If you're looking to cut calories, you might start by cutting your food into smaller pieces. So suggests a study reported Tuesday in Zurich, Switzerland, at the international conference for the Society for the Study of Ingestive Behavior.
Arizona State University researchers gave 301 hungry college students either a whole bagel or the same bagel cut into four separate pieces. Twenty minutes later, both groups of students were treated to a free lunch.
What the researchers found was that the college students in both groups ended up eating roughly the same amount of each bagel; however the students that ate the bagel cut in four pieces ate roughly 25 percent less of their free lunch than the students who ate the uncut bagel.
The phenomenon appeared to hold true in animals as well. As part of the same study, the researchers also found that when hungry rats were given a choice to look for food either as a single large pellet or 30 small pellets, the rats ran faster and more frequently to the small pellets...
Tuesday, July 10, 2012
Binge Eating Improves With Deep Brain Stimulation Surgery
Deep brain stimulation reduces binge eating in mice, suggesting that this surgery, which is approved for treatment of certain neurologic and psychiatric disorders, may also be an effective therapy for obesity. Presentation of the results took place June 25 at The Endocrine Society's 94th Annual Meeting in Houston.
"Doing brain surgery for obesity treatment is a controversial idea," said the study's presenting author, Casey Halpern, MD, a fifth-year neurosurgery resident physician at the University of Pennsylvania, Philadelphia. "However, binge eating is a common feature of obese patients that frequently is associated with suboptimal treatment outcomes."
Currently the U.S. Food and Drug Administration has approved deep brain stimulation for use in various conditions that affect the brain, including Parkinson's disease and essential tremor. The procedure does not destroy any part of the brain and typically does not cause pain, Halpern said.
Available treatments of obesity may inadequately address the neural basis of this compulsive overeating behavior, he suggested. A region of the brain called the nucleus accumbens is known to be dysregulated in both rodents and people who binge eat. Therefore, Halpern and his co-workers targeted that brain region with deep brain stimulation in a strain of obesity-prone mice.
The surgery involved implanting an electrode in the nucleus accumbens. Wires connected the electrode to an external neurostimulator, a device similar to a pacemaker. When switched on, the stimulator triggers the electrode to deliver continuous electrical pulses to the brain.
After recovery from surgery, the mice received high-fat food at the same time every day for one hour, and the researchers measured their food consumption. Binge eating was defined as consuming 25 percent or more of the usual daily caloric intake during this period...
"Doing brain surgery for obesity treatment is a controversial idea," said the study's presenting author, Casey Halpern, MD, a fifth-year neurosurgery resident physician at the University of Pennsylvania, Philadelphia. "However, binge eating is a common feature of obese patients that frequently is associated with suboptimal treatment outcomes."
Currently the U.S. Food and Drug Administration has approved deep brain stimulation for use in various conditions that affect the brain, including Parkinson's disease and essential tremor. The procedure does not destroy any part of the brain and typically does not cause pain, Halpern said.
Available treatments of obesity may inadequately address the neural basis of this compulsive overeating behavior, he suggested. A region of the brain called the nucleus accumbens is known to be dysregulated in both rodents and people who binge eat. Therefore, Halpern and his co-workers targeted that brain region with deep brain stimulation in a strain of obesity-prone mice.
The surgery involved implanting an electrode in the nucleus accumbens. Wires connected the electrode to an external neurostimulator, a device similar to a pacemaker. When switched on, the stimulator triggers the electrode to deliver continuous electrical pulses to the brain.
After recovery from surgery, the mice received high-fat food at the same time every day for one hour, and the researchers measured their food consumption. Binge eating was defined as consuming 25 percent or more of the usual daily caloric intake during this period...
Why Do Fat Cells Get Fat? New Suspect Identified
As the world fights obesity at the human level, scientists at the University of Michigan and their colleagues have made a surprising finding at the microscopic level that could help fuel that fight.
Their work helps explain why fat-storing cells get fatter, and burn fat slower, as obesity sets in. If their findings from mice can be shown to apply to humans, they may provide a new target for obesity-fighting drugs.
By studying the tiny signals that fat-storing cells send to one another, the team has shown a crucial and previously unknown role for a molecule called Sfrp5.
The results, which appear online June 25 and will be in the July issue of the Journal of Clinical Investigation, surprised them.
In a series of experiments, the team showed that Sfrp5 influences a signaling pathway known as WNT to stimulate fat cells -- called adipocytes -- to grow larger and to suppress the rate at which fat is burned in the mitochondria inside them.
By stopping cells from making Sfrp5, they were able to make mice that didn't get as fat as quickly because their adipocytes didn't grow large -- even when the mice were fed a high-fat diet. They even showed the impact when transplanting fat from Sfrp5 -- deficient mice into other mice...
Their work helps explain why fat-storing cells get fatter, and burn fat slower, as obesity sets in. If their findings from mice can be shown to apply to humans, they may provide a new target for obesity-fighting drugs.
