6 December, 2008
Volume 8, Issue 6

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Volume 8, Issue 6

On the cover: A delicate balance governs the cholesterol content of mammalian cell membranes. Using a new method to quantify cholesterol in the endoplasmic reticulum (ER) membrane, Radhakrishnan et al. (pp. 512–521) demonstrate a switch governing activation of the transcription factor SREBP-2 that operates when cholesterol passes a threshold value of 5% of total ER lipids. The cover depicts the system and its components, including cholesterol (yellow), the transcription factor SREBP-2 (magenta), the escort protein Scap (green), the MELADL hexapeptide sequence (red dot), CopII protein (orange), and the ER retention protein Insig (blue).

On the Cover

  • A delicate balance governs the cholesterol content of mammalian cell membranes. Using a new method to quantify cholesterol in the endoplasmic reticulum (ER) membrane, Radhakrishnan et al. demonstrate a switch governing activation of the transcription factor SREBP-2 that operates when cholesterol passes a threshold value of 5% of total ER lipids.


Most Read Papers

  • These are the Top 20 Papers by download from the Cell Metabolism web site for the last 30 days.

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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.

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Current Issue

Volume 8, Issue 6: December 3, 2008
Next issue: January 7, 2009

Featured Article

The Featured Article is freely available to all readers.

Identification of Adropin as a Secreted Factor Linking Dietary Macronutrient Intake with Energy Homeostasis and Lipid Metabolism

Kumar et al.


Obesity and nutrient homeostasis are linked by mechanisms that are not fully elucidated. Here we describe a secreted protein, adropin, encoded by a gene, Energy Homeostasis Associated (Enho), expressed in liver and brain. Liver Enho expression is regulated by nutrition: lean C57BL/6J mice fed high-fat diet (HFD) exhibited a rapid increase, while fasting reduced expression compared to controls. However, liver Enho expression declines with diet-induced obesity (DIO) associated with 3 months of HFD or with genetically induced obesity, suggesting an association with metabolic disorders in the obese state. In DIO mice, transgenic overexpression or systemic adropin treatment attenuated hepatosteatosis and insulin resistance independently of effects on adiposity or food intake. Adropin regulated expression of hepatic lipogenic genes and adipose tissue peroxisome proliferator-activated receptor gamma, a major regulator of lipogenesis. Adropin may therefore be a factor governing glucose and lipid homeostasis, which protects against hepatosteatosis and hyperinsulinemia associated with obesity.

Featured Previews

A Gut Feeling for Obesity: 7TM Sensors on Enteroendocrine Cells

Maja S. Engelstoft, Kristoffer L. Egerod, Birgitte Holst, and Thue W. Schwartz
10.1016/j.cmet.2008.11.004
Related paper: Reimann et al.

A Cholesterol Toggle Switch

Randolph Y. Hampton
10.1016/j.cmet.2008.11.006
Related paper: Radhakrishnan et al.


In This Issue

Glucose Sensing in L Cells: A Primary Cell Study
Reimann et al.
Insig Regulates HMG-CoA Reductase by Controlling Enzyme Phosphorylation in Fission Yeast
Burg et al.
The Serine Protease Matriptase-2 (TMPRSS6) Inhibits Hepcidin Activation by Cleaving Membrane Hemojuvelin
Silvestri et al.
Macrophage EP4 Deficiency Increases Apoptosis and Suppresses Early Atherosclerosis
Babaev et al.