The developments highlighted in the bolus today reinforce a theme Diabettech has been circling for years: the most meaningful progress in diabetes does not come from squeezing ever more signal out of glucose curves, but from understanding the biology that sits underneath them.
Not all of these are from the past 24 hours, but all present an interesting, and in some cases, different take on what might be useful or effective in the Diabetes world.
From drugs that appear to slow organ ageing independent of glycaemia, to immune therapies that aim to retrain rather than suppress, to imaging tools that finally let us see early tissue damage, this is a reminder that diabetes complications are not abstract risks — they are structural, vascular, and immunological processes unfolding long before numbers drift out of range.
The Killifish Breakthrough: SGLT2i as “Age-Blockers”
In a study published in Kidney International, researchers at the MDI Biological Laboratory used the African turquoise killifish—a creature that ages decades in a matter of months—to solve a major mystery. We know SGLT2 inhibitors (like Jardiance or Farxiga) protect kidneys in people with Type 2 diabetes, but we haven’t fully understood how.
The study showed that these drugs don’t just lower glucose; they actively preserve kidney structure and calm inflammation at a cellular level. By keeping the killifish’s kidneys “young” as it aged, researchers proved that these medications are potent organ-protectors regardless of blood sugar levels. This adds heavy weight to the argument for using SGLT2is as a primary defense for anyone with kidney risk, not just those with high A1c.
Anastasia Paulmann, Matthew D. Cox, Tom Boewer, Hannah M. Somers, Heath Fuqua, Ryan P. Seaman, Joel H. Graber, Anchal Mahajan, Cory P. Johnson, Laura L. Beverly-Staggs, Sonia Sandhi, Heiko Schenk, Hermann Haller. Sodium-glucose co-transporter 2 inhibition improves age-dependent kidney microvascular rarefaction. Kidney International, 2025; DOI: 10.1016/j.kint.2025.12.011
Ahead Therapeutics: Accelerating the “Inverse Vaccine”
In a major funding update, Breakthrough T1D (formerly JDRF) awarded a grant to Ahead Therapeutics to accelerate their ASIT (Antigen-Specific Immunotherapy) platform.
This isn’t standard immunosuppression. The technology uses “nanoliposomes” to retrain the immune system to tolerate insulin-producing cells rather than attacking them. It’s often described as an “inverse vaccine.” If the next phase of trials holds up, it could provide a way to stop the progression of Type 1 diabetes shortly after diagnosis without the side effects of traditional immune-suppressing drugs.
Microvascular imaging: complications are vascular diseases first
Also published recently: a new high-resolution imaging approach (“fast-RSOM”) designed to visualise tiny blood vessels non-invasively and detect early microvascular dysfunction before symptoms. While positioned as a general cardiovascular tool, diabetes is the obvious elephant in the room: retinopathy, nephropathy, neuropathy and wound failure are all microvascular stories long before they’re “glucose stories.”
If this kind of portable, early-dysfunction imaging translates clinically, it could become a genuinely useful biomarker layer alongside CGM—something that reflects tissue damage risk, not just interstitial glucose trajectories.
Hailong He, Angelos Karlas, Nikolina-Alexia Fasoula, Chiara Fischer, Ulf Darsow, Michael Kallmayer, Juan Aguirre, Hans-Henning Eckstein, Vasilis Ntziachristos. Single-capillary endothelial dysfunction resolved by optoacoustic mesoscopy. Light: Science, 2026; 15 (1) DOI: 10.1038/s41377-025-02103-6
The Diabettech Take
What links these stories is not novelty, but direction of travel.
SGLT2 inhibitors increasingly look less like “glucose-lowering drugs with benefits” and more like organ-protective agents that happen to lower glucose. The killifish data strengthens a case that’s already uncomfortable for guideline writers: risk stratification based on A1c alone is biologically naïve.
Ahead Therapeutics’ ASIT platform sits at the opposite end of the diabetes timeline, but asks an equally important question: what if we stopped treating autoimmunity as something to blunt, and instead taught it tolerance? If successful, inverse vaccines would represent a genuine shift away from chronic management toward disease interception.
And fast-RSOM imaging underlines a hard truth clinicians already know but rarely measure: by the time glucose metrics deteriorate, microvascular damage is often already underway. Tools that expose endothelial dysfunction early could do more to prevent complications than another decade of marginal CGM accuracy gains.
Taken together, today’s news argues for a recalibration of priorities. Better diabetes care will not come from louder alarms or smarter nudges layered onto glucose traces. It will come from earlier detection of tissue stress, durable modification of immune and vascular pathways, and therapies judged by organ outcomes, not dashboards.
That’s not the easiest story to commercialise — but it’s the one most likely to change lives.
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