Obesity is prevalent today all over the world and in some places more than others. Not only does it take a significant toll on an individual’s health and cause different kinds of complications, it takes a toll on a person’s family and their loved ones who watch them struggle. Researchers like Dr. Jen Beshel, John Dubnau, Holger Henneicke, and Sarah Kim have discovered promising information to help us combat the ongoing pandemic of obesity.
In the article A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila, Dr. Jennifer Beshel, Josh Dubnau, and others have all studied the neuropeptide Leptin which is typically an adipose tissue derived hormone which has a function in weight regulation. Dr. Beshel and the researchers all found that in drosophila there is an unpaired 1 ligand that acts to regulate feeding behaviors just as leptin does in human brains. Also, they found that the neuropeptide F that has regulatory effects on feeding behavior and mediates other obesity-type traits is homologous to the Neuropeptide Y regulator that is found in humans. These findings are significant in the search of obesity treatments because they allow scientists to manipulate the variables in drosophila to attempt to decrease weight gain or obesity related behaviors. However, this search has not been easy, the search for an effective treatment has been made increasingly difficult since leptin receptors can develop a resistance causing excess leptin not to bind to the receptors and thereby inhibiting the suppression of obese-type traits and behaviors causing further weight gain.
Because Leptin resistance is what prevents doctors from prescribing leptin to obese patients for weight loss, it is important that researchers find out the source of leptin resistance. In the article Skeletal glucocorticoid signaling determines leptin resistance and obesity in aging mice, Holger Henneicke, Sarah Kim, and others found that skeletal glucocorticoid signaling determines leptin resistance and obesity in aging mice. The researchers studied mice that were lacking glucocorticoid signaling in osteoblasts and osteocytes (HSD2OB/OCY mice), and their wild-type littermates for 3, 6. 12 and 18 months of age. They also assessed leptin sensitivity by the arcuate nucleus STAT3 phosphorylation and the resulting inhibition of feeding. The researchers found that as the mice aged, wild-type mice became obese. The obesity that resulted from leptin resistance because of an impaired ability of exogenous leptin to suppress food intake and phosphorylate hypothalamic STAT3 from 6 months of age and onwards. This information is significant because it underlines the importance of the skeletal system in regulating weight and highlights a factor associated to the cause of leptin resistance.
These studies open a door of opportunity to finding a new treatment for obesity that will help contain and reverse this global issue. By combining the information learned about leptin resistance in humans with the information about a potential source of the resistance, researchers might be able to target the source and develop different therapies that way.
Citations:
Beshel J, Dubnau J, Zhong Y. A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila.
In the article A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila, Dr. Jennifer Beshel, Josh Dubnau, and others have all studied the neuropeptide Leptin which is typically an adipose tissue derived hormone which has a function in weight regulation. Dr. Beshel and the researchers all found that in drosophila there is an unpaired 1 ligand that acts to regulate feeding behaviors just as leptin does in human brains. Also, they found that the neuropeptide F that has regulatory effects on feeding behavior and mediates other obesity-type traits is homologous to the Neuropeptide Y regulator that is found in humans. These findings are significant in the search of obesity treatments because they allow scientists to manipulate the variables in drosophila to attempt to decrease weight gain or obesity related behaviors. However, this search has not been easy, the search for an effective treatment has been made increasingly difficult since leptin receptors can develop a resistance causing excess leptin not to bind to the receptors and thereby inhibiting the suppression of obese-type traits and behaviors causing further weight gain.
Because Leptin resistance is what prevents doctors from prescribing leptin to obese patients for weight loss, it is important that researchers find out the source of leptin resistance. In the article Skeletal glucocorticoid signaling determines leptin resistance and obesity in aging mice, Holger Henneicke, Sarah Kim, and others found that skeletal glucocorticoid signaling determines leptin resistance and obesity in aging mice. The researchers studied mice that were lacking glucocorticoid signaling in osteoblasts and osteocytes (HSD2OB/OCY mice), and their wild-type littermates for 3, 6. 12 and 18 months of age. They also assessed leptin sensitivity by the arcuate nucleus STAT3 phosphorylation and the resulting inhibition of feeding. The researchers found that as the mice aged, wild-type mice became obese. The obesity that resulted from leptin resistance because of an impaired ability of exogenous leptin to suppress food intake and phosphorylate hypothalamic STAT3 from 6 months of age and onwards. This information is significant because it underlines the importance of the skeletal system in regulating weight and highlights a factor associated to the cause of leptin resistance.
These studies open a door of opportunity to finding a new treatment for obesity that will help contain and reverse this global issue. By combining the information learned about leptin resistance in humans with the information about a potential source of the resistance, researchers might be able to target the source and develop different therapies that way.
Citations:
Beshel J, Dubnau J, Zhong Y. A Leptin Analog Locally Produced in the Brain Acts via a Conserved Neural Circuit to Modulate Obesity-Linked Behaviors in Drosophila.
Henneicke, Holger, et al. “Skeletal Glucocorticoid Signalling Determines Leptin Resistance and Obesity in Aging Mice.” Molecular Metabolism, Elsevier, 10 Oct. 2020,
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