According to a new study, published in the December issue of Cell Reports, microglia, the brain’s immune cells responsible for its response to infection or injury, may also regulate the brain’s response to diet, and, thus play a role in obesity.
The brain’s mediobasal hypothalamus (MBH) is able to sense fatty acids (FAs) and this process is involved in the control of food intake, thermogenesis and metabolism.
Chronic consumption of saturated fat leads to inflammation in the adipose tissue, liver, and skeletal muscle, and in the periphery, the hallmark of this over-nutrition or ‘metabolic inflammation’ is the extensive accumulation of macrophages. This type of inflammation also occurs in the hypothalamus, with accumulation of astrocytes and microglia, the brain’s analogs of macrophages, but it is unclear what orchestrates this process.
In the Cell Reports study a research team from UC San Francisco identifies hypothalamic microglia as sensors of saturated fat that are activated by rising levels of FAs, and that control the intensity of a highly localized form of inflammation in cases of high dietary intake. Microglial cells appear to mediate key changes in hypothalamic function that occur in response to consuming excess saturated fat, which include the reduction of the hypothalamic responsiveness to leptin, thus impacting food intake.
According to Suneil Koliwad, the senior author of this study, “microglial activation in the brain may be a part of a normal physiological process to remodel brain function in response to changes in the composition of food intake”.
See also: Leptin: What Is It & Why Should We Care?