Socs3 deficiency in the brain elevates leptin sensitivity and confers resistance to diet-induced obesity

By H. Mori, Reiko Hanada, Toshikatsu Hanada, Daisuke Aki, R. Mashima, Hitomi Nishinakamura, T. Torisu, K. Chien, H. Yasukawa, A. Yoshimura. Nature Medicine, 2004

651 citations recorded by the source corpus.

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

View Paper: https://www.semanticscholar.org/paper/7d4def57084dcd55ec81a9b9dae0c1483d269b48

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In Endocrine and Autonomic Systems

In Epidemiology

In Nutrition and Dietetics

Citations in the corpus

Conditional ablation of Stat3 or Socs3 discloses a dual role for reactive astrocytes after spinal cord injury (2006, background): “To further investigate the relationship between Stat3 signaling and function of reactive astrocytes, we analyzed SCI in Nes-Socs3 −/− mic”
Inflammation, stress, and diabetes. (2005, positive): “SOCS3 has also been demonstrated to regulate central leptin action, and both whole body reduction in SOCS3 expression ( SOCS3 +/– ) and neural SOCS3 disruption result in resistance to high-fat diet–induced obesity and insulin resistance (69, 70).”
Adipose Tissue in Obesity-Related Inflammation and Insulin Resistance: Cells, Cytokines, and Chemokines (2013, neutral): “Recently, it has been proposed that SOCS3 could be involved in negative regulation of leptin-induced intracellular signal transduction in the brain [46].”
The Human Obesity Gene Map: The 2005 Update (2006, background): “Cerebrum and hypothalamusspecific loss of Socs3 Floxed gene transgenic Cre expressed from Syndecan I promoter Decreased BW and resistant to dietinduced obesity (561)”
Astrocyte reactivity and reactive astrogliosis: costs and benefits. (2014, background): “The effect on astrocyte activation may be mediated via the gp-130/activator of transcription 3 (STAT3) signaling pathway, phosphorylation, and nuclear translocation of STAT3 in astrocytes (225) as well as indirectly through the effects of these molecules on other cell types such as microglia, neuron”
Mechanisms of obesity-associated insulin resistance: many choices on the menu. (2007, background): “Intriguingly, leptin and insulin both induce the expression of SOCS-3, and sensitivity to both insulin and leptin is augmented in mice with reduced neuronal expression of SOCS-3 (Mori et al. 2004).”
Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training (2013, positive): “In addition, findings in adipocytes suggest that resistin is also capable of activating Socs3 that was previously shown to cause impaired insulin action (612).”
The Hormonal Control of Food Intake (2007, positive): “Indeed, although complete lack of Socs-3 is embryonic lethal, mice with only one functional copy of Socs-3 or those with neuronal deletion of Socs-3 are lean and leptin sensitive (Howard et al., 2004; Kievit et al., 2006; Mori et al., 2004).”