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Integrated Neurohormonal Mechanisms and Therapeutic Applications

Jonathan D. Roth, PhD; Holly Maier, PhD; Steve Chen, MD; Barbara L. Roland, PhD

Arch Neurol. 2009;66(3):306-310.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

Amylin receptor agonism is emerging as part of an integrated neurohormonal therapeutic approach for managing diabetes mellitus (DM) and body weight. Pramlintide acetate, an analogue of the pancreatic hormone amylin, has been studied in the United States as an antihyperglycemic agent in patients with type 1 or type 2 DM treated with mealtime insulin.¹ Further clinical testing of pramlintide in subjects with obesity demonstrated that pramlintide monotherapy induced significant, sustained, and dose-dependent weight loss.² Recent clinical observations point to its compatibility as a combination therapy with the hormone leptin, eliciting double-digit weight loss in patients with overweight and obesity.³ Herein, we link amylin activation of central neural circuits to these therapeutic effects, and we speculate on other potential therapeutic applications of amylin receptor agonism.

PHYSIOLOGIC EFFECTS OF AMYLIN

Amylin is a 37–amino acid peptide hormone cosecreted with insulin from pancreatic . . . [Full Text of this Article]

AMYLIN BINDING SITES AND NEURONAL ACTIVATION

THE AMYLIN NEURAL CIRCUIT

Area Postrema

Nucleus of the Solitary Tract, Lateral Parabrachial Nucleus, and Central Amygdala

Hypothalamus

Other Regions of the Brain

CURRENT AND POTENTIAL THERAPEUTIC APPLICATIONS

Diabetes Mellitus

Obesity

Neuropsychiatric Disease

CONCLUSIONS

AUTHOR INFORMATION

Author Affiliations: Amylin Pharmaceuticals, Inc, San Diego, California.

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