ArticleJournal of applied physiology (Bethesda, Md. : 1985)2012
Endothelial leptin receptor mutation provides partial resistance to diet-induced obesity.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2012. 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, 15 citations in OpenAlex.
- Deletion of endothelial leptin receptors in mice promotes diet-induced obesity.Scientific reports · 2023Article
- Leptin Receptor Expression in Mouse Intracranial Perivascular Cells.Frontiers in neuroanatomy · 2018Article
- Obesity and neuroinflammatory phenotype in mice lacking endothelial megalin.Journal of neuroinflammation · 2017Article
- Role of Astrocytes in Leptin Signaling.Journal of molecular neuroscience : MN · 2015Article
- Leukocyte infiltration into spinal cord of EAE mice is attenuated by removal of endothelial leptin signaling.Brain, behavior, and immunity · 2014Article
- Hypersomnolence and reduced activity in pan-leptin receptor knockout mice.Journal of molecular neuroscience : MN · 2013Article
- Loss of astrocytic leptin signaling worsens experimental autoimmune encephalomyelitis.Brain, behavior, and immunity · 2013Article
- Diminished leptin signaling can alter circadian rhythm of metabolic activity and feeding.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Article
- Endothelial cell leptin receptor mutant mice have hyperleptinemia and reduced tissue uptake.Journal of cellular physiology · 2013Article
- Astrocytic leptin-receptor knockout mice show partial rescue of leptin resistance in diet-induced obesity.Journal of applied physiology (Bethesda, Md. : 1985) · 2013Article
- Upregulation of astrocytic leptin receptor in mice with experimental autoimmune encephalomyelitis.Journal of molecular neuroscience : MN · 2013Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Leptin, a polypeptide hormone produced mainly by adipocytes, has diverse effects in both the brain and peripheral organs, including suppression of feeding. Other than mediating leptin transport across the blood-brain barrier, the role of the endothelial leptin receptor remains unclear. We recently generated a mutant mouse strain lacking endothelial leptin receptor signaling, and showed that there is an increased uptake of leptin by brain parenchyma after its delivery by in situ brain perfusion. Here, we tested the hypothesis that endothelial leptin receptor mutation confers partial resistance to diet-induced obesity. These ELKO mice had similar body weight and percent fat as their wild-type littermates when fed with rodent chow, but blood concentrations of leptin were significantly elevated. In response to a high-fat diet, wild-type mice had a greater gain of body weight and fat than ELKO mice. As shown by metabolic chamber measurement, the ELKO mice had higher oxygen consumption, carbon dioxide production, and heat dissipation, although food intake was similar to that of the wild-type mice and locomotor activity was even reduced. This indicates that the partial resistance to diet-induced obesity was mediated by higher metabolic activity in the ELKO mice. Since neuronal leptin receptor knockout mice show obesity and diabetes, the results suggest that endothelial leptin signaling shows opposite effects from that of neuronal leptin signaling, with a facilitatory role in diet-induced obesity.
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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.