May, 2008: 7 (5)
"Ghrelin and Hedonic Food Response"
[Cover Caption]
| Pages | |
|---|---|
| TORCing Up Metabolic Control in the Brain Ville Hietakangas and Stephen M. Cohen | 357 |
| Location, Location, Location… Ruth B.S. Harris and Rudolph L. Leibel | 359 |
| The CAMplexities of Central Ghrelin Mark W. Sleeman and Esther Latres | 361 |
| Type 3 Deiodinase in Hypoxia: To Cool or to Kill? Sabrina Diano and Tamas L. Horvath | 363 |
| Pages | |
| HDL, ABC Transporters, and Cholesterol Efflux: Implications for the Treatment of Atherosclerosis Alan R. Tall, Laurent Yvan-Charvet, Naoki Terasaka, Tamara Pagler, and Nan Wang | 365 |
| Pages | |
| Hypothalamic CaMKK2 Contributes to the Regulation of Energy Balance Kristin A. Anderson, Thomas J. Ribar, Fumin Lin, Pamela K. Noeldner, Michelle F. Green, Michael J. Muehlbauer, Lee A. Witters, Bruce E. Kemp, and Anthony R. Means | 377 |
| Hypothalamic Fatty Acid Metabolism Mediates the Orexigenic Action of Ghrelin Miguel López, Ricardo Lage, Asish K. Saha, Diego Pérez-Tilve, María J. Vázquez, Luis Varela, Susana Sangiao-Alvarellos, Sulay Tovar, Kawtar Raghay, Sergio Rodríguez-Cuenca, Rosangela M. Deoliveira, Tamara Castañeda, Rakesh Datta, Jesse Z. Dong, Michael Culler, Mark W. Sleeman, Clara V. Álvarez, Rosalía Gallego, Christopher J. Lelliott, David Carling, Matthias H. Tschöp, Carlos Diéguez, and Antonio Vidal-Puig | 389 |
| Ghrelin Modulates Brain Activity in Areas that Control Appetitive Behavior Saima Malik, Francis McGlone, Diane Bedrossian, and Alain Dagher | 400 |
| Beneficial Effects of Subcutaneous Fat Transplantation on Metabolism Thien T. Tran, Yuji Yamamoto, Stephane Gesta, and C. Ronald Kahn | 410 |
| IRS1-Independent Defects Define Major Nodes of Insulin Resistance Kyle L. Hoehn, Cordula Hohnen-Behrens, Anna Cederberg, Lindsay E. Wu, Nigel Turner, Tomoyuki Yuasa, Yousuke Ebina, and David E. James | 421 |
| The Insulin-Regulated CREB Coactivator TORC Promotes Stress Resistance in Drosophila Biao Wang, Jason Goode, Jennifer Best, Jodi Meltzer, Pablo E. Schilman, Jian Chen, Dan Garza, John B. Thomas, and Marc Montminy | 434 |
| IRE1β Inhibits Chylomicron Production by Selectively Degrading MTP mRNA Jahangir Iqbal, Kezhi Dai, Tracie Seimon, Rivka Jungreis, Miho Oyadomari, George Kuriakose, David Ron, Ira Tabas, and M. Mahmood Hussain | 445 |
| Amino Acids Activate mTOR Complex 1 via Ca2+/CaM Signaling to hVps34 Pawan Gulati, Lawrence D. Gaspers, Stephen G. Dann, Manel Joaquin, Takahiro Nobukuni, Francois Natt, Sara C. Kozma, Andrew P. Thomas, and George Thomas | 456 |
Cover Caption
The gut hormone ghrelin is a potent stimulator of appetite. On pages 400–409 of this issue, Malik et al. use functional magnetic resonance imaging (fMRI) to visualize ghrelin's effect on brain activity. Ghrelin increased response to food pictures versus a scenery control in a circuit controlling hedonic evaluation of visual stimuli. The cover depicts individuals looking at pictures of food (right) or scenery (left); above, coronal brain images of corresponding subjects show statistical maps of increased cerebral blood flow. Pictures of food activate the insula, amygdala, and hippocampus. Illustration by Yvonne Blanco.
Featured Article
- Hypothalamic CaMKK2 Contributes to the Regulation of Energy Balance
Kristin A. Anderson, Thomas J. Ribar, Fumin Lin, Pamela K. Noeldner, Michelle F. Green, Michael J. Muehlbauer, Lee A. Witters, Bruce E. Kemp, and Anthony R. Means
[Summary] [Full Text] [PDF] [Supplemental Data] - Detailed knowledge of the pathways by which ghrelin and leptin signal to AMPK in hypothalamic neurons and lead to regulation of appetite and glucose homeostasis is central to the development of effective means to combat obesity. Here we identify CaMKK2 as a component of one of these pathways, show that it regulates hypothalamic production of the orexigenic hormone NPY, provide evidence that it functions as an AMPKα kinase in the hypothalamus, and demonstrate that it forms a unique signaling complex with AMPKα and β. Acute pharmacologic inhibition of CaMKK2 in wild-type mice, but not CaMKK2 null mice, inhibits appetite and promotes weight loss consistent with decreased NPY and AgRP mRNAs. Moreover, the loss of CaMKK2 protects mice from high-fat diet-induced obesity, insulin resistance, and glucose intolerance. These data underscore the potential of targeting CaMKK2 as a therapeutic intervention.



