Author: Staff

Epigenetic drugs could protect blood vessels in obesity and diabetes

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.

Can diabetic macular edema be controlled with fewer injections?

A short-term retrospective study published in Eye Discovery compared a new “1 + 1 + PRN” sequential regimen to the standard “3 + PRN” anti-VEGF approach for diabetic macular edema (DME). The research was done by teams at the Third Affiliated Hospital of Wenzhou Medical University, the Primasia International Eye Research Institute at the Chinese University of Hong Kong, and collaborators.

What they tested

  • “1 + 1 + PRN” group: 1-2 anti-VEGF injections, then a dexamethasone intravitreal implant 4 weeks later, followed by anti-VEGF only as needed.
  • “3 + PRN” group: 3 monthly anti-VEGF injections, then anti-VEGF as needed.
  • Why try this? Anti-VEGF drugs target VEGF-driven leakage, but DME also involves inflammation. Dexamethasone implants work via a different anti-inflammatory mechanism and release drug slowly, potentially cutting injection frequency.

Study details

  • Size: 28 eyes from 23 treatment-naïve patients
  • Follow-up: 25 weeks
  • Outcomes measured: Best-corrected visual acuity, central macular thickness, hyperreflective foci, and cystic changes in the deep capillary plexus using OCTA

Key findings

  1. Visual + anatomical results: Both groups showed significant improvements from baseline in vision and retinal thickness. No statistically significant differences between groups, though the “1 + 1 + PRN” group showed a trend toward earlier, more stable visual gains and smoother reduction in central macular thickness.
  2. Injection burden: Mean injections over 25 weeks were 2.58 for “1 + 1 + PRN” vs 4.94 for “3 + PRN”. Most sequential-group eyes needed only 2-3 injections total.
  3. Safety: Elevated intraocular pressure occurred in both groups, controlled with topical meds, with no significant difference. No severe adverse events like cataract progression, retinal detachment, vitreous hemorrhage, or endophthalmitis were seen.

Limitations
The authors note this was small, retrospective, non-randomized, and short-term. Treatment was chosen by shared decision-making, not random assignment. Different anti-VEGF agents were used, and not all “1 + 1 + PRN” eyes got the same number of initial anti-VEGF shots.

Takeaway: The “1 + 1 + PRN” approach cut injection frequency nearly in half without clearly compromising early visual or anatomical outcomes at 25 weeks. The results are exploratory — larger, longer randomized trials are needed before this could become a standard option. Fewer injections could mean lower cost, less clinic burden, and reduced treatment anxiety for DME patients.

Boosting Protein Folding Could Help Protect Insulin-Producing Cells in Diabetes

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.

Diabetes linked to higher risk of tooth and implant loss

A University of Gothenburg thesis by dentist Anna Trullenque Eriksson found that people with diabetes face greater risks for oral health problems, based on a large dataset from seven Swedish registers.

Key findings:

  • Periodontitis & tooth loss:
  • Type 1 diabetes: Risk increased only with poor blood sugar control. Over 10 years, 43.5% with poor control lost one or more teeth vs. 25.3% with good control and 29.0% of controls without diabetes.
  • Type 2 diabetes: Risk was elevated regardless of glycemic control, but strongest with poor control. 54.9% with poor control lost one or more teeth over 10 years vs. 44.0% with good control and 37.8% of controls.
  • Dental implants: Both type 1 and type 2 diabetes were associated with higher risk of peri-implantitis (inflammation/bone loss around implants) and implant loss. Poor blood sugar control was a key factor for worse outcomes.
  • Complications & social factors: Periodontitis was linked to higher risk of diabetes-related eye and kidney complications in both types. Complete tooth loss risk was especially high for people with diabetes who had lower income or less education. Data included Sweden and Denmark.

The study reinforces the link between diabetes and oral disease and suggests dental care should be part of diabetes prevention. It also provides new evidence that diabetes may affect long-term success of dental implants. Anna Trullenque Eriksson notes that collaboration between healthcare and dental providers is important.

DCCBs and Kidney Outcomes in Type 2 Diabetes

A new study found that dihydropyridine calcium-channel blockers (DCCBs) — a widely used blood pressure medication — may be linked to worse kidney outcomes in people with type 2 diabetes (T2D), even when patients are already on modern kidney-protective drugs.

Study details:

  • Data analyzed: 31,031 adults with T2D from 2016–2021, all taking both RAS inhibitors and SGLT2 inhibitors, the current standard kidney-protective therapies for diabetic kidney disease (DKD).
  • Groups: 12,172 patients (39.2%) also took DCCBs; 18,859 (60%) took other antihypertensives.
  • Follow-up: Median ~3.5 years.

Results: After adjusting for baseline differences, DCCB use was associated with a 33% higher risk of major adverse kidney events compared to other blood pressure treatments. These events included a ≥40% drop in eGFR or progression to end-stage kidney disease requiring dialysis/transplant.

Why this might happen: Researchers suggest DCCBs may worsen kidney damage by relaxing blood vessels entering the kidney’s filtering units but not those exiting, potentially increasing pressure and strain within the kidneys. The increased risk persisted even with SGLT2 inhibitors, which were thought to possibly offset harm.

Context:

  • DKD is a leading cause of kidney failure worldwide, driven by high blood sugar damaging kidney blood vessels.
  • DCCBs are commonly prescribed as second-line blood pressure meds for DKD patients.
  • RAS and SGLT2 inhibitors are now standard of care for DKD due to their kidney-protective effects.