By studying the tiny signals that fat-storing cells send to one another, the team has shown a crucial and previously unknown role for a molecule called Sfrp5.
The results, which appear online June 25 and will be in the July issue of the Journal of Clinical Investigation, surprised them.
In a series of experiments, the team showed that Sfrp5 influences a signaling pathway known as WNT to stimulate fat cells -- called adipocytes -- to grow larger and to suppress the rate at which fat is burned in the mitochondria inside them.
By stopping cells from making Sfrp5, they were able to make mice that didn't get as fat as quickly because their adipocytes didn't grow large -- even when the mice were fed a high-fat diet. They even showed the impact when transplanting fat from Sfrp5 -- deficient mice into other mice...
Scientists Identify Target for Obesity and Atherosclerosis
Scientists claim that an enzyme already implicated in the control of tumorigenesis through p53 activation may also directly act to control obesity and atherosclerosis. Wip1 phosphatase is a known negative regulator of ataxia telangiectasia mutated (Atm)-dependent signaling, and knocking out the Wip1 gene, which is amplified in a range of primary human cancers, has been shown to result in tumor resistance in a number of cancer-prone mouse models. Dmitry V. Bulavin, Ph.D., at the Institute of Molecular and Cell Biology and the Singapore Bioimaging Consortium (SBIC) have now found that Wip1 deficiency also makes mice resistant to diet-induced obesity and prevents the development of atherosclerosis in ApoE-knockout animals.
Their findings, reported in Cell Metabolism, indicate that Wip1’s role in controlling obesity and atherosclerosis is dependent on an Atm-mTOR signaling pathway that doesn’t involve p53. Instead, knocking out Wip1 prevents the accumulation of lipid droplets in macrophages and their conversion into foam cells through increased autophagy. Dr Bulavin, et al’s published paper is titled “Wip1-Dependent Regulation of Autophagy, Obesity, and Atherosclerosis.”
Atherosclerosis starts to develop when low-density lipoprotein (LDL) is oxidised by free radicals to generate oxLDL, which damages arterial walls and triggers repair mechanisms. The repair process involves the recruitment of monocytes to the damaged arterial walls, and their differentiation into macrophages that ingest oxLDL and accumulate cholesterol in the form of lipid droplets, leading to the formation of foam cells. Because the cells can’t process the oxLDL, they continue to grow and eventually rupture, depositing even more oxidized cholesterol in the arterial wall, and propagating further immune responses.
Studies by the Singapore team in engineered mice now suggest that Wip1 phosphatase promotes atherosclerosis, as well as diet-induced weight gain and fat accumulation. They found that genetic-knockout animals lacking ApoE and Wip1 put on far less weight when fed a high-fat western diet than ApoE knockouts that retained wild-type Wip1. In comparison with the wild-type Wip1 animals, the double knockouts had far less body fat and lighter livers with evidence of suppressed steatosis. They also ate less and expended more energy. Importantly, the ApoE/Wip1 knockout mice demonstrated higher usage of fat as an energy source...
Their findings, reported in Cell Metabolism, indicate that Wip1’s role in controlling obesity and atherosclerosis is dependent on an Atm-mTOR signaling pathway that doesn’t involve p53. Instead, knocking out Wip1 prevents the accumulation of lipid droplets in macrophages and their conversion into foam cells through increased autophagy. Dr Bulavin, et al’s published paper is titled “Wip1-Dependent Regulation of Autophagy, Obesity, and Atherosclerosis.”
Atherosclerosis starts to develop when low-density lipoprotein (LDL) is oxidised by free radicals to generate oxLDL, which damages arterial walls and triggers repair mechanisms. The repair process involves the recruitment of monocytes to the damaged arterial walls, and their differentiation into macrophages that ingest oxLDL and accumulate cholesterol in the form of lipid droplets, leading to the formation of foam cells. Because the cells can’t process the oxLDL, they continue to grow and eventually rupture, depositing even more oxidized cholesterol in the arterial wall, and propagating further immune responses.
Studies by the Singapore team in engineered mice now suggest that Wip1 phosphatase promotes atherosclerosis, as well as diet-induced weight gain and fat accumulation. They found that genetic-knockout animals lacking ApoE and Wip1 put on far less weight when fed a high-fat western diet than ApoE knockouts that retained wild-type Wip1. In comparison with the wild-type Wip1 animals, the double knockouts had far less body fat and lighter livers with evidence of suppressed steatosis. They also ate less and expended more energy. Importantly, the ApoE/Wip1 knockout mice demonstrated higher usage of fat as an energy source...
Fat Fighting Is Part of the Apple's Peel
Eating unpeeled apples may keep extra pounds and obesity-related diseases at bay, a study in PLoS ONE suggests.
