Category: Treatment

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.

Researchers have discovered a new mechanism linking gestational diabetes to pregnancy complications. The study found that gestational diabetes alters the placenta’s processing of genetic messages, leading to incorrect assembly of hundreds of genetic messages and potentially disrupting placental function. The researchers identified a key protein, SRSF10, that appears to contribute to this disrupted process. Targeting SRSF10 may help mitigate the effects of gestational diabetes on offspring. The study’s findings provide new insights into the underlying biology of gestational diabetes and open up new avenues for intervention to improve pregnancy outcomes.

A new clinical study has found that a healthy Nordic diet, rich in whole grains, fruits, and vegetables, can effectively reduce liver fat and improve blood sugar control in people with type 2 diabetes and non-alcoholic fatty liver disease. The diet, which is high in dietary fibre and low in saturated fat, outperformed both a low-carbohydrate diet and the Nordic Nutrition Recommendations in a one-year trial.

The study, led by Ulf Risérus, Professor of Clinical Nutrition and Metabolism at Uppsala University, found that participants who followed the healthy Nordic diet saw a 20% reduction in liver fat and improved blood sugar control. Over half of the participants also experienced a remission of their fatty liver disease.

A groundbreaking study has found that reversing prediabetes through lifestyle changes can cut the risk of heart attack, heart failure, and premature death by 50%. Researchers analyzed data from over 2,400 people with prediabetes and found that those who normalized their blood glucose levels had a significantly lower risk of cardiovascular disease. A fasting blood glucose value of ≤ 97 mg/dL is a simple marker for lower heart disease risk. The study’s findings suggest that sustained normalization of blood glucose should be a key target for clinical guidelines, adding a fourth pillar to cardiovascular prevention.

A new genetic risk score can predict who’s at high risk of developing type 1 diabetes, and it could be used in large-scale health studies to identify adults who could benefit from new treatments. The score uses genetic information to predict risk and feeds into an online clinical calculator that’s already available to clinicians. This is a big deal because new drugs like teplizumab can delay the onset of type 1 diabetes by up to three years, but they only work if given before symptoms develop. The genetic risk score can help identify who should get autoantibody testing to see if they’re eligible for these new treatments.

A recent study led by Hiddo Lambers Heerspink, a clinical pharmacologist at the University Medical Center Groningen, has found that the drug finerenone can reduce protein excretion in the urine of patients with type 1 diabetes and chronic kidney disease. This reduction indicates a protective effect on kidney function and suggests that finerenone may be an effective treatment for kidney disease in type 1 diabetes.

Key Findings

• Finerenone reduces protein excretion: The study found that finerenone reduced protein excretion in the urine by about 25% in patients with type 1 diabetes and chronic kidney disease.
• Safe and well-tolerated: Finerenone was found to be safe and well-tolerated, except for a slightly elevated potassium level in the blood.
• First new drug in 30 years: Finerenone is the first new drug in over 30 years that has shown to be effective and safe for treating kidney disease in patients with type 1 diabetes.

Implications

The study’s findings suggest that finerenone may be a valuable treatment option for patients with type 1 diabetes and chronic kidney disease. The drug’s ability to reduce protein excretion in the urine is a promising indicator of its potential to slow kidney disease progression.

Researchers at the University of Chicago have developed a new model, DOMUS, that predicts the risk of complications and treatment outcomes for patients with type 2 diabetes. The model uses data from nearly 130,000 patients and takes into account various factors, including blood sugar levels, weight, cholesterol, and blood pressure.

Key Findings

• Early treatment matters: The model shows that early treatment of diabetes can make a significant difference in preventing long-term complications.
• Predicts 14 complications: DOMUS predicts the risk of 14 different complications, including heart attacks, kidney failure, and depression.
• Models disease progression: The model predicts how risk factors such as weight, cholesterol, and A1C levels change over time.

Implications

The DOMUS model has the potential to inform clinical decision-making and policy decisions related to diabetes treatment and management. It can help clinicians and policymakers understand the potential benefits and costs of different treatment approaches and make more informed decisions about resource allocation.

Future Directions

The researchers are working on external validation of the model using different data sources and plan to apply it to study racial and ethnic disparities in predicted outcomes. The model has the potential to be used by insurers, policymakers, and public health agencies to guide decisions about diabetes treatment and management.

A recent study published in JAMA has found that an AI-powered diabetes prevention program (DPP) app can reduce the risk of diabetes in adults with prediabetes similarly to traditional human-led programs. The study, funded by the National Institutes of Health, compared the effectiveness of an AI-powered DPP app to human-led programs in over 368 participants.

Key Findings

• Similar outcomes: Both the AI-powered DPP app and human-led programs achieved similar rates of diabetes risk reduction, with 31.7% and 31.9% of participants meeting the CDC-defined composite benchmark, respectively.
• Higher initiation and completion rates: The AI-powered DPP app had higher rates of program initiation (93.4% vs 82.7%) and completion (63.9% vs 50.3%) compared to traditional human-led programs.

Implications

The study suggests that AI-powered DPPs could be an effective alternative to existing human-coached programs, especially for patients with logistical constraints. The AI-powered app’s ability to provide personalized interventions and always be available could extend its reach and make it a valuable tool in diabetes prevention.

Future Directions

The study team plans to explore how the AI app outcomes translate to broader, underserved patient populations and investigate patient preference, engagement, and costs associated with AI-led DPPs. This research has the potential to inform the development of more effective and accessible diabetes prevention programs.

A recent study by Kyoto University researchers highlights the persistence of diabetes stigma among medical students and residents in Japan. Despite growing awareness, nearly half of the 921 respondents held misconceptions about diabetes, such as believing it’s always genetic or that people with diabetes have shorter life expectancy .

Key Findings

• Awareness of diabetes stigma: 57% of respondents reported awareness of diabetes stigma, while 25.9% were aware of advocacy efforts.
• Misconceptions: About half of medical students and residents held misconceptions about diabetes, with residents more likely to hold stigma-related beliefs.
• Limited impact of clinical education: Clinical lectures increased awareness, but subsequent training had limited impact on reducing stigma.

Implications

The study suggests that medical education curricula need to be revised to address diabetes stigma and promote accurate knowledge. The researchers plan to conduct a follow-up survey to assess the effectiveness of their efforts.

Importance

Diabetes stigma can lead to social isolation, psychological distress, and poor disease management. By addressing these issues in medical education, future physicians can become agents of change, fostering environments where diabetes is understood accurately and without stigma.