Receiving national recognition is always meaningful, but for Dr. Qutuba Karwi it is even more validating to have been singled out for it by his peers.

In late September, the Canadian Society of Pharmacology and Therapeutics (CSPT) presented the Faculty of Medicine researcher with its 2026 Junior Investigator Award.

The award is presented to a CSPT member for significant contributions to the advancement and extension of knowledge in the field of basic and clinical pharmacology.

The recognition comes as new findings from Dr. Karwi’s laboratory suggest a critical cellular message disrupted in a common form of heart failure could be restored pharmacologically, leading to improving how those hearts work.

“I am very happy to receive this award, especially since it comes through a nomination from colleagues,” he said. “To see people ready to put the time and effort into nominating me for an award is very nice.”

Mitochondrial messenger

Dr. Karwi has been examining insulin’s role on cellular energy production.

While insulin is best known for helping cells absorb glucose from the bloodstream, he and his team have shown its job does not end there.

“We discovered recently that insulin does more than that to help cells use glucose to generate their energy,” he said. “And not just at the cell membrane level, but actually inside the cells and, to be more specific, at the mitochondrial level.”

Mitochondria generate most of the energy needed for normal cell function.

Dr. Karwi’s research group wanted to understand how insulin, which acts at the cell’s surface, could communicate with mitochondria deep within the cell.

“We thought there must be a messenger that takes that message to the mitochondria to tell it to use that glucose and burn it to produce energy. We found one protein called AKT, also known as protein kinase B, carries that message and when we inhibited this travelling, we abolished the signal.”

Rewiring the message

Dr. Karwi says that’s when things really got interesting.

His main area of research is a condition called heart failure with preserved ejection fraction, or HFpEF.

For individuals with the condition, their hearts continue to pump normally but struggle to relax and refill between beats.

Working with mouse models, Dr. Karwi’s group previously found that the insulin-to-mitochondria message is missing or impaired, resulting in low levels of glucose oxidation, or the process cells use to convert glucose into usable energy.

“We asked the question: Can we rewire that message?” he said.

Using a compound that activates AKT, they treated HFpEF mice for three weeks and discovered that they can improve glucose oxidation in HFpEF hearts.

“What was even more interesting is that this improvement in cardiac energy metabolism by stimulating glucose oxidation was also associated with improved function, mainly diastolic function, which is the main issue in HFpEF,” Dr. Karwi said.

He presented the work at a conference last year, where it attracted attention from researchers and ultimately led to the award nomination.

Questions remain

Despite the team’s promising results, many questions remain.

Dr. Karwi says they still don’t know why the signal is lost in HFpEF or how AKT produces its effects once it reaches the mitochondria.

Those questions are now driving their next phase of the research.

“The next step is using very complex techniques — proteomics and metabolomics — to compare mitochondria from hearts exposed to insulin with those that have not been stimulated,” he said.

The ultimate goal?

Identify precise biological targets that can one day lead to better treatments for patients living with HFpEF.