FGF1 and Type 2 Diabetes: What the 2014 Salk Mouse Study Found

Blood sugar gauges from the Salk Institute: an untreated diabetic mouse (left) and the same reading after FGF1 (right). Image: Salk Institute for Biological Studies

Short answer: in July 2014, scientists at the Salk Institute in California reported that a single injection of a natural protein called FGF1 brought blood sugar back into a healthy range in obese mice with a type 2 style of diabetes, and that repeated doses reversed their insulin resistance. It was a striking animal result, published in Nature. It was not a cure for people, and more than a decade later there is still no approved FGF1 medicine for diabetes.

Here is what the experiment did, why it caught attention, what it could not show, and what researchers have learned since.

Why insulin resistance is the target

In type 1 diabetes, the immune system destroys the cells in the pancreas that make insulin, so the body cannot produce enough of the hormone that moves sugar out of the blood and into cells. Type 2 diabetes works differently. The body still makes insulin, but muscles, fat and the liver stop responding to it well. This is called insulin resistance.

For a while the pancreas compensates by pumping out more insulin. Over the years it often cannot keep up, and blood sugar rises. Many treatments therefore try to make the body more sensitive to its own insulin. One older class, the thiazolidinediones (such as pioglitazone, sold as Actos), does this but has been linked to side effects including weight gain, fluid retention and bone fractures. A drug that improved insulin sensitivity without those problems would be valuable, which is why the Salk work drew headlines.

What the Salk team did

The study was led by Ronald Evans and Michael Downes at the Salk Institute's gene expression laboratory, with first author Jae Myoung Suh and collaborators in the Netherlands, Australia and elsewhere in the United States. They focused on fibroblast growth factor 1 (FGF1), a protein better known for its role in cell growth and wound repair.

Earlier work had hinted that FGF1 mattered for metabolism: mice bred without it became diabetic quickly when fed a high-fat diet. So the team tried the reverse, injecting FGF1 into the bloodstream of obese mice whose diabetes had been caused by diet.

The main findings

• One dose: a single injection brought blood glucose down into a healthy range for more than two days, according to the institute's announcement.
• Repeated doses: continued treatment did more than lower sugar. It reversed insulin insensitivity, the underlying problem.
• No crash: even at high doses, the mice did not develop dangerously low blood sugar (hypoglycaemia), a real risk with insulin and some older drugs.
• Fewer familiar side effects: the researchers did not see the weight gain or other problems they looked for with comparison drugs.

Commentary at the time, including a piece in The Conversation, noted that FGF1 had no obvious effect in healthy mice and did not help mice that make no insulin at all. That pattern suggested the protein works alongside insulin rather than replacing it.

Liver tissue from obese diabetic mice before (A) and after (B) repeated FGF1 treatment. Image: Salk Institute for Biological Studies

The microscope slides above show one of the more visual results. In panel A, liver tissue from obese diabetic mice is crowded with pale, round fat droplets. In panel B, after a course of FGF1, far fewer droplets remain and the tissue looks closer to that of a healthy animal. The Salk team described these liver cells as having shed fat and begun taking up sugar from the blood again.

Evans summed up the excitement in the institute's release: "FGF1 offers a new method to control glucose in a powerful and unexpected way." He also said the protein would need to be refined into a drug before any human trials.

What the study could not show

The early headlines, such as "one injection reverses diabetes without side effects," went further than the evidence. Three limits matter.

1. It was in mice. Mouse models of diet-induced diabetes are useful, but many treatments that work in rodents fail or behave differently in people.
2. "No side effects" meant "none observed." The researchers checked for specific problems over a limited period. That is not the same as showing a treatment is safe for years in humans.
3. FGF1 is a growth factor. Proteins that encourage cell growth raise an obvious question about long-term risks, including abnormal tissue growth. Any drug would need to separate the sugar-lowering effect from the growth effect.

What came after 2014

The idea did not fade. In 2016, a team led by Michael Schwartz at the University of Washington reported in Nature Medicine that a single injection of FGF1 directly into the brain, at about a tenth of the dose needed in the bloodstream, produced lasting remission of diabetes in both mouse and rat models. The animals did not lose weight to achieve this and did not develop hypoglycaemia, and the authors said the mechanism was not yet fully understood. That finding pointed to the brain as a possible player in how the body regulates blood sugar.

Researchers have also worked on modified versions of FGF1 meant to keep the metabolic effect while reducing growth-promoting activity. A review published in April 2025 still described FGF1 as a promising target and summarised early human testing, but its own authors concluded that larger and longer trials are needed, and some of its citations for clinical results are hard to trace. As of late 2026, no FGF1-based diabetes medicine has been approved.

What this means if you have diabetes

The FGF1 story is a good example of how basic research works: a surprising animal result, a wave of excitement, then years of slower work on mechanism, safety and dosing. It is genuinely interesting science, but it is not something to try or to wait for in place of current care.

Today's established approaches for type 2 diabetes, including lifestyle changes, metformin and newer drug classes, have large human trials behind them. If you are living with diabetes and are curious about new research, the best step is to talk to a doctor, who can explain which options are proven and which are still experimental.

Another early lab result that is easy to over-read: 3D-Printed Corneas: What Newcastle's 2018 Research Demonstrated.

Sources: Salk Institute news release, 16 July 2014: One injection stops diabetes in its tracks; Suh et al., Nature (2014): Endocrinization of FGF1 produces a neomorphic and potent insulin sensitizer; Scarlett et al., Nature Medicine (2016): central injection of FGF1 in rodents; Bu et al., Diabetes, Metabolic Syndrome and Obesity (2025): FGF1 as a therapeutic target in type 2 diabetes; The Conversation, 2014: natural protein could beat insulin resistance; Originally reported by IFL Science.

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