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Comment
. 2008 Oct;149(10):4765-7.
doi: 10.1210/en.2008-0932.

Paying the price for eating ice cream: is excessive GLP-1 signaling in the brain the culprit?

Hans-Rudolf Berthoud  1
Affiliations
Comment

Paying the price for eating ice cream: is excessive GLP-1 signaling in the brain the culprit?

Hans-Rudolf Berthoud. Endocrinology. 2008 Oct.
No abstract available

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Figures

Figure 1
Figure 1
GLP-1 is produced and released from enteroendocrine L-cells in the small intestine, taste receptor cells, and neurons in the brainstem. Peripheral GLP-1 is signaling via vagal and taste afferents to the nucleus of the solitary (NTS) tract in the brainstem and via the blood circulation to the stomach, pancreas, heart, and brain. A different receptor may also mediate effects of circulating GLP-1 on liver and muscle. Areas of the hypothalamus involved in glucose homeostasis and appetite control are differentially affected by GLP-1 released from NTS neuronal projections and/or circulating GLP-1 freely crossing the blood brain barrier. Knauf et al. (16) now demonstrate that blockade of GLP-1 signaling in the brain, but not peripherally, prevents development of insulin resistance in mice fed a high-fat diet. The findings suggest that nutritional abundance as during high-fat feeding causes over-stimulation of brain GLP-1 receptors, leading to inhibition of muscle glucose uptake and hepatic glycogen synthesis through changes in autonomic outflow. The critical brain GLP-1 receptor population and the involvement of brain stem GLP-1 expressing neurons remains to be identified. AP, Area postrema; ARC, arcuate nucleus; DMV, dorsal motor nucleus of the vagus; DMN, dorsomedial nucleus of the hypothalamus; LH, lateral hypothalamic area; NTS, nucleus tractus solitarius; PVH, paraventricular nucleus of the hypothalamus; SPM, sympathetic premotor neurons.
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