Eddy Edson
Well-Known Member
- Relationship to Diabetes
- Type 2
The newly approved GLP-1R agonist anti-obesity drug, not the name. Gila monsters are too classy for stupid names like "Wegovy".
www.vox.com
After learning that the venom of a Gila monster lizard contained hormones that can regulate blood sugar, Daniel Drucker started wondering why. And could the venom somehow help treat diabetes?
Drucker is a scientist and endocrinologist at the University of Toronto who has dedicated his career to understanding the universe of hormones in the body, which do everything from regulating appetite to helping with digestion. His curiosity about the Gila monster led to a call with a zoo in Utah. In 1995, Drucker had a lizard shipped from Utah to his lab and began experiments on the deadly venom.
Ten years later, a synthetic version of a hormone in the venom became the first medicine of its kind approved to treat type 2 diabetes. Known as a GLP-1 (for glucagon-like peptide-1) receptor agonist, the medicine set off a cascade of additional venom-inspired discoveries.
After doctors noticed mice and humans on the drug for diabetes appeared to lose weight, they began to consider its use in obesity science. In June 2021, another effective treatment, this one for obesity, got Food and Drug Administration approval. Called semaglutide and marketed as Wegovy, it also takes its structure from the lizard’s venom.
The article has a nice brief description of what these drugs do:
To understand how semaglutide causes some people to eat less, it’s helpful to understand what hormones do. They’re the body’s traveling messengers: Manufactured in one area, they move to another to deliver messages through receptors — molecules that bind to specific hormones — in distant organs and cells.
The gut makes dozens of hormones, and many of them travel to the brain receptors that either curb appetite or stimulate it, Drucker explains. GLP-1 is one such gut hormone. It’s unleashed in the gut in response to food and stimulates the pancreas to make more insulin after a meal, which lowers blood sugar. (GLP-1 is also made in the brain stem, where it may modify appetite.)
“It sends a signal to our brain that says, ‘You know, we’ve had enough to eat,’” says Drucker.
Enter semaglutide, one of a class of medicines — the GLP-1-receptor agonists — that imitate GLP-1, helping the body lower glucose (in the case of people with diabetes) and, researchers suspect, curb appetite (in the case of people living with obesity who may also have diabetes).
The precise way the drug works on obesity is still unknown, in part because scientists don’t understand exactly how appetite works. But researchers generally agree that the drug harnesses the brain’s GLP-1 receptors to curb food intake. When researchers delete the GLP-1 receptors from the brains of mice, the drug loses its appetite-suppressing effects, says Krashes.
Obesity is “primarily an issue of our brain biology, and the way it’s processing info about the environment we live in,” says Randy Seeley, a University of Michigan researcher focused on obesity treatments, who also consults with Novo Nordisk.
With semaglutide, the idea is that “we’re changing your brain chemistry for your brain to believe you should be at a lower weight,” Seeley added.
This brain-based pharmacological approach is likely to be more successful than diet and exercise alone, Seeley says, because “the most important underlying part of somebody’s weight has to do with how their brain operates,” not a lack of willpower.
A lizard’s venom inspired a promising weight loss drug
Semaglutide is the start of a new chapter in obesity treatments.
www.vox.com
After learning that the venom of a Gila monster lizard contained hormones that can regulate blood sugar, Daniel Drucker started wondering why. And could the venom somehow help treat diabetes?
Drucker is a scientist and endocrinologist at the University of Toronto who has dedicated his career to understanding the universe of hormones in the body, which do everything from regulating appetite to helping with digestion. His curiosity about the Gila monster led to a call with a zoo in Utah. In 1995, Drucker had a lizard shipped from Utah to his lab and began experiments on the deadly venom.
Ten years later, a synthetic version of a hormone in the venom became the first medicine of its kind approved to treat type 2 diabetes. Known as a GLP-1 (for glucagon-like peptide-1) receptor agonist, the medicine set off a cascade of additional venom-inspired discoveries.
After doctors noticed mice and humans on the drug for diabetes appeared to lose weight, they began to consider its use in obesity science. In June 2021, another effective treatment, this one for obesity, got Food and Drug Administration approval. Called semaglutide and marketed as Wegovy, it also takes its structure from the lizard’s venom.
The article has a nice brief description of what these drugs do:
To understand how semaglutide causes some people to eat less, it’s helpful to understand what hormones do. They’re the body’s traveling messengers: Manufactured in one area, they move to another to deliver messages through receptors — molecules that bind to specific hormones — in distant organs and cells.
The gut makes dozens of hormones, and many of them travel to the brain receptors that either curb appetite or stimulate it, Drucker explains. GLP-1 is one such gut hormone. It’s unleashed in the gut in response to food and stimulates the pancreas to make more insulin after a meal, which lowers blood sugar. (GLP-1 is also made in the brain stem, where it may modify appetite.)
“It sends a signal to our brain that says, ‘You know, we’ve had enough to eat,’” says Drucker.
Enter semaglutide, one of a class of medicines — the GLP-1-receptor agonists — that imitate GLP-1, helping the body lower glucose (in the case of people with diabetes) and, researchers suspect, curb appetite (in the case of people living with obesity who may also have diabetes).
The precise way the drug works on obesity is still unknown, in part because scientists don’t understand exactly how appetite works. But researchers generally agree that the drug harnesses the brain’s GLP-1 receptors to curb food intake. When researchers delete the GLP-1 receptors from the brains of mice, the drug loses its appetite-suppressing effects, says Krashes.
Obesity is “primarily an issue of our brain biology, and the way it’s processing info about the environment we live in,” says Randy Seeley, a University of Michigan researcher focused on obesity treatments, who also consults with Novo Nordisk.
With semaglutide, the idea is that “we’re changing your brain chemistry for your brain to believe you should be at a lower weight,” Seeley added.
This brain-based pharmacological approach is likely to be more successful than diet and exercise alone, Seeley says, because “the most important underlying part of somebody’s weight has to do with how their brain operates,” not a lack of willpower.