Researchers are conjuring up ways to harness the power of daylight and cold temperatures for helping with weight loss. Recent discoveries about brown fat, also known as brown adipose tissue (BAT), have brought a research focus on how to stimulate production of brown fat in humans to help with weight loss.
Scientists at The University of Nottingham have now found that daylight and cold are factors that greatly contribute to controlling brown fat, and they are trying to find ways to help humans lose weight by promoting BAT activity.
Brown fat burns energy instead of storing it, making us overweight. White fat is the kind that hangs over our belts, and jiggles under the arms.
Research led by Michael Symonds, Professor of Developmental Physiology in the School of Clinical Sciences at The University of Nottingham found that brown fat activity correlates closely with daylight, and to a lesser degree with ambient temperature. Brown fat is activated by cold.
The scientists say that global warming and indoor heating has diminished out ability to produce energy burning, beneficial brown fat, leading to obesity. Brown fat produces heat. Because our heat requirements have decreased, our bodies produce less brown fat, making it harder to lose weight.
Professor Symonds says, “Our research demonstrates a very strong seasonal variation in the presence of BAT. The study focused on the impact of daylight and ambient temperature as these are two key factors in determining BAT function in small mammals. Our exciting new findings may help us find novel interventions aimed at promoting BAT activity particularly in the winter.” The findings, published in the journal Diabetes, studied over 3500 patients, leading to the findings that stimulating brown fat could be a useful tool to help with weight loss.
If the researchers can find a way for the body make more brown fat (BAT), it would be easy to burn calories and lose weight. Brown fat is capable of producing up to 300 times more heat per unit mass compared with all other tissues.
The scientists feel they may have found a novel mechanism that could use daylight to help with weight loss and fight obesity. The researchers say promoting brown adipose activity in humans could provide a new treatment for losing weight.
Symonds says, “Our research has suggested a previously unknown mechanism for controlling BAT function in humans and this could potentially lead to new treatments for the prevention or reversal of obesity.” The obesity epidemic could become a reason to fight global warming. We need to lose weight.
пятница, 26 ноября 2010 г.
понедельник, 22 ноября 2010 г.
Here Is Another Piece Of The Weight-Control Puzzle
Controlling body weight is a complicated process, as any frustrated dieter might attest. But as scientists continue to investigate the brain’s intricate neurocircuitry and its role in maintaining energy balance, they are forming a clearer picture of the myriad events that lead to weight gain and weight loss.
In the August 10 on-line issue of 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.”
In the August 10 on-line issue of 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.”
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