Category: Treatment

New research to be presented at the Annual Meeting of the European Association for the Study of Diabetes (EASD) in Milan (Sept 28 – Oct 2) — from Prof. Dominic Ehrmann, Research Institute Diabetes Academy Mergentheim, Germany, and colleagues.

Goal of the study:
To understand how day-to-day blood sugar patterns affect quality of life in people with diabetes. The PRO-MENTAL study, funded by the German Centre for Diabetes Research (DZD), looked at whether CGM data from one day predicts quality of life the next day.

How it was done:

• 400 people with diabetes: 72% type 1, 28% type 2, 55% female, average age 47, average HbA1c 7.6%
• 14 consecutive days of monitoring
• Quality of life was rated daily using ecological momentary assessment (EMA) based on the WHO-5 questionnaire, which asks about feeling cheerful, calm, active, rested, and interested in daily life. Sleep quality, perceived stress, mood and energy (0-10 scale) were also recorded daily.
• CGM parameters analyzed: time below range (<70 mg/dL), time above range (>180 mg/dL), time in normal range (70-140 mg/dL), and glucose variability.
• Models adjusted for age, sex, diabetes type, and previous-day quality of life.

Key findings:

1. More time in the normal range (70-140 mg/dL) on one day was associated with better quality of life the next day.
2. Higher glucose variability — while still within safe limits — on one day was also associated with better quality of life the next day.
3. Time above range and time below range showed no significant link to next-day quality of life.
4. Better sleep quality the previous night and higher energy levels the previous day were also linked to better next-day quality of life.
5. Same-day glucose parameters were not associated with same-day quality of life.

Authors’ interpretation:
The researchers suggest that while good blood sugar control is important for well-being, trying to minimise fluctuations too strictly — even when staying within safe limits — may carry a burden that reduces enjoyment. The constant effort and restriction needed to keep glucose completely flat could prevent people from engaging in activities they enjoy.

The study does not suggest that looser control is better, but that the psychological and practical burden of very strict control may affect day-to-day quality of life.

This is conference research that has not yet been through full peer-reviewed publication, so findings should be considered preliminary.

A class of medicines used for type 2 diabetes that also reduces risk of heart and kidney disease. They carry a rare but serious side effect: ketoacidosis — where lack of insulin leads to high ketone production, disrupting the body’s acid-base balance and potentially becoming life-threatening.

What the study did:
Published in The Lancet Diabetes & Endocrinology, researchers analyzed national health registry data from Sweden, Denmark and Norway. It included more than 280,000 patients with type 2 diabetes treated with SGLT2 inhibitors, looking at how often ketoacidosis occurred and what factors increased risk. Collaboration with Statens Serum Institut (Denmark) and NTNU (Norway).

Key findings on who is at higher risk:

• Highest risk factors: history of previous ketoacidosis, high blood glucose levels, low body weight or signs of malnutrition
• Also linked to higher risk: previous episodes of hypoglycaemia (low blood sugar)
• Most common trigger: infection was the most common triggering or co-occurring event when ketoacidosis happened
• Other acute conditions were more common in affected patients, including kidney impairment, stroke, and major surgery

Timing of risk:
Previous studies focused on the early months of treatment. This study found risk is highest in the first few months, but remains elevated throughout the entire time a patient is on the medication.

What it means for clinical care:
Lead author Peter Ueda, Assistant Professor at Department of Medicine, Solna, Karolinska Institutet, said the goal is not to avoid treatment — SGLT2 inhibitors benefit many patients — but to better identify high-risk patients and use the drugs more safely.

Researchers hope the findings help clinicians with treatment decisions and with guidance on when to temporarily pause the medication, for example during acute illness or before surgery.

Next steps are to study in more detail the patients who do develop ketoacidosis on treatment, and to investigate other rare but serious side effects of modern diabetes medicines.

Researchers at UC Berkeley have identified a compound that could treat obesity, diabetes, and fatty liver disease differently than current GLP-1 drugs like Ozempic, Wegovy, Mounjaro and Zepbound.

