Back in 2011, Reuters reported on a study led by Tim Spector of King’s College London, which resulted in the discovery that the KLF14 gene is the mastermind of the obesity epidemic, ruling other genes like a mob boss and ordering them to wreak havoc in the human body. The story says:
In a report of their study, the researchers explained that other genes found to be controlled by KLF14 are linked to a range of metabolic traits, including body mass index, obesity, cholesterol, insulin and glucose levels…. They found a link between the KLF14 gene and the levels of many other distant genes found in fat tissue, showing that KLF14 acts as a master switch to control these genes.
Not long after that announcement, a pseudonymous blogger published a very comprehensible explanation of the different kinds of genetic research. The medical profession has learned a lot from family studies of diseases caused by change in a lone gene. But obesity, hypertension, and diabetes are complex disorders described here as “not single entities, but instead, a collection of different pathogeneses with similar clinical endpoints.” The writer goes on to say:
In the example of severe childhood obesity, we already know that there is a clear genetic cause of disease in about one in 20 cases…. It is clear that many other inherited causes of obesity remain to be discovered, and that there are similar, very strong genetic effects hidden among sufferers of other complex disorders.
By gaining familiarity with the various genes that have been implicated, a person is better prepared for the astonishment provoked by a certain brand of fatlogic.
Previously, we saw how scientists, not content with the identification of several “fat gene” suspects, began to suggest that combinations of genes working together could cause more obesity than anyone had previously suspected. Additional British research found a variation in a gene called FTO that affects one person in six. Because it causes higher levels of ghrelin in the blood, along with increased sensitivity to the “hunger hormone” once it reaches the brain, these people are much more likely to develop obesity.
A study of more than 2,000 pediatric patients with severe early-onset obesity found that a gene called KSR2, if it suffers a mutation, can cause sluggish metabolism and increased appetite. Then, McGill University’s Patricia Silveira announced that yet another gene affects the reward system of the brain, especially in girls. She said,
We found that a variation in a gene that regulates the activity of dopamine, a major neurotransmitter that regulates the individual’s response to tasty food, predicted the amount of ‘comfort’ foods – highly palatable foods such as ice cream, candy or calorie-laden snacks – selected and eaten by the children.
At University College London, scientists are exploring how multiple genes work together. A team created a conceptual tool called the Polygenic Risk Score, or PRS, accounting for “28 common obesity-related single nucleotide polymorphisms” (or DNA sequence variations). Dr. Clare Llewellyn, the lead author on the stufy, told the press,
As expected, we found that children with a higher PRS (more obesity-risk genetic variants) were likely to have larger BMI and waist circumference. But more importantly, we also found that these children were more likely to have low satiety responsiveness.
In other words, the children’s brains don’t know how to tell their bodies when they have eaten enough. Not long afterward, Germany’s Ulm University Medical Center released the news that “congenital leptin deficiency is a rare autosomal recessive monogenic obesity syndrome caused by mutations in the leptin gene.”
(Next time: the reason for touching on all these pieces of genetic news.)
Your responses and feedback are welcome!
Source: “Scientists find “master switch” gene for obesity,” Reuters.com, April 16, 2011
Source: “Answers in the genes,” blogspot.com, June 27, 2011
Source: “Scientists find how ‘obesity gene’ makes people fat,” ht.ly, July 15, 2013
Source: “Genetic mutation linked to childhood obesity,” Healio.com, October 24, 2013
Source: “Gene linked to childhood obesity identified,” Daijiworld.com, November 30, 2013
Source: “Satiety sensitivity may explain predisposition to childhood obesity,” Healio.com, February 17, 2014
Source: “Monogenic forms of childhood obesity due to mutations in the leptin gene,” MolCellPed.com, September 4, 2014
Image by Micah Baldwin