Posts tagged obesity
Articles and news from the latest research reports.
Study of link between night eating and the peculiar internal clock of fat cells
When researchers at the University of Pennsylvania messed with the internal clocks of mouse fat cells, a surprising thing happened.
The mice got fat.
Figuring out why led to more surprises. Mice usually eat at night, but the altered mice ate more of their food during the day. They got fat even though they ate the same number of calories as regular, nocturnal-feeding mice.
And when the researchers gave altered mice two of the key ingredients in fish oil, the animals didn’t get fat.
That’s a lot to digest, but it has potential implications for humans as we enter the season of stuffed refrigerators that beckon some to eat when they should be resting.
Risk of childhood obesity can be predicted at birth
A simple formula can predict at birth a baby’s likelihood of becoming obese in childhood, according to a study published in the open access journal PLOS ONE.
The formula, which is available as an online calculator, estimates the child’s obesity risk based on its birth weight, the body mass index of the parents, the number of people in the household, the mother’s professional status and whether she smoked during pregnancy.
The researchers behind the study hope their prediction method will be used to identify infants at high risk and help families take steps to prevent their children from putting on too much weight.
BrainHealth Team Studies Overeating as a Type of Addiction
A similar, insidious craving plagues all addicts, no matter the substance of choice. A new study published in NeuroImage from Center for BrainHealth scientists Dr. Francesca Filbey, assistant professor in the School of Behavioral and Brain Sciences, and doctoral student Samuel DeWitt has found that for binge-eaters, as with all addiction sufferers, the compulsion to overeat is rooted in the brain’s reward center.
“Obese but Happy Gene” Challenges the Common Perception of Link Between Depression and Obesity
Researchers at McMaster University have discovered new genetic evidence about why some people are happier than others.
McMaster scientists have uncovered evidence that the gene FTO – the major genetic contributor to obesity – is associated with an eight per cent reduction in the risk of depression. In other words, it’s not just an obesity gene but a “happy gene” as well.
The research appears in a study published in the journal Molecular Psychiatry. The paper was produced by senior author David Meyre, associate professor in clinical epidemiology and biostatistics at the Michael G. DeGroote School of Medicine and a Canada Research Chair in genetic epidemiology; first author Dr. Zena Samaan, assistant professor, Department of Psychiatry and Behavioural Neurosciences, and members of the Population Health Research Institute of McMaster University and Hamilton Health Sciences.
“The difference of eight per cent is modest and it won’t make a big difference in the day-to-day care of patients,” Meyre said. “But, we have discovered a novel molecular basis for depression.”
In the past, family studies on twins, and brothers and sisters, have shown a 40 per cent genetic component in depression. However, scientific studies attempting to associate genes with depression have been “surprisingly unsuccessful” and produced no convincing evidence so far, Samaan said.
The McMaster discovery challenges the common perception of a reciprocal link between depression and obesity: That obese people become depressed because of their appearance and social and economic discrimination; depressed individuals may lead less active lifestyles and change eating habits to cope with depression that causes them to become obese.
“We set out to follow a different path, starting from the hypothesis that both depression and obesity deal with brain activity. We hypothesized that obesity genes may be linked to depression,” Meyre said.
The McMaster researchers investigated the genetic and psychiatric status of patients enrolled in the EpiDREAM study led by the Population Health Research Institute, which analyzed 17,200 DNA samples from participants in 21 countries.
In these patients, they found the previously identified obesity predisposing genetic variant in FTO was associated with an eight per cent reduction in the risk of depression. They confirmed this finding by analyzing the genetic status of patients in three additional large international studies.
Meyre said the fact the obesity gene’s same protective trend on depression was found in four different studies supports their conclusion. It is the “first evidence” that an FTO obesity gene is associated with protection against major depression, independent of its effect on body mass index, he said.
This is an important discovery as depression is a common disease that affects up to one in five Canadians, said Samaan.
(Source: newswise.com)
Hormone Combination Effective and Safe for Treating Obesity in Mice
Scientists at Indiana University and international collaborators have found a way to link two hormones into a single molecule, producing a more effective therapy with fewer side effects for potential use as treatment for obesity and related medical conditions.
The studies were carried out in the laboratories of Richard DiMarchi, the Standiford H. Cox Distinguished Professor of Chemistry and the Linda & Jack Gill Chair in Biomolecular Sciences in the IU Bloomington College of Arts and Sciences, and of Matthias Tschöp, professor of medicine and director of the Institute of Diabetes and Obesity, Helmholtz Center Munich, Germany. Results were published online this week by the journal Nature Medicine.
Researchers combined a peptide hormone from the digestive system, GLP-1, with the hormone estrogen and administered it to obese laboratory mice. While both GLP-1 and estrogen have demonstrated efficacy as therapy for obesity and adult-onset diabetes, the combination was more effective in producing weight loss and other beneficial results than using either compound on its own. And it produced fewer adverse effects, such as excessive tissue growth linked to tumor formation.
"We find that combining the hormones as a single molecule dramatically enhanced their efficacy and their safety," DiMarchi said. "The combination improves the ability to lower body weight and the ability to manage glucose, and it does so without showing the hallmark toxicities associated with estrogen."
Fat cells store excess energy and signal these levels to the brain. In a new study this week in Nature Medicine, Georgios Paschos PhD, a research associate in the lab of Garret FitzGerald, MD, FRS director of the Institute for Translational Medicine and Therapeutics, Perelman School of Medicine, University of Pennsylvania, shows that deletion of the clock gene Arntl, also known as Bmal1, in fat cells, causes mice to become obese, with a shift in the timing of when this nocturnal species normally eats. These findings shed light on the complex causes of obesity in humans.