How it works:

• GLP-1s work by reducing appetite and food intake, which can cause side effects like nausea, nutritional deficiencies, and muscle loss.
• The new compound, 5-tetradecyloxy-2-furoic acid (TOFA), works on the other side of the energy equation: it increases energy expenditure.
• TOFA has a dual mechanism. It is an ACC inhibitor that blocks production of lipids like cholesterol and triglycerides, AND it activates cellular receptors PPARα and PPARδ that turn on genes to help cells take up fat and burn it for energy.

Results in mice, published in Science Advances:

• Cells burned up to 18% more energy with no change in food intake, physical activity, or body temperature.
• Obese mice lost weight from fat with no significant loss of lean muscle mass.
• Improved insulin sensitivity, glucose control, lowered triglycerides, and improved features of fatty liver disease.
• Unlike other ACC inhibitors that reached mid-stage clinical trials, TOFA did not raise triglycerides, a major heart risk that has prevented approval of others in this class.

Combination potential:

• When researchers gave mice two separate drugs to replicate TOFA’s two actions, it was less effective than TOFA alone.
• When combined with GLP-1 drugs semaglutide and tirzepatide, TOFA worked additively or synergistically, leading to greater improvements in weight, glucose, insulin, and triglycerides than either alone. Researchers view it as complementary, not a replacement.

TOFA was first discovered in the 1970s. The study was led by senior author Anders Näär, professor of metabolic biology and nutrition at UC Berkeley, and first author Justin Y. Lee.

A new review published in Genes & Diseases identifies trained immunity — a long-lasting adaptation of the innate immune system — as a key mechanism in diabetes and its complications.

Here is a summary of the press release:

What is trained immunity?
It’s a form of immune memory where innate immune cells like monocytes and macrophages undergo lasting changes after exposure to metabolic stress or inflammation. They become primed to react more aggressively to future triggers, creating a state of chronic, low-grade inflammation that can persist even after blood sugar normalizes.

What triggers it in diabetes?
The review found that common diabetes-related factors can activate these pathways, including:

• Hyperglycemia (high blood sugar)
• Obesity
• Lipid abnormalities
• Changes in the gut microbiome

Why it matters for disease progression:
This sustained inflammatory response can:

• Promote insulin resistance
• Impair insulin-producing beta cell function
• Accelerate tissue damage

Beyond diabetes itself, trained immunity may help explain major complications, including atherosclerosis and cardiovascular disease, diabetic kidney disease, delayed wound healing, tissue fibrosis, and vascular dysfunction.

New treatment opportunities:
The authors suggest future therapies should target the immune mechanism itself, not just blood glucose. Promising directions highlighted include:

• Targeting inflammatory pathways like the NLRP3 inflammasome
• Modifying cellular metabolism (immunometabolism)
• Improving gut microbial balance through diet and microbiome-focused therapies
• Exploring vaccination strategies that reprogram immune responses

The overall shift is from viewing diabetes as purely a metabolic disorder to understanding it as a disease with a persistent innate immune component — opening new avenues for prevention and treatment of its long-term complications.

A new mouse study published this week in the Journal of Virology suggests that GLP-1 agonists — drugs commonly used for type 2 diabetes and weight loss — could help prevent pulmonary fibrosis in diabetic patients with Long COVID.

Key findings:

• The problem: People with type 2 diabetes have ∼4x higher risk of severe Long COVID symptoms than non-diabetics. Pulmonary fibrosis, a severe Long COVID condition where lung tissue becomes scarred and thickened, is driven by immune cells called macrophagesAmerican Society for Microbiology.
• The research: Led by virologist Runhong Zhou, Ph.D., at the University of Hong Kong, researchers compared blood samples from COVID-19 patients with and without diabetes months after hospitalization. Diabetic patients showed increased monocyte activity and genetic pathways linked to fibrosis.
• The mouse experiments: Mice with diabetes and SARS-CoV-2 infection developed overactive fibrosis-related genes. When treated with GLP-1 agonists, those genes normalized and macrophages were “reprogrammed,” leading to reduced lung scarring compared to untreated mice.
• Why GLP-1s?: The GLP-1 receptor is highly expressed in lung cells, and earlier lab work hinted at anti-inflammatory effects against pneumonia-related fibrosis. This is the first test in animal models after severe COVID-19 infection.

