0-16 amylin-induced reductions in body weight did not persist beyond treatment cessation. Since amylin enhances adult DIO ARC signaling via an IL-6-dependent mechanism, we assessed ARC-PVN pathway competency in IL-6 knockout mice and found that the AgRP, but not the α-MSH, ARC-PVN pathway was reduced. These results suggest that both leptin and amylin are important neurotrophic factors for the postnatal development of the ARC-PVN pathway. Amylin might act as a direct neurotrophic factor in DIO rats to enhance both the number of POMC neurons and their α-MSH ARC-PVN pathway development. This suggests important and selective roles for amylin during ARC hypothalamic development.
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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.