Doctors and researchers will often footnote their advice or clinical study findings saying something like, “While the new information looks promising, there is no ‘magic bullet’, no ‘on-off switch’ for (whatever). More study is needed before a drug can be developed”… Well, it sounds like one is very near, here!
No On-Off switch…
But now a new discovery by researchers from Columbia University, U.S., say hey might found the basis for just that – an ‘on-off switch’ for brain impulses that tell us when we’re full and satiated, and could be useful in the treatment of of obesity.
What they did
Researchers studied the effects of a newly discovered hormone, called Lipocalin-2 (LCN2), on then brain and the mechanism that usually tells us when we’ve eaten enough.
“LCN2 acts as a signal for satiety after a meal, leading mice to limit their food intake, and it does this by acting on the hypothalamus within the brain,” explains Study Lead Author Peristera-Ioanna Petropoulou, who was a Postdoctoral Research Scientist at Columbia University at the time the study was carried out. “We wanted to see whether LCN2 has similar effects in humans, and whether a dose of it would be able to cross the blood-brain barrier.”
An abstract of the Study explains: “The team first analysed data from four different studies of people in the US and Europe who were either normal weight, overweight or living with obesity. The people in each study were given a meal after an overnight fast, and the amount of LCN2 in their blood before and after the meal was studied.”
What they found
The researchers found that in those who were of normal weight, there was an increase in LCN2 levels after the meal, which coincided with how satisfied they felt after eating. The researchers found that in those who were of normal weight, there was an increase in LCN2 levels after the meal, which coincided with how satisfied they felt after eating.
By contrast, in people who were overweight or had obesity, LCN2 levels decreased after a meal. Based on this post-meal response, the researchers grouped people as non-responders or responders. Non-responders, who showed no increase in LCN2 after a meal, tended to have a larger waist circumference and higher markers of metabolic disease – including BMI, body fat, increased blood pressure and increased blood glucose.
Taken together, these results mirror those seen in mice, and suggest that this loss of post-meal LCN2 regulation is a new mechanism contributing to obesity and could be a potential target for weight-loss treatments.
Hoo-RAH! But I hasten to point out that the doctors behind these new studies, though enthusiastic about the results, call it ‘just a beginning’, saying scientists have much more work to do before they can even consider developing a drug based on it. They’ve already got to the stage where humans are involved in the studies. I say, if it’s so promising, then get off your duffs and give it the ‘Operation Warp Speed’ treatment so we can get the drug and start reducing the billions and billions of dollars a year that the obesity epidemic is costing the world’s healthcare systems!