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New key brain target of fat hormone
January 19, 2006Researchers have identified a new area of the brain that responds to the fat hormone leptin in regulating body weight and energy expenditure. They said that the region seems to be particularly important in enabling the body to resist weight gain from a high-fat diet. Their discovery, they said, indicates that leptin acts on more brain areas than previously believed, to regulate body weight.
Leptin is secreted by fat tissue into the bloodstream, where it travels to the brain and other tissues. It acts on leptin receptors in areas of the hypothalamus to trigger fat loss and decreased appetite.
Bradford Lowell and his colleagues published their findings in mice in the January 19, 2006, issue of Neuron. They reported that an area called the ventromedial hypothalamus (VMH) is also important in leptin response, in addition to the area called the arcuate nucleus (ARC) of the hypothalamus, which is already known to be a target of leptin signaling.
Even though leptin was known to act on the neurons of the ARC, wrote the researchers, knocking out leptin receptors in those neurons caused only mild obesity in mice, compared to the effects of knocking out such receptors throughout the brain. Such findings, they said, hinted at the role of another region of the hypothalamus as a leptin target. The VMH constituted a good candidate for such a leptin target region because neurons there express leptin receptors, said the researchers. Also, they noted, destroying the VMH produces massive obesity in mice.
To explore the role of the VMH in leptin signaling, Lowell and his colleagues generated mice lacking leptin receptors only in specific neurons in the VMH. Electrophysiological studies of the VMH neurons in these altered mice showed that they were not triggered by leptin to fire, as were such neurons in normal mice.
The researchers found that the mice lacking VMH leptin receptors showed the same degree of body weight gain as those engineered to lack leptin receptors in the ARC. What's more, the researchers found that knocking out both types of neurons showed an additive effect on weight gain in the animals. Their measurements in the mice revealed that such weight gain was due to an increase in fat stores.
Importantly, when the researchers fed the mice deficient in VMH leptin receptors a high-fat, high-sugar diet, they found that the animals rapidly gained weight throughout the feeding period. In contrast, normal mice gained some weight, but leveled off during the feeding period. The knockout mice continued to gain weight, found the researchers, because they did not suppress their food intake, as did normal mice.
The researchers noted that the combined effects on obesity of the deficiency of VMH leptin receptors and high-fat feeding "were greater than expected from the individual components added together.
"This synergistic interaction strongly suggests that leptin action on [the VMH neurons] plays a particularly important role in resisting high-fat-diet-induced obesity."
Lowell and his colleagues concluded that "In total, these findings suggest that the ability of leptin to restrain body weight is distributed to a number of different sites in the brain.\\\
Cell Press
Even though leptin was known to act on the neurons of the ARC, wrote the researchers, knocking out leptin receptors in those neurons caused only mild obesity in mice, compared to the effects of knocking out such receptors throughout the brain. Such findings, they said, hinted at the role of another region of the hypothalamus as a leptin target. The VMH constituted a good candidate for such a leptin target region because neurons there express leptin receptors, said the researchers. Also, they noted, destroying the VMH produces massive obesity in mice.
To explore the role of the VMH in leptin signaling, Lowell and his colleagues generated mice lacking leptin receptors only in specific neurons in the VMH. Electrophysiological studies of the VMH neurons in these altered mice showed that they were not triggered by leptin to fire, as were such neurons in normal mice.
The researchers found that the mice lacking VMH leptin receptors showed the same degree of body weight gain as those engineered to lack leptin receptors in the ARC. What's more, the researchers found that knocking out both types of neurons showed an additive effect on weight gain in the animals. Their measurements in the mice revealed that such weight gain was due to an increase in fat stores.
Importantly, when the researchers fed the mice deficient in VMH leptin receptors a high-fat, high-sugar diet, they found that the animals rapidly gained weight throughout the feeding period. In contrast, normal mice gained some weight, but leveled off during the feeding period. The knockout mice continued to gain weight, found the researchers, because they did not suppress their food intake, as did normal mice.
The researchers noted that the combined effects on obesity of the deficiency of VMH leptin receptors and high-fat feeding "were greater than expected from the individual components added together.
"This synergistic interaction strongly suggests that leptin action on [the VMH neurons] plays a particularly important role in resisting high-fat-diet-induced obesity."
Lowell and his colleagues concluded that "In total, these findings suggest that the ability of leptin to restrain body weight is distributed to a number of different sites in the brain.\\\
Cell Press
Canadian scientists link fat hormone to death from potentially deadly blood infection
A new Canadian study has found that lower-than-normal levels of a naturally-occurring fat hormone may increase the risk of death from sepsis-an overwhelming infection of the blood which claims thousands of lives each year.
Insulin sensitizer also serves as energy-conserving signal to the brain
A fat-derived protein known for its effects on the liver and skeletal muscle might also serve as an energy-conserving signal to the brain during periods of starvation.
Lean for life
Infant formula and other baby foods that provide permanent protection from obesity and diabetes into adulthood could be on shop shelves soon, reports Lisa Melton in Chemistry & Industry, the magazine of the SCI.
Promising antiobesity drug fails to produce clinically meaningful weight loss
A drug designed to target a powerful hunger-stimulating factor that has long been considered a prime target for antiobesity therapy failed to produce clinically meaningful weight loss in obese people in a long-term clinical trial.
Weight control protein may yield antiobesity drugs
A weight control protein with a key role in the brain's ability to monitor body fat content may yield new approaches for treating obesity and type 2 diabetes, according to a new report in the August issue of Cell Metabolism.
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