ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Leptin stimulates neuropeptide Y and cocaine amphetamine-regulated transcript coexpressing neuronal activity in the dorsomedial hypothalamus in diet-induced obese mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 74 citations in OpenAlex.
- Diet-Driven Microglial Activation: Region-Specific Neuroinflammation in the Mouse Brain.Brain sciences · 2025Article
- Central leptin pathways in metabolic homeostasis.Clinical science (London, England : 1979) · 2025Review
- Leptin and Associated Neural Pathways Underlying Obesity-Induced Hypertension.Comprehensive Physiology · 2025Review
- Article
- Molecular Characterization and Expression Pattern ofBiology · 2023Article
- Paraventricular nucleus-Medullary interactions: How they help enable endocrine responses to metabolic stress.Current opinion in endocrine and metabolic research · 2022Article
- The contribution of astrocytes to obesity-associated metabolic disturbances.Journal of biomedical research · 2022Article
- Review
- The physiological control of eating: signals, neurons, and networks.Physiological reviews · 2022 · on this mapArticle
- Hypothalamic control of energy expenditure and thermogenesis.Experimental & molecular medicine · 2022Review
- Hypothalamic Kisspeptin Neurons and the Control of Homeostasis.Endocrinology · 2022Review
- Article
- Transcriptional study reveals a potential leptin-dependent gene regulatory network in zebrafish brain.Fish physiology and biochemistry · 2021Article
- Review
- Research and prospect of peptides for use in obesity treatment (Review).Experimental and therapeutic medicine · 2020Review
- Transcriptional study of appetite regulating genes in the brain of zebrafish (Danio rerio) with impaired leptin signalling.Scientific reports · 2019Article
- Convergent neuronal projections from paraventricular nucleus, parabrachial nucleus, and brainstem onto gastrocnemius muscle, white and brown adipose tissue in male rats.The Journal of comparative neurology · 2019Article
- Role of POMC and AgRP neuronal activities on glycaemia in mice.Scientific reports · 2019Article
- Diet-induced obesity suppresses cortical bone accrual by a neuropeptide Y-dependent mechanism.International journal of obesity (2005) · 2018Article
- Leptin Signaling in the Control of Metabolism and Appetite: Lessons from Animal Models.Journal of molecular neuroscience : MN · 2018Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Neuropeptide Y (NPY) neurons in both the arcuate nucleus of the hypothalamus (ARH) and the dorsomedial hypothalamus (DMH) have been implicated in food intake and obesity. However, while ARH NPY is highly expressed in the lean animal, DMH NPY mRNA expression is observed only after diet-induced obesity (DIO). Furthermore, while ARH NPY neurons are inhibited by leptin, the effect of this adipokine on DMH NPY neurons is unknown. In this study we show that in contrast to the consistent expression in the ARH, DMH NPY mRNA expression was undetectable until after 10 weeks in mice fed a high-fat diet, and peaked at 20 weeks. Surprisingly, electrophysiological experiments demonstrated that leptin directly depolarized and increased the firing rate of DMH NPY neurons in DIO mice. To further differentiate the regulation of DMH and ARH NPY populations, fasting decreased expression of DMH NPY expression, while it increased ARH NPY expression. However, treatment with a leptin receptor antagonist failed to alter DMH NPY expression, indicating that leptin may not be the critical factor regulating mRNA expression. Importantly, we also demonstrated that DMH NPY neurons coexpress cocaine amphetamine-regulated transcript (CART); however, CART mRNA expression in the DMH peaked earlier in the progression of DIO. This study demonstrates novel and important findings. First, NPY and CART are coexpressed in the same neurons within the DMH, and second, leptin stimulates DMH NPY neurons. These studies suggest that during the progression of DIO, there is an unknown signal that drives the expression of the orexigenic NPY signal within the DMH, and that the chronic hyperleptinemia increases the activity of these NPY/CART neurons.
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