A ketogenic diet may influence how the pancreas functions in people with type 2 diabetes, according to a small clinical study comparing a high-fat, low-carbohydrate diet with a low-fat approach. Researchers found changes in a biomarker linked to stress on insulin-producing cells, suggesting the diet may affect how the body regulates blood sugar.

The study, published in Journal of the Endocrine Society, followed 51 adults with type 2 diabetes over three months. While the findings point to a potential metabolic effect of a ketogenic diet, the study did not show that the diet reverses diabetes or improves long-term health outcomes.

Researchers focused on the proinsulin-to-C-peptide ratio, a laboratory measure that reflects how efficiently the pancreas produces and processes insulin. Higher levels can indicate that insulin-producing beta cells are under stress. Lower levels suggest those cells may be functioning more effectively.

Participants were assigned to either a ketogenic diet or a low-fat diet, both designed to maintain weight. At the end of the study, the ketogenic group showed a greater reduction in this ratio compared with the low-fat group, a change associated with improved beta-cell function.

“We showed that three months of a ketogenic diet was able to improve beta-cell function in patients with type 2 diabetes, and these improvements were associated with changes in the proinsulin-C-peptide ratio, a biomarker of pancreas stress,” said Marian Yurchishin of the University of Alabama at Birmingham.

Both groups lost a modest amount of weight, even though the diets were intended to be weight-maintaining. That makes it difficult to fully separate the effects of diet composition from the effects of weight change, which is already known to influence insulin function.

The study also focused on a surrogate marker rather than clinical outcomes. It did not measure changes in A1C, medication use or rates of diabetes remission. While improved beta-cell function is considered a positive sign, it does not necessarily translate into meaningful changes in disease progression on its own.

Researchers noted that most strategies known to improve beta-cell function involve significant weight loss or surgical intervention.

“Other than bariatric surgery or large-volume intentional weight loss, interventions for improving beta-cell function in type 2 diabetes do not currently exist,” Yurchishin said.

That context makes the findings worth exploring, particularly because the study attempted to isolate dietary effects independent of major weight loss. Still, the sample size was small, the study duration was short and longer-term outcomes remain unknown.

The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases, along with research centers at the University of Alabama at Birmingham and support from the National Heart, Lung, and Blood Institute.

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