Neuronal PTP1B regulates body weight, adiposity and leptin action

By K. Bence, M. Delibegović, B. Xue, Cem Z. Gorgun, G. Hotamisligil, B. Neel, B. Kahn. Nature Medicine, 2006

639 citations recorded by the source corpus.

Subfields: Endocrine and Autonomic Systems, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/e90a88697de018cc4da087a5072a36933c1d9da1

How researchers see this paper

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

In Endocrine and Autonomic Systems

1. S. O’Rahilly
2. M. Myers
3. I. S. Farooqi
4. J. Oakhill
5. A. Coll
6. S. Galic
7. G. Steinberg
8. David M. Sabatini

In Molecular Biology

1. S. O’Rahilly
2. Philippe Froguel
3. I. S. Farooqi
4. Kassem Makki
5. A. Coll
6. I. Wolowczuk
7. G. Steinberg

In Physiology

1. S. O’Rahilly
2. Philippe Froguel
3. Kassem Makki
4. J. Oakhill
5. S. Galic
6. I. Wolowczuk
7. G. Steinberg
8. M. Laplante

Citations in the corpus

• Mechanisms of leptin action and leptin resistance. (2008, background): “Indeed, although neuronal deletion of PTP1B renders animals lean and leptin sensitive, the effect of PTP1B on adiposity is independent of DIO (that is, the increased leanness of neuronal PTP1B knockout mice relative to controls does not differ by diet) (105).”
• Endoplasmic reticulum stress plays a central role in development of leptin resistance. (2009, background): “, 2000; Flier, 2004; Myers, 2004) and tyrosine phosphatase 1 B (PTB1B) have been shown to play important roles in the blockade of leptin signaling (Bence et al., 2006).”
• Adipose Tissue in Obesity-Related Inflammation and Insulin Resistance: Cells, Cytokines, and Chemokines (2013, positive): “Moreover, neuronal deletion as well as whole-body knock-out of protein tyrosine phosphatase 1B (PTP1B) increased leptin and insulin sensitivity, preventing body weight gain in a diet-induced obesity animal model [47, 48], hence suggesting that, likewise SOCS3, PTP1B also orchestrates leptin resistan”
• The Hormonal Control of Food Intake (2007, positive): “Finally, recent data that demonstrate that mice with a neuron-specific lack of the tyrosine phosphatase PTP1B are rendered hypersensitive to leptin point to this molecule having an important role in the development of leptin resistance (Bence et al., 2006).”
• Adipose tissue as an endocrine organ. (2010, background): “Consistent with this, whole-body and neuron-specific PTP1B knockout mice are resistant to diet-induced obesity and show improved leptin sensitivity (Bence et al., 2006).”