The Brain–Liver Connection Between BDNF and Glucose Control

  1. Streamson C. Chua Jr.
  1. Division of Endocrinology, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York
  1. Corresponding author: Streamson C. Chua, Jr., streamson{at}gmail.com.

Growing knowledge of the control of glucose metabolism permits the testing of alternative treatments to insulin to maintain euglycemia. Diminishing glucagon action on the liver (1) and increasing leptin (2) are prime examples of promising peptide hormone treatments that could be useful in glucose regulation. A report from Morton and colleagues (3) in this issue provides data that a systems biology model could integrate these two points of view of glucose regulation.

Brain-derived neurotrophic factor (BDNF) and its cognate receptor TrkB are involved in the regulation of energy balance and glucose homeostasis via its effects in the central nervous system. Perturbed BDNF signaling in the brain triggers hyperphagia and obesity in mice, suggesting that BDNF acts as an anorexigenic signaling molecule (46). However, the cellular mechanisms underlying the anorexigenic effects of BDNF have not been clearly defined. As a neurotrophic factor, BDNF promotes survival, induces differentiation of neurons in the developing and adult central nervous system (7), and forms appropriate synaptic connections at central synapses (8). Thus, the obesity phenotype observed in BDNF- and TrkB-mutant animals can be, in part, due to neurodevelopmental anomalies (6,9 …

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