Selective deletion of leptin receptor in neurons leads to obesity.

By P. Cohen, Connie Zhao, Xiaoli Cai, J. Montez, S. Rohani, P. Feinstein, Peter Mombaerts, J. Friedman. Journal of Clinical Investigation, 2001

608 citations recorded by the source corpus.

Subfields: Endocrine and Autonomic Systems, Epidemiology, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/a05902b7cf2582731ce8050b4b07251a8aab77c8

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrine and Autonomic Systems

1. G. Frühbeck
2. Haiming Cao
3. G. Hotamışlıgil

In Epidemiology

1. B. Spiegelman
2. G. Frühbeck
3. E. Rosen
4. S. Kajimura
5. Haiming Cao
6. G. Hotamışlıgil

In Nutrition and Dietetics

1. G. Frühbeck

Citations in the corpus

• The Human Obesity Gene Map: The 2005 Update (2006, background): “7) Lepr 1p31 LEPR Neuronal-specific deletion of leptin receptor Floxed gene Cre transgene expressed from the Syndecan 1 promoter Obesity (449,450)”
• Molecular mechanisms of cancer development in obesity (2011, background): “The major physiological site of leptin action is in the central nervous system, but the leptin receptor (OBR; also known as LEPR) is also expressed at lower levels in peripheral tissue”
• Intracellular signalling pathways activated by leptin. (2006, background): “Selective deletion of all OB-R isoforms in neurons has been shown to lead to obesity in mice, providing evidence for the relevance of neuronal leptin action in body mass regulation [68].”
• Leptin Receptor-expressing mesenchymal stromal cells represent the main source of bone formed by adult bone marrow (2014, unknown): “Mice All mice were maintained in a C57BL/6 background, including Lepr-cre (DeFalco et al., 2001), Leprfl/fl (Cohen et al., 2001), Ptenfl/fl (Groszer et al., 2001), Scf-GFP (Ding et al., 2012), Cxcl12-DsRed (Ding and Morrison, 2013), Ubc-creER (Ruzankina et al., 2007),…”
• Leptin regulation of bone mass, appetite and energy expenditure relies on its ability to inhibit serotonin synthesis in the brainstem (2009, unknown): “Genetic inactivation of ObRb in all neurons and chemical destruction of the arcuate nuclei of hypothalamus increases appetite (Cohen et al., 2001), yet inactivation of ObRb selectively in arcuate, VMH or in both nuclei does not when mice are fed a normal diet (Balthasar et al., 2004).”
• Leptin directly activates SF1 neurons in the VMH, and this action by leptin is required for normal body-weight homeostasis. (2006, unknown): “Central nervous system (CNS)-specific deletion of LEPRs results in marked obesity ( Cohen et al., 2001 ), whereas transgenic, brainspecific reconstitution of LEPRs in leptin-receptor-deficientLeprdb/db mice ameliorates obesity (Kowalski et al.,”