Kaushik et al.¹ report that a similar pathway operates in AgRP neurons, with consequences that seem to extend beyond fuel utilization. They propose that AgRP neurons accumulate free fatty acids from the blood during food deprivation and that these fatty acids are then quickly converted into triglyceride fats and stored in lipid droplets (Fig. 1). These lipids are rapidly remobilized through autophagy of the lipid droplet, and free fatty acids are re-formed for use as fuel. The authors suggest that this circuitous pathway provides a mechanism for regulatory control over the accumulation of free fatty acids in the cell, so that they can be used in an orderly fashion. It remains to be seen whether this process operates in other neurons.   一种吞噬作用把脂肪酸吸收

A key finding from these experiments is that Agrp expression, which promotes eating, is increased by free fatty acids. In addition, this effect on gene expression requires lysosomal processing, as would be expected of the autophagy pathway.

These results¹ should be considered in the light of other studies demonstrating a role for fatty-acid metabolism in the regulation of Agrp expression. For example, Agrp expression is reduced when fatty-acid utilization is inhibited by eliminating an uncoupling protein involved in the activity of the mitochondrion, the cell's energy-producing organelle⁶. One implication is that the autophagy pathway could be linked to the transport of fatty acids for mitochondrial metabolism. Then there is the question of how cellular fatty acids regulate Agrp. One possibility for future investigation is the involvement of the transcription factor FoxO1, which regulates Agrp expression according to hunger status⁷.

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Could blocking this cannibalistic process be used to reduce body weight? Possibly, but the autophagy pathway is ubiquitous in cells throughout the body, so extensive investigation will be needed to find selective points of entry for therapeutic interference in obesity and eating disorders.

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