PPARgamma ligands increase expression and plasma concentrations of adiponectin, an adipose-derived protein.

By N. Maeda, Masahiko Takahashi, T. Funahashi, S. Kihara, H. Nishizawa, K. Kishida, H. Nagaretani, M. Matsuda, R. Komuro, N. Ouchi and 5 more. Diabetes, 2001

1,772 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/d56b6a50f44518917432ff97fe0c1810010c7b6b

How researchers see this paper

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

In Epidemiology

1. Herbert Tilg
2. B. Spiegelman
3. A. Moschen
4. E. Rosen
5. I. Shimomura
6. Yuji Matsuzawa
7. T. Funahashi
8. P. Ferré

In Molecular Biology

1. B. Spiegelman
2. E. Rosen
3. Herbert Tilg
4. P. Havel
5. S. Kahn
6. Bart Staels
7. P. Ferré
8. M. Matsuda

In Oncology

1. B. Spiegelman

Citations in the corpus

• Induction of adiponectin, a fat-derived antidiabetic and antiatherogenic factor, by nuclear receptors. (2003, background): “Consistent with the previous reports (28,29), PPARligands augmented adiponectin mRNA levels in white adipose tissues (Fig.”
• Endothelial dysfunction in diabetes mellitus (2007, neutral): “…and, possibly, leptin expression; suppress lipolysis and thus decrease plasma free fatty acid concentrations and increase plasma adiponectin levels (Hauner et al 2001, 2002) and exert direct effects on insulin-mediated glucose transport in skeletal muscle and the heart (BishopBailey et al 2000;…”
• Adiponectin: action, regulation and association to insulin sensitivity (2005, background): “The potential importance of adiponectin as a target for the insulin-sensitizing action of TZD is underscored by the substantial increase in plasma adiponectin levels in response to treatment with TZDs (72,78,83).”
• Adipokines Mediate Inflammation and Insulin Resistance (2013, background): “In contrast PPARγ antagonists stimulate the expression of adiponectin in adipocytes (Maeda et al., 2001).”
• Inflammatory Mechanisms in the Regulation of Insulin Resistance (2008, background): “Weight loss induces adiponectin synthesis (37), as activation of peroxisome-proliferator– activated receptor γ (PPARγ) by its ligands thiazolidinediones (TZDs), which are used in the treatment of T2D (38).”
• Adipocytokines: mediators linking adipose tissue, inflammation and immunity (2006, background): “, as is activation of peroxisome-proliferator-activated receptor-γ ( PPARγ ) by its ligands thiazolidinediones, which are important for the treatment of type 2 diabetes mellitu”
• The biology of peroxisome proliferator-activated receptors: relationship with lipid metabolism and insulin sensitivity. (2004, background): “A number of articles have now shown that TZD treatment increases adiponectin expression and secretion in insulin-resistant humans and rodents (52,53).”
• Regulation of adiponectin by adipose tissue-derived cytokines: in vivo and in vitro investigations in humans. (2003, background): “Previous studies have demonstrated that the reduced circulating adiponectin levels could be reversed partially after induction of weight loss in obese and in insulin-resistant subjects (21, 40) as well as after treatment with insulin-sensitizing drugs such as thiazolidinediones (8, 27).”