The secrets of longevity protein!

Longevity protein? A new study published in Nature could have implications for therapies developed focused on treating a wide range of medical conditions. They range from diabetes, obesity, to certain types of cancer, the researchers said.

Klotho Proteins

Named after the Greek goddess who spins the thread of life, Klotho proteins play an important role in regulating longevity and metabolism.** Klotho family receptor families are found on the surface of cells in specific tissues. The proteins bind to a family of hormones, called endocrine FGFs. They regulate critical metabolic processes in the liver, kidneys and brain, among others.

The researchers’ analysis served to generate several ideas

First, beta-Klotho is the primary receptor that binds to FGF21, a key hormone produced by starvation. When bound to beta-Klotho, it stimulates insulin sensitivity and glucose metabolism, causing weight loss. “Like insulin, FGF21 stimulates metabolism, including glucose absorption. In animals and in some clinical trials involving FGF21, it is shown that it can increase calorie burning without changing food intake and we now understand how to improve its biological activity,” said Joseph Schlessinger. Senior author and chair of pharmacology at Yale School of Medicine. The authors also describe a new variant of FGF21 that has 10 times more potency and cellular activity. Additionally, the research team presented evidence of how a structurally related enzyme, glycosidase, which breaks down sugars, evolved to become a receptor for a hormone that lowers blood sugar. Which may not be a coincidence, Schlessinger added. By developing drugs that improve the pathway, he said, researchers can attack diabetes and obesity. On the contrary, using agents that block it presents opportunities to explore therapies for diseases. Such as liver cancer and bone diseases, among others. “The next step will be to make better hormones, create new powerful blockers, do animal studies and move forward,” Schlessinger said.