Researchers at the Johns Hopkins University, in a recent study, have demonstrated the ability of fat cells to participate in a form of two-way communication with nerve cells outside the brain. This study provides the first definitive research that fat cells can directly influence the action of neurons not located within the brain. This has important consequences on research aimed at understanding the storage and burning of fat, obesity and diseases like diabetes.
Historically, fat cells were only known to communicate with neurons in the brain by making substances that were exported and carried in the blood stream. The brain is known to control the rate of fate burning and respond to signals of this process by sending nervous impulses through the spinal cord and to the fat deposits in the body. The Hopkins study provides the first definitive proof that nerve and fat cells can communicate directly outside the brain.
"It's been known for a long time that neurons outside of the brain communicate to fat cells, but no one has thought much about whether fat cells can signal back to the neurons," says first author Christine Turtzo, an M.D.-Ph.D. candidate at The Johns Hopkins University School of Medicine. "We now have evidence that fat cells directly signal neurons and influence their behavior. Unless you had both types of cells growing together, you would not know."
Nerve cells were obtained from rats and the fat cells came from mice. The fat cells were similar to human fat tissue called white adipose tissue, which constitutes most of the energy-storing fat deposits in human.
In addition, fat cells were shown by the study to affect the ability of nerve cells to produce neuropeptide Y (NPY), a protein that is strongly associated with feeding behavior, sexual function, anxiety responses and vascular resistance. Turtzo discovered that nerve cells grown in proximity to fat cells produce more than seven times the NPY than nerve cells grown by themselves. Turtzo also found that when insulin was injected onto the mixed cultures of fat and neural cells the production of NPY dropped, but NPY levels were not affected in isolated neural cell cultures.
"Because insulin doesn't affect these nerve cells, but does affect fat cells, we believe the insulin is acting on the fat cells, which in turn affect the neurons," Turtzo explained.
Based on the results of this study, the Hopkin's scientist claim that NPY is secreted from nerve cells outside the brain to prevent fat deposits from being consumed by the body, and that the fat cells are apparently participating in the regulation of the NPY levels.
"The effects of NPY outside the brain make sense with what we know about it in the brain," says Lane, who oversaw Turtzo's research. "In the brain, high levels of NPY cause animals to eat ravenously, and in the periphery it seems to block the mobilization of fat. If you're eating, you don't need to burn stored fat."
According to Daniel Lane, Ph.D., lead investigator of the study and professor of biological chemistry at the Hopkins Institute for Basic Biomedical Sciences, the fats cells are also secreting a compound, yet to be identified, that is affecting the nerve cells. He believes that human neural and fat cells might be similarly affected.
Some of the problems associated with obesity appear to stem from the extensive saturation of fat deposits in the abdomen with nerve cells compared with fat found elsewhere in the body.
"We don't know why the two different types of fat cells behave differently, but we know that fat in the abdomen has a greater amount of nerves associated with them," said Turtzo.
"Cross-talk between the neurons and the fat cells in the abdomen may be particularly important in controlling what these fat cells make and secrete," says Lane. "Many investigators believe that these secreted factors act on liver function in a manner, as yet unknown, to promote the onset of Type 2 diabetes, for example. Our approach may well shed light on these issues."
"If you can control what the fat cell is doing then you might be able to control the problem [of obesity]," Lane said. The study was reported on Oct. 16 in the Proceedings of the National Academy of Sciences, an online journal.
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