Fat literally accrues in the brain of mice consuming a diet high in fat. Exercise was unable to reverse the fat accumulation. The consequences of hypothalamic lipid accumulation may include neural dysfunction and problems with brain regulation.
Adipocytes are cells whose specific function is to take up fat. However, fat can also be stored in other cells, a process called lipotoxicity. Excessive fat accumulation in non-adipose tissue can lead to cellular dysfunction and in extreme cases, cell death or apoptosis.
The central nervous system can be affected by lipotoxicity. In a study published this month in the Journal of Physiology, fat content in the hypothalamus region of the brain was observed in mice fed a high-fat diet (Consumption of a high-fat diet, but not regular endurance exercise training, regulates hypothalamic lipid accumulation in mice, 2012, Melissa L Borg, et al.). Fats generally are not a source of fuel for the brain (glucose is the brain's primary fuel and fat-derived ketone bodies substitute when the body is starved of carbohydrates). Yet, fatty acids can cross the blood-brain barrier and reach the hypothalamus for regulatory purposes. The hypothalamus is the body's hunger and body weight regulator. In addition to neuronal signals, the hypothalamus receives input from the levels of fatty acids in the cerebral spinal fluid. The hypothalamus has a limited means of oxidizing fatty acids; therefore, high levels of fatty acids result in fat being stored in the hypothalamus.
The study found that a high fat diet resulted in an increased amount of lipotoxicity in the hypothalamus. Surprisingly, exercise did not reduce the amount of lipids in the high fat diet mice. The mice were fed a high fat diet (59% of calories from fat) or low fat diet (5% of calories from fat) for twelve weeks. Half of the high fat diet mice were exercised six weeks into the study. As the graph below shows, exercise in the high fat diet mice was able to drop most of the added body weight.
The high fat diet increased a variety of fats in the hypothalamus. Phospholipids, glycerol lipids, saturated fatty acids and monounsaturated fatty acids were all increased in the hypothalamus as a result of a high fat diet. In addition, high fat feeding increased hypothalamic lipid species known to cause insulin resistance. Yet, exercise was unable to reverse the increase in hypothalamus lipids.
The figure above demonstrates that a substantial, 6-week exercise program was not able to substantially reduce the hypothalamus lipid content in mice fed a high fat diet. This suggests that the only way to control fat accumulation in the brain is through diet. Since exercise is not a viable means of reversing fat accumulation in the hypothalamus, other means of reducing lipid accumulation, and the harm it may cause to brain regulation, must be sought.
In conclusion, excess lipid accumulation in non-adipose tissue causes cellular dysfunction leading to diseases such as diabetes. Therefore, lipid accumulation in the hypothalamus due to a high fat diet probably harms regulatory processes in the brain. In the study discussed, exercise was found not to reverse hypothalamus lipid accumulation. The fat content of one's diet should be monitored even in people with a healthy body weight.