Adipose-specific disruption of signal transducer and activator of transcription 3 increases body weight and adiposity.
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Summary
Findings demonstrate that adipocyte STAT3 regulates body weight homeostasis in part through direct effects of leptin on adipocytes, which may partially explain the increased cell size.
- Type
- article
- Published
- 2008-04-01
- Cited by
- 89
- References
- 56
- Access
- Open access
- OpenAlex
- https://openalex.org/W1979647427
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:2404739
Keywords
Internal medicine, Endocrinology, Adipocyte, Adipose tissue, Adipogenesis
References
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- The biology of white adipocyte proliferation
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- The Regulation and Activation of Ciliary Neurotrophic Factor Signaling Proteins in Adipocytes*
- Distinct Transcriptional Profiles of Adipogenesisin Vivo and in Vitro *
- Beyond insulin resistance in NASH: TNF‐α or adiponectin?
- Obese Gene Expression Alters the Ability of 30A5 Preadipocytes to Respond to Lipogenic Hormones*
- Adipose-specific peroxisome proliferator-activated receptor γ knockout causes insulin resistance in fat and liver but not in muscle
- The glucose fatty-acid cycle. Its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus.
- Disappearance of body fat in normal rats induced by adenovirus-mediated leptin gene therapy.
- Direct effects of leptin on brown and white adipose tissue.
- Disruption of neural signal transducer and activator of transcription 3 causes obesity, diabetes, infertility, and thermal dysregulation.
- Free fatty acid-induced insulin resistance is associated with activation of protein kinase C theta and alterations in the insulin signaling cascade.
Cited by
- Signal transducer and activator of transcription 3 (STAT3) regulates adipocyte differentiation via peroxisome‐proliferator‐activated receptor γ (PPARγ)
- Dietary saturated fat modulates the association between STAT3 polymorphisms and abdominal obesity in adults.
- Hepatic Acetyl CoA Links Adipose Tissue Inflammation to Hepatic Insulin Resistance and Type 2 Diabetes
- Adipose tissue and ceramide biosynthesis in the pathogenesis of obesity.
- Exploiting knowledge of mesenchymal stromal cells in vivo for bone disease therapy development
- Knockout of STAT3 in skeletal muscle does not prevent high-fat diet-induced insulin resistance
- Effects of High Fat Feeding on Adipose Tissue Gene Expression in Diabetic Goto-Kakizaki Rats
- Stat3β mitigates development of atherosclerosis in apolipoprotein E-deficient mice
- Identification of STAT target genes in adipocytes
- Comparative pathophysiology, toxicology, and human cancer risk assessment of pharmaceutical-induced hibernoma.
- Adipose Tissue Deficiency and Chronic Inflammation in Diabetic Goto-Kakizaki Rats
- Stat3 pathway correlates with the roles of leptin in mouse liver fibrosis and sterol regulatory element binding protein-1c expression of rat hepatic stellate cells.
- Adipocyte-specific deficiency of Janus kinase (JAK) 2 in mice impairs lipolysis and increases body weight, and leads to insulin resistance with ageing
- Association of STAT3 Common Variations with Obesity and Hypertriglyceridemia: Protective and Contributive Effects
- Adipocyte-specific Inactivation of Acyl-CoA Synthetase Fatty Acid Transport Protein 4 (Fatp4) in Mice Causes Adipose Hypertrophy and Alterations in Metabolism of Complex Lipids under High Fat Diet*
- Cyclooxygenase-2 inhibition reverts the decrease in adiponectin levels and attenuates the loss of white adipose tissue during chronic inflammation.
- The role of JAK-STAT signaling in adipose tissue function
- Leptin, insulin and thyroid hormones in a cohort of Egyptian obese Down syndrome children: a comparative study
- Chronic leptin treatment stimulates lipid oxidation in immortalized and primary mouse skeletal muscle cells.
- Real-time monitoring of adipocyte differentiation using a capacitance sensor array.
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