Endoplasmic reticulum stress plays a central role in development of leptin resistance.

By L. Ozcan, A. S. Ergin, Allen Lu, Jason Chung, S. Sarkar, Duyu A. Nie, M. Myers, U. Ozcan. Cell Metabolism, 2009

882 citations recorded by the source corpus.

Subfields: Cell Biology, Endocrine and Autonomic Systems, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/3a9f5a2c618ebc79b5a3d067aa4e7b5804ff13fd

How researchers see this paper

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

In Cell Biology

1. I. Tabas
2. Herbert Tilg
3. Jianping Ye
4. D. Ron
5. A. Moschen
6. R. Kaufman
7. C. Hetz
8. J. Malhotra

In Endocrine and Autonomic Systems

1. Herbert Tilg
2. Jianping Ye
3. A. Moschen

In Nutrition and Dietetics

1. Jianping Ye
2. I. Tabas
3. Herbert Tilg
4. A. Moschen

Citations in the corpus

• Mechanisms of insulin resistance in obesity (2013, background): “It was then reported as a risk factor of insulin resistance [99] and leptin resistance in obesity [100].”
• Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress (2011, background): “Both have been used in humans for a variety of disorders and have beneficial effects in various mouse models of pathologic ER stres”
• Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “XBP1 has evolved as a critical molecule that is able to regulate all aspects of NAFLD, namely lipid synthesis/accumulation, leptin resistance, adipogenesis, inflammation, and insulin signaling/ resistance.(93,94) Autophagy has recently evolved as an additional pathway affecting hepatic lipid metabol”
• Lipotoxicity and the gut-liver axis in NASH pathogenesis. (2018, background): “recognized as an additional target of lipotoxicity, and hypothalamic inflammation and ER-stress have been implicated in the resistance to leptin and insulin, contributing to obesity [10].”
• Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, neutral): “However, a similar pattern is also reported in a brain-specific XBP1 deficiency mouse model, which revealed increased levels of phosphorylated PERK and decreased leptin sensitivity associated with a higher food intake and increased body weight compared to control animals (Ozcan et al., 2009).”
• Treatment of Obesity with Celastrol (2015, neutral): “On the other hand, overexpression of spliced form of XBP1 (XBP1S) in in vitro and in vivo settings increases leptin sensitivity (Ozcan et al., 2009; Williams et al., 2014).”