Caveats: Zhou notes the results are preliminary and only involved a small number of mice. But the team sees it as proof of concept worth further investigation, especially since Long COVID continues to affect many people, particularly the elderly.

The study was announced by the American Society for Microbiology on 9 July 2026.

A review published 23 June 2026 in Diabetes Care from the Immunology of Diabetes research group at the Germans Trias i Pujol Research Institute (IGTP) examines whether physical activity could serve as a complementary strategy for type 1 diabetes beyond blood sugar management.

Key points from the review:

• Focus: Type 1 diabetes is autoimmune — the immune system destroys insulin-producing beta cells. The paper looks at exercise’s potential to influence that immune process.
• Preclinical evidence: In animal models, exercise may reduce immune cell infiltration into pancreatic islets, protect beta cells, and increase anti-inflammatory mediators.
• Human data: Still limited, but some studies link physical activity to longer partial remission periods and anti-inflammatory immune profiles.
• What it isn’t: Authors stress exercise does not cure type 1 diabetes or replace insulin. It’s a potential low-risk, patient-centered complement.

Next steps called for:

• More clinical studies to identify optimal exercise type, intensity, duration, and timing
• Development of immunological markers to measure impact
• Integration with emerging early detection and immunotherapy strategies

Goal: Understand how exercise affects autoimmunity to potentially help restore immune tolerance, preserve remaining beta cells, and reduce complications.

First author Daniel A. Cook notes that specific studies are needed to clarify mechanisms and position exercise as both a complement to insulin therapy and a preconditioning strategy for immunotherapy.

Researchers at the University of Zurich, University Hospital Zurich, and University of Pisa found that targeting epigenetic “readers” in perivascular fat — the fat layer surrounding blood vessels — can reduce inflammation and improve vessel health in both mice and human tissue. This approach may help prevent vascular damage in people with obesity and type 2 diabetes.

Why perivascular fat matters
Perivascular fat actively communicates with vessel walls to control relaxation and inflammation. In obesity and metabolic disease, this fat becomes inflamed, stores lipids abnormally, and releases molecules that stiffen vessels and impair function, contributing to early vascular disease, heart attacks, and strokes.

What the study did
Instead of targeting single downstream molecules, the team used BET protein inhibitors — epigenetic drugs that modulate how genes are “read” — to retune the entire gene activity program in perivascular fat cells.

Results

• In lab tests on mice and human tissue, the drugs shifted fat cells away from an inflammatory profile.
• Blood vessels surrounded by reprogrammed fat relaxed more easily and showed fewer signs of damage.
• A key driver identified was the enzyme hexokinase 2, which regulates sugar metabolism. Overactive hexokinase 2 makes fat cells store more fat and release inflammatory signals that harm vessels. Lowering its activity, either via epigenetic modulation or direct inhibition, blunted inflammation and restored normal vessel function in samples.

Potential impact
Led by UZH cardiologist Francesco Paneni, the study suggests epigenetic therapies could complement current treatments for blood pressure, cholesterol, and blood sugar. Rather than only managing downstream risk factors after damage starts, this approach aims to reprogram the tissue processes that cause vascular damage, potentially reducing progression to heart attack or stroke in obesity and metabolic disease.

Published June 1, 2026 in Proceedings of the National Academy of Sciences by researchers at Sanford Burnham Prebys Medical Discovery Institute and the University of Michigan. Senior author: Randal J. Kaufman, PhD.

The Core Problem
In healthy beta cells, proteins must fold into precise 3D shapes to work — like origami. As prediabetes progresses to diabetes, proinsulin, the precursor to insulin, often misfolds. Misfolded proinsulin builds up, stresses beta cells, and contributes to their failure to meet insulin demand.

What They Studied
The team investigated how beta cells manage proinsulin folding, focusing on the chaperone protein binding immunoglobulin protein (BiP) and its partner proteins. To track BiP, they engineered mice with a 3xFLAG-tagged version of BiP in beta cells.

