Insulin Isn’t the Only Blood Sugar Regulator

Written by Amy Norton HealthDay Reporter >

Wednesday, January 5, 2022 – Scientists have known for 100 years that insulin is the body’s main mechanism for controlling blood sugar levels, but researchers have now discovered that a second hormone performs the same function slightly differently – and they say it could be a new target for treating diabetes.

The hormone FGF1 is produced in fatty tissues of the body. Like insulin, it rapidly lowers blood sugar levels, but researchers have found in mice that it works independently of insulin, and by a different mechanism.

Type 2 diabetes arises when the body becomes resistant to insulin, resulting in chronically high levels of glucose (sugar) in the blood. Over time, this can affect the arteries and nerves of the body, leading to complications such as heart and kidney disease, stroke, vision problems, and permanent nerve damage.

In the new study, scientists found that FGF1 suppresses the breakdown of fat tissue, which reduces the liver’s ability to produce glucose. Insulin also does these things, but FGF1 achieves them via a different “signaling pathway” in the body.

And in mice with insulin resistance, injections of FGF1 significantly lower blood sugar.

“This mechanism is essentially a second loop, with all the advantages of a parallel pathway,” said study author Jencer Sankar, a postdoctoral researcher at the Salk Institute in La Jolla, California.

“In insulin resistance, insulin signaling is impaired,” Sankar said in an institute news release. “However, by using a different signaling sequence, if one is not working, so can the other. That way you can still control the [fat breakdown] Regulating blood sugar.

However, it remains to be seen whether the findings in the animals will eventually translate to patients with type 2 diabetes.

One question is whether people who are insulin resistant will also be resistant to FGF1, noted Dr. Emily Gallagher, an endocrinologist who was not involved in the study.

It’s also possible, she said, that targeting FGF1 may be effective in some people with type 2 diabetes, but not others.

“Type 2 diabetes is a complex condition in which different individuals have different metabolic features,” explains Gallagher, MD, assistant professor in the division of endocrinology, diabetes, and orthopedics at the Icahn School of Medicine at Mount Sinai in New York City.

The scientists knew something about FGF1’s way of working. In previous studies, Salk researchers found that it lowered blood sugar in lab mice, and when given consistently reduced insulin resistance in animals.

The new study, published Jan. 4 in the journal cell metabolism It delves into exactly how the hormone works.

The researchers found that FGF1, similar to insulin, prevents the breakdown of fats, which in turn helps control blood sugar. But the way it works is different: Insulin works 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 pathway, we can learn its role in the body’s energy balance and how to deal with it,” said study senior author Michael Downs, a Salk scientist.

It’s “interesting” that FGF1 can have insulin-like effects in fat tissue, Gallagher said. But there is still much to learn.

She said more lab research is needed to understand the long-term effects of FGF1 on insulin signaling and insulin resistance.

“For humans, it will be important to understand more about the systemic effects of FGF1 administration, as FGF1 affects many organ systems – including the inflammatory system – and can also alter tumor growth,” Gallagher said.

Whether manipulating the hormone, or the proteins it regulates, would be appropriate for people with type 2 diabetes “remains to be determined,” Gallagher said.

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