Can't stop eating? Blame it on your genes
Obesity is a medical condition where excess body fat accumulates to the extent of causing adverse effect on health which may lead to reduced life expectancy with increased health problems. It increases the likelihood of different diseases especially the heart disease, cancer as well as type two diabetes. Obesity tends to run in families. Weights of adults selected during studies reveal that their weights are closer to their biological parents’ weights.
A recent study done by Guey-Ying Liao and his colleagues (2012) suggests that human obesity may possibly be caused by mutations in the Bdnf gene as it produces transcripts having either short or long 3’ un translated regions (3’ UTRs). However, in regulation of energy balance, the precise role of brain-derived neurotrophic factor (BDNF) is unknown. The relationship between Bdnf mRNA with along 3’ UTR which means long 3’ UTR Bdnf mRNA, leptin neural activation and the body weight is shown. Long 3’ UTR Bdnf mRNA has been found to be enriched in dendrites of hypothalamic neurons. It has also been found that insulin and leptin could possibly stimulate its translation in dendrites.
Mice harboring a truncated long Bdnf 3’ UTR furthermore developed acute hyperphagic obesity. However, this was completely reversed by viral expression of somewhat long 3’ UTR Bdnf mRNA found in the hypothalamus. The ability of leptin in activating hypothalamic neurons and inhibiting food intake was compromised despite the presence of leptin receptors, in the mice. The results obtained revealed a novel mechanism which linked leptin action to BDNF expression happening during hypothalamic mediated body weight regulation and this also implicated dentritic protein synthesis in the process.
Researchers claim to have found a single mutant gene is the one to blame for the inability of brain to tell obese people when to stop eating. The brain derived neurotrophic factor in mice either stops or slows passage of leptin as well as the insulin signals through the brain. In the humans the aforementioned hormones are released at somewhere at the time when one can see the bottom of the colonel’s sixteen piece bucket. It is not usually the guiltiness that tells one to stop but the brain dictates when the climax is reached. In cases where the signals fail to reach the locations that are of concern in the area in brain signaling satiety.
Such discovery may possibly open up novel strategies which help the brain control body weight. The Bdnf does not only control body weight, but notably in failure to development of one of Bdnf gene, there is a flow effect resulting in deficits in learning and memory in mice. Neurons rarely talk to each other in case there is a problem with Bdnf gene and as such, the leptin and insulin signals become effective without modification of appetite. Faulty transmission line can be repaired by the strategy where missing Bdnf would be produced using virus based gene therapy despite the difficult of delivering across the brain blood barrier.
The lack of a single gene has been found to cause obesity. Leptin appears linked to human disease in which case several childhood diseases have been associated with mutations in leptin genes. Leptin however plays a big role in the body of human beings today. As an issue of concern in human science, research findings should be well administered so as to ensure that the risks of obesity associated with gene mutations are effectively curbed.
Obesity is a medical condition where excess body fat accumulates to the extent of causing adverse effect on health which may lead to reduced life expectancy with increased health problems. It increases the likelihood of different diseases especially the heart disease, cancer as well as type two diabetes. Obesity tends to run in families. Weights of adults selected during studies reveal that their weights are closer to their biological parents’ weights.
A recent study done by Guey-Ying Liao and his colleagues (2012) suggests that human obesity may possibly be caused by mutations in the Bdnf gene as it produces transcripts having either short or long 3’ un translated regions (3’ UTRs). However, in regulation of energy balance, the precise role of brain-derived neurotrophic factor (BDNF) is unknown. The relationship between Bdnf mRNA with along 3’ UTR which means long 3’ UTR Bdnf mRNA, leptin neural activation and the body weight is shown. Long 3’ UTR Bdnf mRNA has been found to be enriched in dendrites of hypothalamic neurons. It has also been found that insulin and leptin could possibly stimulate its translation in dendrites.
Mice harboring a truncated long Bdnf 3’ UTR furthermore developed acute hyperphagic obesity. However, this was completely reversed by viral expression of somewhat long 3’ UTR Bdnf mRNA found in the hypothalamus. The ability of leptin in activating hypothalamic neurons and inhibiting food intake was compromised despite the presence of leptin receptors, in the mice. The results obtained revealed a novel mechanism which linked leptin action to BDNF expression happening during hypothalamic mediated body weight regulation and this also implicated dentritic protein synthesis in the process.
Researchers claim to have found a single mutant gene is the one to blame for the inability of brain to tell obese people when to stop eating. The brain derived neurotrophic factor in mice either stops or slows passage of leptin as well as the insulin signals through the brain. In the humans the aforementioned hormones are released at somewhere at the time when one can see the bottom of the colonel’s sixteen piece bucket. It is not usually the guiltiness that tells one to stop but the brain dictates when the climax is reached. In cases where the signals fail to reach the locations that are of concern in the area in brain signaling satiety.
Such discovery may possibly open up novel strategies which help the brain control body weight. The Bdnf does not only control body weight, but notably in failure to development of one of Bdnf gene, there is a flow effect resulting in deficits in learning and memory in mice. Neurons rarely talk to each other in case there is a problem with Bdnf gene and as such, the leptin and insulin signals become effective without modification of appetite. Faulty transmission line can be repaired by the strategy where missing Bdnf would be produced using virus based gene therapy despite the difficult of delivering across the brain blood barrier.
The lack of a single gene has been found to cause obesity. Leptin appears linked to human disease in which case several childhood diseases have been associated with mutations in leptin genes. Leptin however plays a big role in the body of human beings today. As an issue of concern in human science, research findings should be well administered so as to ensure that the risks of obesity associated with gene mutations are effectively curbed.
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