Key Findings

1. p58IPK is a critical helper: Removing p58IPK, a BiP cochaperone, caused misfolded proinsulin to accumulate in cell lines. Mice lacking p58IPK made less proinsulin and insulin.
2. p58IPK can’t replace BiP, but helps it: Reintroducing p58IPK restored proper proinsulin folding and trafficking, but only when BiP was also present. Overexpressing BiP without p58IPK gave only modest improvements.
3. It’s a team effort: “Like a single tennis player trying to play a doubles match, BiP cannot just go it alone,” said lead author Insook Jang, PhD.
4. Other players involved: Additional partner proteins also help with proinsulin folding and quality control, but their exact roles need more study.

Why It Matters
Current diabetes drugs mainly help tissues absorb sugar or boost insulin release — they don’t fix the root problem of beta cell stress from misfolded proteins. This work shows proinsulin folding is vulnerable to the same cellular stresses that drive type 2 diabetes.

If researchers can figure out how to support BiP and its cochaperones like p58IPK, they may develop treatments that promote proper proinsulin folding, protect beta cells, and intervene earlier in diabetes progression.

A new study presented at the 28th European Congress of Endocrinology (ECE 2026) in Prague, 9–12 May, found that dementia risk varies by diabetes type and treatment, with insulin users facing the greatest risk.

Key findings:

• Researchers from Kyung Hee University Hospital at Gangdong and Samsung Medical Center tracked over 1.3 million South Korean adults aged 40+ without dementia from 2013–2024.
• Compared to people without diabetes:
  • Type 2 diabetes on oral meds: ∼1.3x higher risk of dementia
  • Type 2 diabetes using insulin: 2.1x higher risk
  • Type 1 diabetes: 2.4x higher risk
• The pattern held for both Alzheimer’s disease and vascular dementia.

Why it matters:
Lead author Prof. Ji Eun Jun noted this suggests “not all types of diabetes carry the same risk” and that people with insulin-dependent treatment “may be particularly vulnerable to cognitive decline”. Recurrent hypoglycemia and greater glucose fluctuations in insulin-treated patients may partly explain the link.

Implications:
The authors recommend recognizing diabetes as a brain health risk factor, not just metabolic. Prevention strategies like earlier cognitive monitoring and improving long-term glucose stability, such as continuous glucose monitoring, should be considered in routine diabetes care.

The study was published in Diabetes, Obesity and Metabolism.

The FreeDM2 clinical trial found that real-time continuous glucose monitoring (CGM) significantly improves blood sugar control in adults with type 2 diabetes who use basal insulin, compared to traditional finger-prick testing.

Study Details

• Published in: The Lancet Diabetes and Endocrinology on 23 April 2026. Findings also presented at the Diabetes UK Professional Conference in Liverpool.
• Led by: Dr Emma Wilmot, University of Nottingham/University Hospitals of Derby and Burton NHS Foundation Trust, and Dr Lala Leelarathna, Imperial College London/Imperial College Healthcare NHS Trust.
• Participants: 303 adults with type 2 diabetes on basal insulin, randomly assigned to either real-time CGM or finger-prick monitoring.
• Duration: 16-week self-management period, followed by 16 weeks of clinician-supported care.

Results

• CGM users had significantly greater reductions in HbA1c (the key measure of long-term blood glucose) at both 16 and 32 weeks.
• Benefits were seen in both the self-management phase and the clinician-guided phase.
• In phase 1, improvements occurred without new medications, suggesting participants used CGM data to make meaningful lifestyle changes.

Context

• Type 2 diabetes makes up ∼90% of diabetes cases globally. High blood glucose increases risk of blindness, amputations, heart disease, and early death.
• CGM uses a small arm sensor that sends glucose readings to a phone/reader, with alarms for high/low levels. It’s less painful than finger-pricks and gives 24/7 data.
• While CGM is standard care for type 1 diabetes in the UK, its role in type 2 has been uncertain, limiting access.

A small peer-reviewed study published in the latest Journal of the Endocrine Society found that a ketogenic diet may help improve beta-cell function in people with type 2 diabetes, potentially aiding diabetes reversal.

