[HTML][HTML] Evidence for a novel functional role of astrocytes in the acute homeostatic response to high-fat diet intake in mice

LB Buckman, MM Thompson, RN Lippert… - Molecular …, 2015 - Elsevier
LB Buckman, MM Thompson, RN Lippert, TS Blackwell, FE Yull, KLJ Ellacott
Molecular metabolism, 2015Elsevier
Objective Introduction of a high-fat diet to mice results in a period of voracious feeding,
known as hyperphagia, before homeostatic mechanisms prevail to restore energy intake to
an isocaloric level. Acute high-fat diet hyperphagia induces astrocyte activation in the rodent
hypothalamus, suggesting a potential role of these cells in the homeostatic response to the
diet. The objective of this study was to determine physiologic role of astrocytes in the acute
homeostatic response to high-fat feeding. Methods We bred a transgenic mouse model with …
Objective
Introduction of a high-fat diet to mice results in a period of voracious feeding, known as hyperphagia, before homeostatic mechanisms prevail to restore energy intake to an isocaloric level. Acute high-fat diet hyperphagia induces astrocyte activation in the rodent hypothalamus, suggesting a potential role of these cells in the homeostatic response to the diet. The objective of this study was to determine physiologic role of astrocytes in the acute homeostatic response to high-fat feeding.
Methods
We bred a transgenic mouse model with doxycycline-inducible inhibition of NFkappaB (NFκB) signaling in astrocytes to determine the effect of loss of NFκB-mediated astrocyte activation on acute high-fat hyperphagia. ELISA was used to measure the levels of markers of astrocyte activation, glial-fibrillary acidic protein (GFAP) and S100B, in the medial basal hypothalamus.
Results
Inhibition of NFκB signaling in astrocytes prevented acute high-fat diet-induced astrocyte activation and resulted in a 15% increase in caloric intake (P < 0.01) in the first 24 h after introduction of the diet.
Conclusions
These data reveal a novel homeostatic role for astrocytes in the acute physiologic regulation of food intake in response to high-fat feeding.
Elsevier