NEW HAVEN, Conn.—A person’s brain may control whether or not he or she has the predisposition to become obese, according to a new study published online in Proceedings of the National Academy of Sciences.
Yale University researchers studied rats bred to be vulnerable to obesity and found they were born with a major difference in the area of the brain that controls hunger. Neurons in the brain that are supposed to signal when enough has been eaten and when the body needs to burn off calories are more sluggish in obese rats because they are inhibited by other cells.
Researchers analyzed the synaptic input organization of the melanocortin system in lean rats that were vulnerable (DIO) or resistant (DR) to diet-induced obesity. They found a distinct difference in the quantitative and qualitative synaptology of anorexigenic proopiomelanocortin (POMC) cells between DIO and DR animals, with a significantly greater number of inhibitory inputs in the POMC neurons in DIO rats compared with DR rats. When exposed to a high-fat diet (HFD), the POMC cells of DIO animals lost synapses, whereas those of DR rats recruited connections. In both DIO rats and mice, the HFD-triggered loss of synapses on POMC neurons was associated with increased glial ensheathment of the POMC perikarya. The altered synaptic organization of HFD-fed animals promoted increased POMC tone and a decrease in the stimulatory connections onto the neighboring neuropeptide Y (NPY) cells. Exposure to HFD was associated with reactive gliosis, that affected the structure of the blood-brain barrier such that the POMC and NPY cell bodies and dendrites became less accessible to blood vessels. The data suggests that consumption of an HFD has a major impact on the cytoarchitecture of the arcuate nucleus in vulnerable subjects, with changes that might be irreversible due to reactive gliosis.
