High-fat diet induces apoptosis of hypothalamic neurons. Export

@article{citeulike:4292700, abstract = {Consumption of dietary fats is amongst the most important environmental factors leading to obesity. In rodents, the consumption of fat-rich diets blunts leptin and insulin anorexigenic signaling in the hypothalamus by a mechanism dependent on the in situ activation of inflammation. Since inflammatory signal transduction can lead to the activation of apoptotic signaling pathways, we evaluated the effect of high-fat feeding on the induction of apoptosis of hypothalamic cells. Here, we show that consumption of dietary fats induce apoptosis of neurons and a reduction of synaptic inputs in the arcuate nucleus and lateral hypothalamus. This effect is dependent upon diet composition, and not on caloric intake, since pair-feeding is not sufficient to reduce the expression of apoptotic markers. The presence of an intact TLR4 receptor, protects cells from further apoptotic signals. In diet-induced inflammation of the hypothalamus, TLR4 exerts a dual function, on one side activating pro-inflammatory pathways that play a central role in the development of resistance to leptin and insulin, and on the other side restraining further damage by controlling the apoptotic activity.}, author = {Moraes, J. C. and Coope, A. and Morari, J. and Cintra, D. E. and Roman, E. A. and Pauli, J. R. and Romanatto, T. and Carvalheira, J. B. and Oliveira, A. L. and Saad, M. J. and Velloso, L. A.}, citeulike-article-id = {4292700}, citeulike-linkout-0 = {http://dx.doi.org/10.1371/journal.pone.0005045}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/19340313}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=19340313}, doi = {10.1371/journal.pone.0005045}, issn = {1932-6203}, journal = {PLoS ONE}, keywords = {diet-induced-obesity, grattan-lab-journal-club, hypothalamus}, number = {4}, posted-at = {2009-04-08 23:12:07}, priority = {2}, title = {High-fat diet induces apoptosis of hypothalamic neurons.}, url = {http://dx.doi.org/10.1371/journal.pone.0005045}, volume = {4}, year = {2009} }

TY - JOUR ID - citeulike:4292700 L3 - citeulike-article-id:4292700 N2 - Consumption of dietary fats is amongst the most important environmental factors leading to obesity. In rodents, the consumption of fat-rich diets blunts leptin and insulin anorexigenic signaling in the hypothalamus by a mechanism dependent on the in situ activation of inflammation. Since inflammatory signal transduction can lead to the activation of apoptotic signaling pathways, we evaluated the effect of high-fat feeding on the induction of apoptosis of hypothalamic cells. Here, we show that consumption of dietary fats induce apoptosis of neurons and a reduction of synaptic inputs in the arcuate nucleus and lateral hypothalamus. This effect is dependent upon diet composition, and not on caloric intake, since pair-feeding is not sufficient to reduce the expression of apoptotic markers. The presence of an intact TLR4 receptor, protects cells from further apoptotic signals. In diet-induced inflammation of the hypothalamus, TLR4 exerts a dual function, on one side activating pro-inflammatory pathways that play a central role in the development of resistance to leptin and insulin, and on the other side restraining further damage by controlling the apoptotic activity. IS - 4 JF - PLoS ONE SN - 1932-6203 TI - High-fat diet induces apoptosis of hypothalamic neurons. VL - 4 KW - diet-induced-obesity KW - grattan-lab-journal-club KW - hypothalamus AU - Moraes, JC AU - Coope, A AU - Morari, J AU - Cintra, DE AU - Roman, EA AU - Pauli, JR AU - Romanatto, T AU - Carvalheira, JB AU - Oliveira, AL AU - Saad, MJ AU - Velloso, LA PY - 2009/// UR - http://dx.doi.org/10.1371/journal.pone.0005045 ER -