Stress induces glucocorticoid and insulin secretion, increasing food motivation and intake and ultimately resulting in obesity. Most individuals change their eating behavior when stressed. Regardless of an increase or decrease in caloric intake, there is a shift in food choice, and therefore in what kinds of calories are consumed. On pages 159–165 of this issue, Mary F. Dallman discusses the emotional and regulatory brain networks that coerce stressed individuals to snack on high fat and sweet foods, rather than more nutritious options such as fruits and vegetables. The cover shows various desserts that would provide tasty options for the stressed.


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92nd Annual ENDO meeting
The Endocrine Society, June 19-22, 2010
Cell
Acid Extrusion from Human Spermatozoa Is Mediated by Flagellar Voltage-Gated Proton Channel
Polina V. Lishko, Inna L. Botchkina, Andriy Fedorenko, Yuriy Kirichok
Cell Metabolism
Hepatic FGF21 expression is induced at birth via PPARα in response to milk intake and contributes to thermogenic activation of neonatal brown fat
Elayne Hondares, Meritxell Rosell, Frank J. Gonzalez, Marta Giralt, Roser Iglesias, Francesc Villarroya
Current Biology
Regulation of gustatory physiology and appetitive behavior by the Drosophila circadian clock
Abhishek Chatterjee, Shintaro Tanoue, Jerry H. Houl, Paul E. Hardin
Trends in Pharmacological Sciences
Emerging role of estrogen in the control of cardiometabolic disease
Andrea Cignarella, Mario Kratz, and Chiara Bolego
The metabolic syndrome, characterized by insulin resistance, fatty liver, increased risk of diabetes, among others, affects ~1/6 of the population of the United States. While 2/3 of the US population is estimated to be overweight or obese, an article published online on 8 March 2010 in Trends in Endocrinology and Metabolism by Roger Unger and Philipp Scherer describes that obesity may in fact protect against metabolic syndrome, by storing lipids in the appropriate place -- in fat.
The authors also address the role of insulin resistance in the metabolic syndrome, as there is much discussion in the field regarding its role as either a cause or feature of the metabolic syndrome. They argue for the latter, i.e. that insulin resistance is merely a byproduct of fat deposition in the liver and muscle, once fat cells reach their storage capacity. Instead, they argue for the important role of leptin, a hormone that increases as fat storage increases, concluding that obesity and hyperleptinemia protect nonadipose organs from lipotoxicity.
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Trends in Endocrinology and Metabolism contains polished and concise reviews, opinions, and discussions of topics at the cutting edge of the field. The articles incorporate clinical and research perspectives and differ from classical reviews with their focus on the more recent developments in each topic. The content is lively and accessible to a broad audience encompassing basic researchers, physician scientists, and clinical endocrinologists. Topics include physiological function of hormones and the tissues that secrete them, and the recent developments in the metabolism field, from lipid biology to diabetes/insulin resistance.
Commissioned Reviews and Opinion articles form the foundation of each monthly issue. Reviews objectively chronicle recent and important developments, while Opinion articles provide a forum for debate and hypothesis. The journal does consider unsolicited proposals.
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Trends in Endocrinology and Metabolism publishes articles online ahead of the print issue. You can find the latest here:
These are the five most downloaded papers for the 30 days preceding March 11, 2010. See full list of most read articles