Key findings

• Study design: 51 adults with type 2 diabetes, ages 55-62, 71% female, were assigned to either a ketogenic diet or a low-fat diet for 3 months. Both diets were designed to be weight-maintaining.
• What improved: The ketogenic diet group showed greater improvement in beta-cell function compared to the low-fat group. Beta cells in the pancreas secrete insulin to control blood sugar, and they often underperform in type 2 diabetes.
• How it was measured: Researchers tracked the proinsulin-to-C-peptide ratio, a biomarker of beta-cell stress. This ratio decreased more in the keto group, indicating reduced stress on the pancreas and better insulin secretion ability.
• Weight loss: Both groups lost a modest amount of weight on average, but the keto diet’s benefits to beta-cell function occurred independently of substantial weight loss.

Why it matters

• Current gap: According to lead author Marian Yurchishin, M.S., of the University of Alabama at Birmingham, “Other than bariatric surgery or large-volume intentional weight loss, interventions for improving beta-cell function in type 2 diabetes do not currently exist.”
• Mechanism: A ketogenic diet is high-fat, low-carb and shifts metabolism to burn fat instead of storing it. The authors suggest this reduces stress on the pancreas and improves beta-cells’ ability to secrete insulin.

Study details

• Authors: Marian Yurchishin, Amanda Finn, Lauren Fowler, and Barbara Gower of UAB; Sara Vere-Whiting of University of Glasgow.
• Funding: National Institute of Diabetes and Digestive and Kidney Diseases, UAB Nutrition Obesity Research Center, UAB Diabetes Research Center, and National Heart, Lung, and Blood Institute.
• Context: The study was small and focused on patients with early type 2 diabetes. More research would be needed to confirm long-term effects and applicability to broader populations.

Researchers at Karolinska Institutet and KTH Royal Institute of Technology in Sweden published a peer-reviewed study in Stem Cell Reports detailing an improved method to create insulin-producing cells from human stem cells.

Key findings

• More reliable production: The new method consistently generates high-quality, mature insulin-producing cells from multiple human stem cell lines, addressing past issues where methods produced mixed, immature cell populations.
• Better function in lab tests: In vitro, the cells secreted insulin and showed strong glucose responsiveness.
• Reversed diabetes in mice: When transplanted into the anterior chamber of the eye of diabetic mice, the cells gradually matured and restored blood sugar regulation for several months.

Why it matters

• Patient-specific potential: Works across different stem cell lines, which could enable personalized cell therapies with reduced immune rejection, per lead authors Per-Olof Berggren and Siqin Wu.
• Solves prior barriers: By refining culture steps and letting cells form 3D clusters themselves, the process eliminates many unwanted cell types and improves glucose responsiveness — two major hurdles in past trials, according to Fredrik Lanner.
• Clinical next steps: The team aims to move toward clinical translation for treating type 1 diabetes.

Context & notes

• Type 1 diabetes results from immune destruction of pancreatic insulin-producing cells, leaving patients unable to regulate blood sugar.
• The eye chamber transplant technique allows minimally invasive monitoring of cell development over time.
• Funded by the Swedish Research Council, Novo Nordisk Foundation, ERC, and others. Some researchers report industry links, including patents and employment at Spiber Technologies AB and Biocrine AB. Karolinska Institutet

A new study led by researchers at Stanford Medicine suggests that about 1 in 10 people may have a genetic resistance to GLP-1 diabetes drugs, such as Ozempic and Wegovy, when these medications are used to control blood sugar in people with Type 2 Diabetes.

The study found that certain variants in the PAM gene, carried by roughly 10% of the population, are linked to a phenomenon researchers call GLP-1 resistance. People with these variants have higher levels of the GLP-1 hormone, but the hormone is less biologically effective, meaning it does not lower blood sugar as well as expected. This was unexpected, since researchers initially thought these individuals would have lower hormone levels.

After experiments in both humans and mice, the researchers confirmed that this resistance is real. In mouse models, GLP-1 activity was reduced despite normal receptor function, suggesting that the problem likely occurs further downstream in the signaling pathway, though the exact mechanism remains unknown.

Analysis of clinical trial data involving more than 1,100 participants showed that people with PAM variants were less likely to reach target HbA1c blood sugar levels after six months of treatment with GLP-1 receptor agonists. Importantly, this reduced response appeared to be specific to GLP-1 drugs, as responses to other diabetes medications like metformin were unaffected.

