ArticleAmerican journal of physiology. Endocrinology and metabolism2015
Leptin in the hindbrain facilitates phosphorylation of STAT3 in the hypothalamus.
Article in American journal of physiology. Endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Leptin in the VMH contributes to the initial overconsumption of palatable diets by rats.American journal of physiology. Endocrinology and metabolism · 2025Article
- Leptin receptor-expressing cells in the ventromedial nucleus of the hypothalamus contribute to enhanced CCK-induced satiety following central leptin injection.American journal of physiology. Endocrinology and metabolism · 2022Article
- The physiological control of eating: signals, neurons, and networks.Physiological reviews · 2022 · on this mapArticle
- Spexin Regulates Hypothalamic Leptin Action on Feeding Behavior.Biomolecules · 2022Article
- Phosphorylation of STAT3 in hypothalamic nuclei is stimulated by lower doses of leptin than are needed to inhibit food intake.American journal of physiology. Endocrinology and metabolism · 2021Article
- Loss of leptin receptor-expressing cells in the hindbrain decreases forebrain leptin sensitivity.American journal of physiology. Endocrinology and metabolism · 2020Article
- Leptin receptor-expressing neurons in ventromedial nucleus of the hypothalamus contribute to weight loss caused by fourth ventricle leptin infusions.American journal of physiology. Endocrinology and metabolism · 2019Article
- Low-dose infusions of leptin into the nucleus of the solitary tract increase sensitivity to third ventricle leptin.American journal of physiology. Endocrinology and metabolism · 2019Article
- Low-dose leptin infusion in the fourth ventricle of rats enhances the response to third-ventricle leptin injection.American journal of physiology. Endocrinology and metabolism · 2017Article
- Fourth-ventricle leptin infusions dose-dependently activate hypothalamic signal transducer and activator of transcription 3.American journal of physiology. Endocrinology and metabolism · 2016Article
- Facilitation of breathing by leptin effects in the central nervous system.The Journal of physiology · 2016Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Leptin receptors (ObRs) in the forebrain and hindbrain have been independently recognized as important mediators of leptin responses. We recently used low-dose leptin infusions to show that chronic activation of both hypothalamic and hindbrain ObRs is required to reduce body fat. The objective of the present study was to identify the brain nuclei that are selectively activated in rats that received chronic infusion of leptin in both the forebrain and hindbrain. Either saline or leptin was infused into third and fourth ventricles (0.1 μg/24 h in the third ventricle and 0.6 μg/24 h in the fourth ventricle) of male Sprague-Dawley rats for 6 days using Alzet pumps. Rats infused with leptin into both ventricles (LL rats) showed a significant increase in phosphorylated (p)STAT3 immunoreactivity in the arcuate nucleus, ventromedial hypothalamus, dorsomedial hypothalamus, and posterior hypothalamus compared with other groups. No differences in pSTAT3 immunoreactivity were observed in midbrain or hindbrain nuclei despite a sixfold higher infusion of leptin into the fourth ventricle than the third ventricle. ΔFosB immunoreactivity, a marker of chronic neuronal activation, showed that multiple brain nuclei were chronically activated due to the process of infusion, but only the arcuate nucleus, ventromedial hypothalamus, dorsomedial hypothalamus, and ventral tuberomamillary nucleus showed a significant increase in LL rats compared with other groups. These data demonstrate that low-dose leptin in the hindbrain increases pSTAT3 in areas of the hypothalamus known to respond to leptin, supporting the hypothesis that leptin-induced weight loss requires an integrated response from both the hindbrain and forebrain.
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