7 January, 2009
Volume 9, Issue 1
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Volume 9, Issue 1
On the cover: The hypothalamic neuropeptide orexin is postulated to play a role in weight control. On pp. 64–76 of this issue, Funato et al. show through genetic and pharmacological means that increased orexin signaling, through the OXR2 receptor, results in resistance to high-fat diet-induced obesity, improved insulin sensitivity, increased energy expenditure, and decreased food intake in mice. The cover depicts a lean transgenic mouse (left), represented with a superimposed structural image of orexin-A, which unlike its wild-type counterpart (right) resists to weight gain on a high-fat diet (represented by a hamburger and fried potatoes). Cover art by Allen Tsai, Makito Sato, and Dave Gresham.
On the Cover
- The hypothalamic neuropeptide orexin is postulated to play a role in weight control. Using genetic and pharmacological manipulations in mice, Funato et al. show that enhanced Orexin/OXR2R signaling counteracts the effects of a high-fat diet, such as one of hamburgers and fried potatoes.
In The News
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Endoplasmic Reticulum Stress Plays a Central Role in Development of Leptin Resistance
Ozcan et al.
January 7 issue
Coverage in:
The Boston Globe | Washington Post
| Reuters | Nature | Scientific American | AFP | The Telegraph
Specific SIRT1 Activation Mimics Low Energy Levels and Protects against Diet-Induced Metabolic Disorders by Enhancing Fat Oxidation
Feige et al.
November 5 issue
Coverage in:
Scientific American | BBC | WebMD | Reuters | National Public Radio
Apelin Stimulates Glucose Utilization in Normal and Obese Insulin-Resistant Mice
Dray et al.
November 5 issue
Coverage in:
National Public Radio
Most Read Papers
- These are the Top 20 Papers by download from the Cell Metabolism web site for the last 30 days.
Cell Press Podcast
In our latest podcast, we hear from Dr. Gokhan Hotamisligil about a new lipid hormone produced by fat that might help to keep you thin. We learn from Dr Ralph Steinman, who discovered dendritic cells 35 years ago, about using these elusive cells to make better vaccines. We also hear from Dr Elizabeth Phelps about regions of the brain that control responses to fearful memories. Finally, stay tuned for our quarterly roundup of exciting research highlights published in the Cell Press family of journals.
You can listen directly by clicking on the player above. To learn about other ways to listen to the podcast, click here.
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Featured Job
Postdoctoral Positions
Molecular Cell Biology of Diabetic Complications
As reviewed in Nature 414:813, 2001, our laboratory focuses on the mechanisms by which hyperglycemia causes vascular damage. Current projects include investigating the molecular basis for “metabolic imprinting”, endothelial progenitor cell dysfunction and impaired vasculogenesis in diabetes, and development of novel therapeutic strategies
for preventing diabetic vascular damage. Candidates should have a strong foundation in molecular and cell biology. Please send CV and names/contact information of 3 references to Dr. M. Brownlee, Diabetes Research Center, Albert Einstein College of Medicine, Jack and Pearl Resnick Campus, 1300 Morris Park Avenue, Bronx, NY 10461, Email: brownlee@aecom.yu.edu. Click here to learn more about the job.
Volume 9, Issue 1: January 7, 2009
Current Issue
Volume 9, Issue 1: January 7, 2009
Next issue: February 4, 2009
Immediate Early Publication
Yatrik M. Shah, Tsutomu Matsubara, Shinji Ito, Sun-Hee Yim, and Frank J. Gonzalez
Featured Article
The Featured Article is freely available to all readers.
Ozcan et al. |
Leptin has not evolved as a therapeutic modality for the treatment of obesity due to the prevalence of leptin resistance in a majority of the obese population. Nevertheless, the molecular mechanisms of leptin resistance remain poorly understood. Here, we show that increased endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) in the hypothalamus of obese mice inhibits leptin receptor signaling. The genetic imposition of reduced ER capacity in mice results in severe leptin resistance and leads to a significant augmentation of obesity on a high-fat diet. Moreover, we show that chemical chaperones, 4-phenyl butyric acid (PBA), and tauroursodeoxycholic acid (TUDCA), which have the ability to decrease ER stress, act as leptin-sensitizing agents. Taken together, our results may provide the basis for a novel treatment of obesity. |
Featured Previews
Kevin D. Hall and Steven B. Heymsfield
10.1016/j.cmet.2008.12.006
Related paper: Tam et al.
David Carling
10.1016/j.cmet.2008.12.007
Related paper: McBride et al.
In This Issue
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