Leptin-replacement therapy for lipodystrophy.

By E. Oral, V. Simha, E. Ruiz, Alexa Andewelt, A. Premkumar, P. Snell, A. Wagner, A. DePaoli, M. Reitman, Simeon I. Taylor and 2 more. New England Journal of Medicine, 2002

1,201 citations recorded by the source corpus.

Subfields: Endocrine and Autonomic Systems, Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/eb7cd2c5e21721d237736da4996374d968d501b6

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. Herbert Tilg
2. A. Moschen
3. S. O’Rahilly
4. I. S. Farooqi
5. K. Frayn
6. Haiming Cao
7. G. Hotamışlıgil
8. Luigi Fontana

In Epidemiology

1. Herbert Tilg
2. B. Spiegelman
3. A. Moschen
4. E. Rosen
5. K. Walsh
6. J. Bastard
7. N. Ouchi
8. K. Frayn

In Molecular Biology

1. B. Spiegelman
2. E. Rosen
3. Herbert Tilg
4. S. O’Rahilly
5. K. Walsh
6. M. Czech
7. I. S. Farooqi
8. A. Moschen

Citations in the corpus

• Narrative Review: The Role of Leptin in Human Physiology: Emerging Clinical Applications (2010, background): “5%, improves hyperlipidemia (57, 58), and reverses hepatic steatosis (53, 54).”
• Physiology of leptin: energy homeostasis, neuroendocrine function and metabolism. (2015, background): “congenital or acquired lipoatrophy, leptin treatment improves several metabolic parameters, including insulin sensitivity, dyslipidemia, and hepatic steatosis [94, 95, 155].”
• Obesity and the role of adipose tissue in inflammation and metabolism. (2006, background): “In a pioneering study, administration of exogenous leptin to individuals with lipoatrophic diabetes resulted in marked reductions in triacylglycerol concentrations, liver volume, and glycated hemoglobin and discontinuation or a large reduction in antidiabetes therapy (30).”
• Adipose tissue as a buffer for daily lipid flux (2002, background): “Treatment of lipodystrophic patients with recombinant leptin also produced marked metabolic improvements [102], although probably mediated at least in part by reduction in food intake.”
• Inflammatory Mechanisms in the Regulation of Insulin Resistance (2008, background): “It also improves glucose homeostasis in lipodystrophic mice and in humans with lipodystrophy or congenital leptin deficiency (49,50).”
• Adipose Tissue in Obesity-Related Inflammation and Insulin Resistance: Cells, Cytokines, and Chemokines (2013, neutral): “Leptin therapy in lipodystrophic patients improves their metabolic state with remarkable improvements in insulin sensitivity, suggesting that leptin acts as a signal that contributes to regulation of total body sensitivity to insulin [53].”
• Adipokines in inflammation and metabolic disease (2011, background): “Leptin has also been shown to be effective at improving metabolic dysfunction in patients with lipodystrophy or congenital leptin deficienc”
• Disordered lipid metabolism and the pathogenesis of insulin resistance. (2007, neutral): “Another way in which ectopic lipid deposits can be reduced in lipodystrophic mice and humans is by replacing leptin, an anorexogenic adipocyte-derived hormone (74, 102).”
• Adipocytes as regulators of energy balance and glucose homeostasis (2006, background): “Leptin also improves glucose homeostasis in lipodystrophic mice, and in humans with lipodystrophy or congenital leptin deficienc”
• Adipocyte dysfunctions linking obesity to insulin resistance and type 2 diabetes (2008, background): “Human and mouse lipodystrophies cause impaired adipokine secretio”