The findings could be an important step toward precision medicine, allowing doctors to use genetic testing to predict which patients are less likely to benefit from GLP-1 therapies and choose better treatments earlier. Researchers also note that longer-acting GLP-1 drugs may help overcome this resistance, though more research is needed, especially regarding effects on weight loss

A new study published on March 31, 2026, demonstrates that reducing or discontinuing diabetes medications (deprescribing) is feasible and safe for patients with type 2 diabetes when lifestyle medicine is integrated into routine primary care.

Key findings:

• A retrospective review of 650 adults with type 2 diabetes found that 6.3% of patients safely reduced or stopped their glucose-lowering medications after showing improvements in weight and blood glucose due to lifestyle-informed care in primary care settings
• These medication reductions happened naturally during routine primary care, not in intensive programs or specialty clinics
• Patients who deprescribed saw an average BMI decrease of 2.2 kg/m² and a blood glucose drop of 50.5 mg/dL, with no adverse events linked to the deprescribing process
• The most common medication changes were metformin dose reduction (34%), metformin discontinuation (19.5%), and insulin dose reduction (19.5%)
• The study suggests that incorporating lifestyle medicine into primary care could lead to significant medication burden reduction, lower costs, and fewer side effects for millions of Americans with type 2 diabetes if these outcomes are replicated nationally

MIT researchers are developing an implantable device that houses insulin-producing islet cells, aiming to let type 1 diabetes patients control blood sugar without daily insulin shots. The device encapsulates the cells to shield them from immune attack and includes an on-board oxygen generator that splits water vapor in the body into oxygen (with hydrogen diffusing away).

In the latest study, published in Device, the team made the device more waterproof, more crack-resistant, and boosted its wireless power delivery so the oxygen generator can keep cells alive longer. In mice and rats, the encapsulated islets survived at least 90 days and produced enough insulin to keep blood sugar in a healthy range. Stem-cell-derived islets also worked, though they didn’t fully reverse diabetes yet.

The researchers hope to extend device life to up to two years and see the platform as a way to deliver other protein therapies—antibodies, enzymes, clotting factors—so drugs could be made inside the body rather than infused repeatedly

A new press release from Kyoto University talks about a new method for assessing beta cell mass in people with type 1 diabetes, which could totally change how we treat it.

Summary:

• The Problem: In type 1 diabetes, the immune system attacks insulin-producing beta cells. Current ways to measure the remaining beta cells are indirect and not always accurate, making it tough to know if new treatments are working.
• The Solution: Researchers developed a noninvasive method using an 18F-labeled PET tracer that targets GLP-1 receptors, which are found on beta cells. This allows for direct imaging of the beta cell mass using PET/CT scans.
• The Findings: In a study at Kyoto University Hospital, people with type 1 diabetes had lower pancreatic uptake of the tracer compared to those without diabetes. This measurement was also linked to lower A1c levels (meaning better blood sugar control) and less daily insulin needed. No major side effects were reported.
• Why It Matters: If more studies confirm these results, this PET/CT method could give doctors a clear, quantitative way to measure beta cell mass. This would be super helpful for staging the disease, tracking its progression, and evaluating new therapies designed to preserve or restore beta cells.

A new study from the German Diabetes Center (DDZ) finds Blood Flow Restriction Training (BFRT) is a game-changer for people with type 2 diabetes.

BFRT uses lighter weights (30% of max strength) with cuffs on thighs to restrict blood flow, and it:

• Boosts muscle strength as much as classic strength training
• Reduces visceral fat (the bad stuff around organs)
• Improves mitochondrial function (energy production)
• Increases blood flow

It’s low-impact, so perfect for those who struggle with heavy weights or mobility issues. Participants felt stronger and more resilient, and some even signed up for gym memberships.

A new study in Israel gave people with type 2 diabetes a discount on their meds if their blood sugar levels improved. Those who got the discount had better blood sugar control compared to those who didn’t. The study suggests offering financial incentives could be a good way to support disadvantaged patients with diabetes.