Ursolic acid is a natural compound found in the waxy coats on apples and other fruits and herbs. Previous research showed that ursolic acid increased the activity of a protein that stimulated muscle growth and glucose metabolism in mice.
Ursolic acid, found in apples' waxy coats, triggered an increase in high-energy brown fat, which is associated with reduced obesity, in mice in an Iowa study.
In this follow-up study, researchers in Iowa tested ursolic acid on mice with diet-induced obesity. For six weeks, one group of mice had unlimited access to a diet of high-fat food proven to cause obesity, glucose intolerance and fatty liver disease. Two other groups of mice had unlimited access to the same diet, but supplemented with either 0.14 grams or 0.27 grams of ursolic acid per 100 grams of food. For comparison, an apple contains 50 milligrams of ursolic acid, equivalent to about 6% of the lowest dose given to the mice.
Ursolic-acid mice developed more skeletal muscle but gained less weight than nonsupplemented mice, even though food intake was higher in ursolic-acid mice. Supplemented mice had greater strength and exercise capacity, and higher resting energy expenditure. Ursolic acid triggered an increase in high-energy brown fat associated with reduced obesity, though it isn't known how, researchers said. The results were the same for both ursolic-acid doses...
Ursolic acid is a natural compound found in the waxy coats on apples and other fruits and herbs. Previous research showed that ursolic acid increased the activity of a protein that stimulated muscle growth and glucose metabolism in mice.
Ursolic acid, found in apples' waxy coats, triggered an increase in high-energy brown fat, which is associated with reduced obesity, in mice in an Iowa study.
In this follow-up study, researchers in Iowa tested ursolic acid on mice with diet-induced obesity. For six weeks, one group of mice had unlimited access to a diet of high-fat food proven to cause obesity, glucose intolerance and fatty liver disease. Two other groups of mice had unlimited access to the same diet, but supplemented with either 0.14 grams or 0.27 grams of ursolic acid per 100 grams of food. For comparison, an apple contains 50 milligrams of ursolic acid, equivalent to about 6% of the lowest dose given to the mice.
Ursolic-acid mice developed more skeletal muscle but gained less weight than nonsupplemented mice, even though food intake was higher in ursolic-acid mice. Supplemented mice had greater strength and exercise capacity, and higher resting energy expenditure. Ursolic acid triggered an increase in high-energy brown fat associated with reduced obesity, though it isn't known how, researchers said. The results were the same for both ursolic-acid doses...
Obesity Vaccine Effective In Mice
New vaccines promote weight loss. A new study, published in BioMed Central's open access journal, Journal of Animal Science and Biotechnology, assesses the effectiveness of two somatostatin vaccinations, JH17 and JH18, in reducing weight gain and increasing weight loss in mice.
Obesity and obesity-related disease is a growing health issue worldwide. Somatostatin, a peptide hormone, inhibits the action of growth hormone (GH) and insulin-like growth factor (IGF-1), both of which increase metabolism and result in weight loss. Vaccination with modified somatostatin causes the body to generate antibodies to somatostatin, effectively removing this inhibition without directly interfering with the growth hormones and subsequently increasing energy expenditure and weight loss.
Keith Haffer from Braasch Biotech LLC, tested the vaccinations in two groups of ten diet-induced obese male mice compared with a control group of ten mice which received saline injections. Mice in all groups had been fed a high fat diet for eight weeks prior to the study and continued to eat the same food for the duration of the six-week study. The vaccinations were administered twice - at the start of the study followed by a booster vaccination on day 22.
Four days after the first injection of modified somatostatin, the vaccinated mice had a 10% drop in body weight (not seen in the control mice). At the end of the study, results showed that both vaccines induced antibodies to somatostatin and significantly reduced body weight, sustaining a 10% lower body weight, without affecting normal levels of the growth hormone IGF-1, or insulin levels...
Obesity and obesity-related disease is a growing health issue worldwide. Somatostatin, a peptide hormone, inhibits the action of growth hormone (GH) and insulin-like growth factor (IGF-1), both of which increase metabolism and result in weight loss. Vaccination with modified somatostatin causes the body to generate antibodies to somatostatin, effectively removing this inhibition without directly interfering with the growth hormones and subsequently increasing energy expenditure and weight loss.
Keith Haffer from Braasch Biotech LLC, tested the vaccinations in two groups of ten diet-induced obese male mice compared with a control group of ten mice which received saline injections. Mice in all groups had been fed a high fat diet for eight weeks prior to the study and continued to eat the same food for the duration of the six-week study. The vaccinations were administered twice - at the start of the study followed by a booster vaccination on day 22.
Four days after the first injection of modified somatostatin, the vaccinated mice had a 10% drop in body weight (not seen in the control mice). At the end of the study, results showed that both vaccines induced antibodies to somatostatin and significantly reduced body weight, sustaining a 10% lower body weight, without affecting normal levels of the growth hormone IGF-1, or insulin levels...
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