Eglantine Balland

TL;DR: Triggering ERK signaling in tanycytes with EGF reestablishes leptin transport, elicits MBH neuron activation and energy expenditure in obese animals, and accelerates the restoration of leptin sensitivity upon the return to a normal-fat diet.

TL;DR: It is reported that insulin and leptin act together on hypothalamic neurons to promote WAT browning and weight loss, and a homeostatic mechanism for coordinating the status of energy stores, as relayed by insulin andptin, with the central control of WATbrowning is identified.

TL;DR: The decrease in blood glucose levels during fasting alters the structural organization of this blood-hypothalamus barrier, resulting in the improved access of metabolic substrates to the arcuate nucleus, and shows a hitherto unappreciated role for tanycytes and the permeable microvessels associated with them in the adaptive metabolic response to fasting.

TL;DR: It is argued that glial–neuronal interactions provide a core hub integrating food-related cues, interoceptive signals, and internal states to adapt a complex set of physiological responses operating on different timescales to finely tune behavior and metabolism according to metabolic status.

TL;DR: It is shown that discrete gray and white hypothalamic structures are consistently identifiable by MRI, and that MRI could also highlight finer structures such as the paraventricular nucleus, the ventromedial nucleus of the hypothalamus and the infundibular (arcuate) nucleus, brain nuclei that play key roles in the regulation of food intake and energy homeostasis.