http://www.eurekalert.org/pub_releases/2014-02/uob-nrs021014.phpPretty cool, but I have some thoughts.
As far as possible mechanisms, lactate produced in astrocytes is transported to neurons via the lactate transporter (MCT1), which triggers depolarization and excitation of neurons.
It's involved on glucose sensing in the hypothalamus, regulating energy and hunger. Usage of glucose leads to the lactate I talked about in the first thought, and the transportation. These shifts modulate neuropeptide expression (shifts sensed largely by Glucokinase), example - hypoglycemia/depleted reserves can induce hypothalamic AMPK expression, leading to NPY and AgRP (and vice versa) expression increased and thus hunger.
As for this study, it makes sense. Lactate production would indicate glycogen depletion and glucose usage. Norepinephrine/epi induce glycogenolysis and such to increase glucose concentrations.
It also fits in w/ my first statement. Norepi/epi (sympathetic nervous system mediators) innervate ghrelin, the main gut hunger hormone, which also acts at the ARC of the hypothalamus to shift to hunger pathways, as described above.
At least, that's how I think about it, iirc