The Penn studies are surprising in two respects. “The first is that a relatively modest shift in food consumption into what is normally the rest period for mice can favor energy storage,” says Paschos. “Our mice became obese without consuming more calories.” Indeed, the Penn researchers could also cause obesity in normal mice by replicating the altered pattern of food consumption observed in mice with a broken clock in their fat cells.
This behavioral change in the mice is somewhat akin to night-eating syndrome in humans, also associated with obesity and originally described by Penn’s Albert Stunkard in 1955.
The second surprising observation relates to the molecular clock itself. Traditionally, clocks in peripheral tissues are thought to follow the lead of the “master clock” in the SCN of the brain, a bit like members of an orchestra following a conductor. “While we have long known that peripheral clocks have some capacity for autonomy – the percussionist can bang the drum without instructions from the conductor – here we see that the orchestrated behavior of the percussionist can, itself, influence the conductor,” explains FitzGerald.
New clues to how the brain and body communicate to regulate weight
Maintaining a healthy body weight may be difficult for many people, but it’s reassuring to know that our brains and bodies are wired to work together to do just that—in essence, to achieve a phenomenon known as energy balance, a tight matching between the number of calories consumed versus those expended. This careful balance results from a complex interchange of neurobiological crosstalk within regions of the brain’s hypothalamus, and when this “conversation” goes awry, obesity or anorexia can result.
Given the seriousness of these conditions, it’s unfortunate that little is known about the details of this complex interchange. Now research led by investigators at Beth Israel Deaconess Medical Center (BIDMC) provides new insights that help bring order to this complexity. Described in the October 26 issue of the journal Cell, the findings demonstrate how the GABA neurotransmitter selectively drives energy expenditure, and importantly, also help explain the neurocircuitry underlying the fat-burning properties of brown fat.
"Our group has built up a research program with the overall goal of unraveling the ‘wiring diagram’ by which the brain controls appetite and the burning of calories," says senior author Bradford Lowell, MD, PhD, a Professor of Medicine in BIDMC’s Division of Endocrinology and Harvard Medical School. "To advance our understanding to this level, we need to know the function of specific subsets of neurons, and in addition, the upstream neurons providing input to, and the downstream neurons receiving output from, these functionally defined neurons. Until recently, such knowledge in the hypothalamus has been largely unobtainable."
Is obesity irreversible? Timing is everything when it comes to weight loss
Joint research between the University of Michigan and the Argentina-based National Council of Science and Technology (CONICET) has shed light on one of the most frustrating mysteries of weight loss – why the weight inevitably comes back.
A novel animal model showed that the longer mice remained overweight, the more “irreversible” obesity became, according to the new study that appeared online ahead of print Oct.24 in the Journal of Clinical Investigation.
Over time, the static, obese state of the mice reset the “normal,” body weight set point to become permanently elevated, despite dieting that initially worked to shed pounds, authors say.
“Our model demonstrates that obesity is in part a self-perpetuating disorder and the results further emphasize the importance of early intervention in childhood to try to prevent the condition whose effects can last a lifetime,” says senior author Malcolm J. Low, M.D., Ph.D., professor of molecular and integrative physiology and internal medicine.
(Source: uofmhealth.org)
Findings reveal brain mechanisms at work during sleep
One in five American adults show signs of chronic sleep deprivation, making the condition a widespread public health problem. Sleeplessness is related to health issues such as obesity, cardiovascular problems, and memory problems.
Today’s findings show that:
• Sleepiness disrupts the coordinated activity of an important network of brain regions; the impaired function of this network is also implicated in Alzheimer’s disease (Andrew Ward, abstract 909.05).
• Sleeplessness plays havoc with communication between the hippocampus, which is vital for memory, and the brain’s “default mode network;” the changes may weaken event recollection (Hengyi Rao, PhD, abstract 626.08).
• In a mouse model, fearful memories can be intentionally weakened during sleep, indicating new possibilities for treatment of post-traumatic stress disorder (Asya Rolls, abstract 807.06).
• Loss of less than half a night’s sleep can impair memory and alter the normal behavior of brain cells (Ted Abel, PhD, abstract 807.13).Other recent findings discussed show:
• How sleep enables the remodeling of memories — including the weakening of irrelevant memories — and the coherent integration of old and new information (Gina Poe, PhD).
• The common logic behind seemingly contradictory theories of how sleep remodels synapses, aiding cognition and memory consolidation (Giulio Tononi, MD, PhD).
Scientists discover novel diabetes and obesity therapy, and potential cause of major side effects from hedgehog inhibitors used as a cancer treatment
Cancer, diabetes, and excess body weight have one thing in common: they alter cellular metabolism. Scientists from the Max Planck Institute of Immunobiology and Epigenetics in Freiburg and the Medical University of Vienna together with an international research team have jointly resolved a new molecular circuit controlling cellular metabolism. The previously unknown signalling pathway, acting downstream of the hedgehog protein enables muscle cells and brown fat cells to absorb sugars without relying on insulin. Substances that selectively activate the signalling pathway could thus be utilized in the treatment of diabetes and obesity. With their results, the researchers are also able to explain why various new anti-cancer agents have induced mysterious pronounced side effects in the clinics.