Obesity-associated improvements in metabolic profile through expansion of adipose tissue.
By Ja-Young Kim, E. van de Wall, M. Laplante, A. Azzará, M. Trujillo, S. Hofmann, T. Schraw, J. Durand, Hua Li, Guangyue Li and 7 more. Journal of Clinical Investigation, 2007
1,316 citations recorded by the source corpus.
Subfields: Endocrine and Autonomic Systems, Epidemiology, Physiology
View Paper: https://www.semanticscholar.org/paper/843b52fa7e7c0035b3a7882180c77b93cafb2b6e
How researchers see this paper
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In Endocrine and Autonomic Systems
- Herbert Tilg
- P. Scherer
- Toshimasa Yamauchi
- Gerald I. Shulman
- S. Summers
- Sushil Kumar Jain
- D. J. Drucker
- William L. Holland
In Epidemiology
- Gerald I. Shulman
- V. Samuel
- B. Spiegelman
- P. Scherer
- S. Kajimura
- Herbert Tilg
- Haiming Cao
- A. Moschen
In Physiology
Citations in the corpus
- Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity (2009, background): “It has been hypothesized that ectopic fat accumulation is caused by an inadequate capacity of adipose tissue to store triglyceride (17, 24).”
- SirT1 gain-of-function increases energy efficiency and prevents diabetes in mice (2008, neutral): “Nonetheless, this phenotype bears similarities with the effect of adiponectin overexpression in ob/ob mice (Kim et al., 2007).”
- Adipose Tissue Distribution, Inflammation and Its Metabolic Consequences, Including Diabetes and Cardiovascular Disease (2020, background): “visceral and hepatic fat accumulation, potentially driving the MHO phenotype (76, 97, 193).”
- Fat Tissue, Aging, and Cellular Senescence (2010, background): “Subcutaneous fat expansion in obesity may actually be protective (Kim et al., 2007; Tran et al., 2008).”
- Adipose tissue plasticity in health and disease (2022, background): “Strikingly, the metabolic dysfunction of ob/ob mice is ameliorated by concomitant overexpression of the insulin-sensitizing hormone adiponectin (adiponectinTG) or by the knockout of collagen 6 (Col6 KO) (Khan et al., 2009; Kim et al., 2007).”
- Adiponectin: mechanistic insights and clinical implications (2012, background): “Transgenic mice overexpressing Adipoq show reduced lipogenic activity at the level of the liver [55], but may be predominantly protected as a result of a healthy, non-inflamed expansion of adipose tissue that can readily accommodate any excess lipids [52, 53].”
- Hypoxia-Inducible Factor 1α Induces Fibrosis and Insulin Resistance in White Adipose Tissue (2009, result): “This is a much more extreme challenge than a simple HFD regimen, although from our previous results, we know that adipose tissue can be further expanded even in the ob/ob background via local overexpression of adiponectin (29).”
- Metabolic Dysregulation and Adipose Tissue Fibrosis: Role of Collagen VI (2008, background): “fat mass with a metabolically healthy phenotype, mimicking chronic exposure to PPAR agonists (15, 28).”
- The Pleiotropic Actions of Adiponectin are Initiated via Receptor-Mediated Activation of Ceramidase Activity (2010, background): “Overexpression of adiponectin from adipose tissue results in improvements in systemic insulin sensitivit”
- Normalization of Obesity-Associated Insulin Resistance through Immunotherapy: CD4+ T Cells Control Glucose Homeostasis (2009, background): “TNF-α can be produced by both adipocytes and, in particular, macrophage”
- Pathophysiology of Type 2 Diabetes Mellitus (2020, neutral): “Adiponectin has insulin-sensitizing properties [260,261].”
- Adipokines Mediate Inflammation and Insulin Resistance (2013, background): “Consistent with this model, TLR4 deficient mice show improved HFD-induced insulin resistance (Kim et al., 2007a).”