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Brain IL-6—Where Amylin and GLP-1 Antiobesity Signaling Congregate

A prerequisite for the homeostatic control of fat mass is the existence of peripheral hormones that, together with nervous afferents, signal the state of energy balance to adipostatic circuits in the brain. It is assumed that the effects of these signals are mediated, at least in part, by changes in key neurotransmitters, especially those located in the hypothalamus. It has been known for many years that leptin from adipose tissue engages neurons producing α-melanocyte–stimulating hormones, while ghrelin from the empty stomach stimulates neurons producing neuropeptide Y/agouti-related peptide/γ-aminobutyric acid. These two neuronal populations in the arcuate nucleus mediate these two counterregulatory canonical signals for energy homeostasis (1). In addition, peripheral energy balance–reporting hormones may act on the brain stem (2).

In this issue of Diabetes , Le Foll et al. (3) report that the pancreatic hormone amylin may use interleukin-6 (IL-6) as a noncanonical signal mediator in the brain. Thus, amylin may be dependent upon expression of IL-6 in the hypothalamus to exert its effects to reduce body weight and to increase leptin sensitivity.

Like leptin and ghrelin, amylin is a periphery-to-brain messenger of importance for energy balance. Proamylin is coreleased with insulin from the β-cells after meals, and amylin decreases blood glucose (4,5). Amylin reduces food intake and body weight and potentiates effects of leptin …