WEDNESDAY, Jan. 5, 2022 (HealthDay News) – Scientists have known for 100 years that insulin is the body’s main control mechanism blood sugar levels, but researchers have now found that another hormone does the same job a little differently – and says it could be a new target for treatment diabetes.
The hormone, called FGF1, is produced in the body fat tissue. As insulin, quickly lowers blood sugar levels, but researchers have found in mice that it acts independently of insulin and a different mechanism.
Type 2 diabetes occurs when the body becomes resistant to insulin, which leads to chronically high levels of glucose (sugar) in the blood. Over time, this can affect the body’s arteries and nerves, leading to complications such as heart and kidney disease, stroke, vision problems and permanent nerve damage.
In a new study, scientists found that FGF1 suppresses the breakdown of adipose tissue, which reduces the liver’s ability to excrete glucose. Insulin also does these things, but FGF1 accomplishes this through a different “signaling pathway” in the body.
And in laboratory mice with insulin resistance, injections of FGF1 significantly lower blood sugar.
“This mechanism is basically a second loop, with all the benefits of a parallel path,” said study author Gencer Sancar, a postdoctoral researcher at the Salk Institute in La Jolla, California.
“IN insulin resistance, insulin signaling is disrupted, “Sancar said in a statement from the institute.” However, with a different signaling cascade, if one doesn’t work, the other can. That way you still have control over it [fat breakdown] and blood glucose regulation. “
However, whether it is found on animals will ultimately translate to humans s type 2 diabetes remains to be seen.
One question is whether people who are insulin resistant will also be resistant to FGF1, noted Dr. Emily Gallagher, endocrinologist who was not included in the study.
She said it is also possible that targeting FGF1 could be effective in some people with type 2 diabetes, but not in others.
“Type 2 diabetes is a complex condition in which different people have different metabolic profiles,” explained Gallagher, an assistant professor in the Department of Endocrinology, Diabetes and Bone Diseases at the Icahn School of Medicine in Mount Sinai, New York.
Scientists knew something about the work of FGF1. In previous studies, researchers from Salka found that it lowers blood sugar in laboratory mice, and when given continuously, it reduces insulin resistance in animals.
A new study, published Jan. 4 in the journal Cell metabolism, immersed in exactly how the hormone works.
Researchers have found that, similar to insulin, FGF1 suppresses fat breakdown, which in turn helps control blood sugar. But its mode of operation is different: insulin acts through an enzyme called PDE3B, which triggers a chain of events called the signaling pathway.
FGF1 uses a different enzyme – called PDE4.
“Now that we have a new path, we can understand its role in energy homeostasis in the body and how to manipulate it,” said senior study author Michael Downes, an employee of Salk.
Gallagher said it was “very interesting” that FGF1 could have insulin-like effects in adipose tissue. But much remains to be learned.
More laboratory research, she said, is needed to understand the long-term effects of FGF1 on insulin signaling and insulin resistance.
“And in humans,” Gallagher said, “it would be important to understand more about the systemic effects of FGF1 administration, since FGF1 affects many organ systems – including the inflammatory system – and can also alter tumor growth.”
Whether manipulating the hormone or proteins it regulates would be appropriate in people with type 2 diabetes remains to be determined, Gallagher said.
The U.S. National Institute on Diabetes and Digestive and Kidney Diseases has more on that type 2 diabetes.
SOURCES: Emily Gallagher, MD, PhD, Assistant Professor, Department of Endocrinology, Diabetes and Bone Diseases, Icahn School of Medicine in Mount Sinai, New York City; Cell metabolism, January 4, 2022; Salk Institute, press release, January 4, 2022