Calorie Restriction May Make Rats Live Longer, But Doesn’t Work For PrimatesСпасибо за наводку jtotheizzoe.
Remember those famous studies in worms, mice and rats that indicated that a restricted-calorie diet increased lifespan? Well, the results of a 30-year study in rhesus monkeys has just been reported, and the results make it pretty clear that it doesn’t apply to primates … likely including us.
The molecular pathways and gene circuits that are activated in our bodies as a result of long-term calorie restriction are immensely complicated. Like a tangled ball of yarn complicated. We don’t understand how they work, frankly, and there’s just no magic bullet when it comes to diet and lifespan in creatures like monkeys and humans (I’m looking at you, resveratrol). It’s certainly good for one’s long-term survival not to overeat into Honey-Boo-Boobesity, but what does current science say about calories, long life and naked apes?
Studies of humans who live past 100 point to genetics as more important than restricting calories. Which genes? Time may tell. And none of this has helped us understand how different diet compositions may affect aging.
Read more at Nature News.
31.08.2012
Ограничение калорий - работает ли для всех видов?
27.05.2011
Антидепрессанты и диабет
21.09.2008
Жир жиру рознь!
Жировые клетки людей с лишним весом отличаются от таковых у стройных товарищей. Об этом - статья на http://www.scientificblogging.com/news_releases/fat_in_fat_people_different_than_fat_in_thin_people
Fat In Fat People Different Than Fat In Thin People
Submitted by News Staff on 27 August 2008 - 12:30am. Microbiology
Not all fat is created equal, it seems. A Temple University study finds fat in obese patients is "sick" when compared to fat in lean patients.
Why 'sick? When our bodies don't work properly, we say we're sick. The study in the September issue of Diabetes finds that the same could be said for fat tissue found in obese patients. The cells in their fat tissue aren't working properly and as a result, are sicker than cells found in lean patients' fat tissue.
Lead author Guenther Boden, M.D. theorizes that "sick fat" could more fully explain the link between obesity and higher risk of diabetes, heart disease and stroke.
Researchers from the departments of endocrinology, biochemistry and surgery at the Temple University School of Medicine took fat biopsies from the upper thighs of six lean and six obese patients and found significant differences at the cellular level.
"The fat cells we found in our obese patients were deficient in several areas," said Boden, Laura H. Carnell Professor of Medicine and chief of endocrinology. "They showed significant stress on the endoplasmic reticulum, and the tissue itself was more inflamed than in our lean patients."
Endoplasmic reticulum (ER) is found in every cell and helps synthesize proteins and monitor how they're folded. The stress that Boden describes causes the ER in fat cells to produce several proteins that ultimately lead to insulin resistance, which has been found to play a major role in the development and progression of obesity-related conditions.
The National Institutes of Health recently reported that each time a body mass index (BMI) over 25 is raised by one point, the risk for diabetes increases 25 percent and the risk for heart disease increases 10 percent.
Reducing weight can help reduce stress on the ER, which can lower the risk of insulin resistance and the resulting conditions. Currently Boden and his team are looking at whether free fatty acids are a potential cause for this ER stress.
Other authors on this study include Xunbao Duan, Carol Homko, Ezequiel J. Molina, WeiWei Song, Oscar Perez, Peter Cheung and Salim Merali of Temple University School of Medicine. Funding for this research was provided by grants from the National Institutes of Heath, the Groff Foundation and a mentor-based training grant from the American Diabetes Association.
23.08.2008
GABA и контроль веса.
Нейротрансмиттеры - такие загадочные субстанции! Оказывается, GABA может влиять на процессы ожирения и похудения. Прочитала на http://www.scientificblogging.com/news_releases/gaba_neurocircuitry_gets_a_look_in_weight_gain_and_decline и вам советую:
GABA Neurocircuitry Gets A Look In Weight Gain (And Decline)
Submitted by News Staff on 10 August 2008 - 12:00am. Research
Controlling body weight is a complicated process but scientists investigating the brain's intricate neurocircuitry and its role in maintaining energy balance are forming a clearer picture of the myriad events that lead to weight gain ... and weight loss.
Writing in Nature Neuroscience, a study led by scientists at Beth Israel Deaconess Medical Center (BIDMC) identifies another piece of this complex puzzle, demonstrating that the neurotransmitter GABA --one of the master communicators among neurons – plays a role in controlling energy balance.
"Body weight maintenance is made up of three basic stages," explains the paper's senior author Bradford Lowell, MD, PhD, an investigator in the Division of Endocrinology, Diabetes and Metabolism at BIDMC whose laboratory is working to identify the specific neurocircuits responsible for controlling food intake and/or energy through functional neuroanatomical mapping studies.
"In the first stage, the brain receives sensory input from the body [including information provided by circulating hormones such as leptin and ghrelin and from fuels such as glucose and fatty acids]," says Lowell, who is also a Professor of Medicine at Harvard Medical School.
In the second stage, he adds, the brain integrates this sensory information with cues it has received from the environment (such as aromas and other enticements) along with information gathered from the organism's emotional state. Then, in the final stage, the brain's neurocircuitry takes over, enabling the brain to make appropriate alterations in food intake and energy expenditure in order to maintain energy balance – and prevent weight gain and obesity.
Previous work had primarily focused on identifying the neuropeptides involved in this process. And indeed, this group of neurotransmitters often proves essential to maintaining energy balance – but not always.
"It is well known that AgRP [Agouti-related protein] neurons play a critical role in feeding and energy balance regulation," explains Qingchun Tong, PhD, a postdoctoral fellow in the Lowell laboratory and the study's first author. "However, the deletion of AgRP and NPY [two neuropeptides released from the AgRP neurons] produces little metabolic effect."
An alternate theory proposed that release of the GABA neurotransmitter was mediating the function of AgRP neurons, an idea that had long been postulated but never examined.
To test this hypothesis, Tong and his colleagues generated a group of mice with disrupted release of GABA specifically from the AgRP neurons. As predicted, the genetically altered mice exhibited profound metabolic changes.
"The mice with AgRP neuron-specific disruption of GABA release were lean, had higher energy expenditure and showed resistance to diet-induced obesity," says Tong. "We also found that these animals showed reduced food intake response to the hormone ghrelin. This suggests to us that the neurocircuit engaging GABA release from the AgRP neurons mediates at least part of ghrelin's appetite-stimulating action."
A series of studies to examine the function of glutamate and GABA release from other groups of neurons are currently underway as investigators continue to dissect the brain's neurocircuitry.
"As these new findings demonstrate, GABA release is an important component that mediates the function of AgRP neurons," says Tong. "Discoveries such as this will ultimately help us to design an efficient strategy to tackle the current epidemic of obesity and metabolic disease."
This work was funded, in part, by grants from the National Institutes of Health and support from the North American Association for the Study of Obesity.
In addition to Lowell and Tong, coauthors include BIDMC investigators Chian-Ping Ye and Juli Jones and University of Texas Southwestern Medical Center investigator Joel Elmquist.

