ArticleEndocrinology2013
Amylin acts in the central nervous system to increase sympathetic nerve activity.
Article in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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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.
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Who cites it
21 citing papers in PubMed, 57 citations in OpenAlex.
- Amylin: A Multi-Functional Pancreatic Hormone-A Review.Diabetes, obesity & metabolism · 2026Review
- The story of amylin: from physiology to therapy.Nature metabolism · 2026Review
- Amylin: emergent therapeutic opportunities in overweight, obesity and diabetes mellitus.Nature reviews. Endocrinology · 2025Review
- Discovery of peptides as key regulators of metabolic and cardiovascular crosstalk.Cell reports · 2025Review
- Amylin: From Mode of Action to Future Clinical Potential in Diabetes and Obesity.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025Review
- Mediators of Amylin Action in Metabolic Control.Journal of clinical medicine · 2022Review
- Mouse Microglial Calcitonin Receptor Knockout Impairs Hypothalamic Amylin Neuronal pSTAT3 Signaling but Lacks Major Metabolic Consequences.Metabolites · 2022Article
- The long-acting amylin/calcitonin receptor agonist ZP5461 suppresses food intake and body weight in male rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Impaired Leptin Signalling in Obesity: Is Leptin a New Thermolipokine?International journal of molecular sciences · 2021Review
- An inducible model of human amylin overexpression reveals diverse transcriptional changes.Neuroscience letters · 2019Article
- Reduced renal sympathetic nerve activity contributes to elevated glycosuria and improved glucose tolerance in hypothalamus-specific Pomc knockout mice.Molecular metabolism · 2017Article
- Traveling from the hypothalamus to the adipose tissue: The thermogenic pathway.Redox biology · 2017Review
- Gut hormones such as amylin and GLP-1 in the control of eating and energy expenditure.International journal of obesity supplements · 2016Review
- FGF21 Mediates Endocrine Control of Simple Sugar Intake and Sweet Taste Preference by the Liver.Cell metabolism · 2016Article
- Hypothalamic-autonomic control of energy homeostasis.Endocrine · 2015Review
- CGRP as a neuropeptide in migraine: lessons from mice.British journal of clinical pharmacology · 2015Review
- Regulation of glucose tolerance and sympathetic activity by MC4R signaling in the lateral hypothalamus.Diabetes · 2015Article
- The brain and brown fat.Annals of medicine · 2015Review
- Amylin at the interface between metabolic and neurodegenerative disorders.Frontiers in neuroscience · 2015Review
- Central nervous system regulation of brown adipose tissue.Comprehensive Physiology · 2014Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The pancreatic hormone amylin acts in the central nervous system (CNS) to decrease food intake and body weight. We hypothesized that amylin action in the CNS promotes energy expenditure by increasing the activity of the sympathetic nervous system. In mice, ip administration of amylin significantly increased c-Fos immunoreactivity in hypothalamic and brainstem nuclei. In addition, mice treated with intracerebroventricular (icv) amylin (0.1 and 0.2 nmol) exhibited a dose-related decrease in food intake and body weight, measured 4 and 24 hours after treatment. The icv injection of amylin also increased body temperature in mice. Using direct multifiber sympathetic nerve recording, we found that icv amylin elicited a significant and dose-dependent increase in sympathetic nerve activity (SNA) subserving thermogenic brown adipose tissue (BAT). Of note, icv injection of amylin also evoked a significant and dose-related increase in lumbar and renal SNA. Importantly, icv pretreatment with the amylin receptor antagonist AC187 (20 nmol) abolished the BAT SNA response induced by icv amylin, indicating that the sympathetic effects of amylin are receptor-mediated. Conversely, icv amylin-induced BAT SNA response was enhanced in mice overexpressing the amylin receptor subunit, RAMP1 (receptor-activity modifying protein 1), in the CNS. Our data demonstrate that CNS action of amylin regulates sympathetic nerve outflow to peripheral tissues involved in energy balance and cardiovascular function.
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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.