Researcher comments: Lead author Dr. Timna Agur noted the findings “raise important questions about whether these medications are always the best option” for DKD patients on modern therapies.

Caveats: The study is observational, so it cannot prove DCCBs directly cause worse outcomes. Dr. Agur called for prospective studies and randomized controlled trials to confirm results and define safest blood pressure strategies. Given how commonly DCCBs are prescribed, even a small risk increase could affect many DKD patients.

Global inequalities in type 1 diabetes are widening among children and adolescents

A new peer-reviewed global analysis found that the burden of type 1 diabetes mellitus (T1DM) in people aged 0–19 has risen sharply from 1990 to 2021, and income-related health gaps have worsened.

Key findings:

  • Incidence and prevalence up: Global T1DM incidence nearly tripled, from 2.71 to 7.42 per 100,000. Prevalence also rose sharply from 20.75 to 56.59 per 100,000.
  • Geographic patterns: In 2021, North America and Europe had the highest incidence and prevalence rates. African regions had the highest burden of years of life lost (YLLs).
  • Widening inequalities: Lower-income countries bear a disproportionate share of T1DM deaths and YLLs. By 2021, countries in the lower half of global income distribution accounted for ∼80% of T1DM mortality burden and ∼86% of T1DM YLL burden. Absolute and relative inequalities both increased since 1990.
  • Drivers: Researchers linked the disparities to unequal access to insulin, glucose monitoring, healthcare resources, and diabetes management systems in resource-limited settings.

Whole organ 3D imaging reveals remaining insulin producing cells in type 1 diabetes

Researchers at Umeå University used advanced 3D imaging to map entire human pancreases at microscopic resolution, comparing non-diabetic donors with a donor who had late-onset type 1 diabetes. Published as a peer-reviewed release.

While most insulin-producing β-cells in the islets of Langerhans were destroyed in the type 1 diabetic pancreas, hundreds of thousands of insulin-positive cells still remained.

Why it matters:

  • Unexpected location: These surviving β-cells were mostly found outside traditional islets — as individual cells or small clusters separated from other endocrine cell types. This is the inverse of non-diabetic pancreases, where β-cells are mainly islet-associated.
  • Challenges old assumptions: Traditional studies focus only on islets, so they likely underestimate how many β-cells actually survive in type 1 diabetes.
  • Therapeutic potential: The cells may be more resistant to autoimmune destruction, or new β-cells might still form. If certain pancreatic microenvironments promote β-cell survival, they could become targets for therapies aimed at stabilizing or expanding remaining β-cells.


Prof. Ulf Ahlgren says the pancreas can retain β-cells “in a way that has not previously been recognized.” Doctoral student Joakim Lehrstrand adds, “we must look beyond the islets when studying β‑cell biology in type 1 diabetes.”

The whole-organ 3D imaging method lets scientists study individual cells throughout the entire organ. The team believes this will be key for future research into type 1 diabetes, type 2 diabetes, and pancreatic cancer, by helping isolate specific regions for molecular analysis.

Over half of Type 2 diabetes cases could be preventable

A UMass Amherst-led study published in Diabetes found that over half of Type 2 diabetes cases could be preventable through lifestyle changes, even for people with high genetic risk.

Key findings from 332,000+ U.K. adults tracked for ~14 years:

  • Lifestyle outweighs genetics: People with the least healthy lifestyles were nearly 7x more likely to develop diabetes vs. those with the healthiest habits. High genetic risk only raised risk 2.6x compared to low genetic risk.
  • Genetics isn’t destiny: Across all genetic risk levels, healthier lifestyles consistently meant lower diabetes rates. “Even if you’ve lost the genetic lottery,” lifestyle changes still cut risk, says senior author Cassandra Spracklen.
  • 55%+ of cases potentially preventable: Researchers estimate that if people with less healthy lifestyles improved their habits, more than 55% of new Type 2 diabetes cases could be avoided.

What counts as a “healthy lifestyle”?
Based on American Heart Association guidelines, the study used 4 factors:

  1. BMI – had the strongest link to risk
  2. Smoking status
  3. Physical activity
  4. Diet – had the smallest independent effect

People with 3+ healthy factors were considered to have a healthy lifestyle. Only 4% of participants developed Type 2 diabetes during the study.

Takeaway: You can’t change genetics, but “better” choices — not necessarily perfect ones — can reduce risk or delay onset, cutting long-term complications. Results held across sexes and ancestry groups, and applied to adults aged 40-69 in the UK Biobank.

New study finds higher dementia risk in insulin-requiring diabetes

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.

Predicting genetic risk for Type 1 diabetes just got more accurate

Researchers at UC San Diego unveiled T1GRS, a new machine learning model that predicts genetic risk for Type 1 diabetes (T1D) more accurately across a broader population. The peer-reviewed study was published April 30, 2026 in Nature Genetics.

What T1GRS does

  • Goes beyond high-risk variants: Unlike existing scores that work best for people with known high-risk genes, T1GRS analyzes complex interactions between 199 risk variants across the genome, including the MHC region on chromosome 6.
  • Earlier, broader detection: It identifies both children and adults at high risk sooner, including people who develop T1D without the well-known high-risk genetic regions.
  • Built on massive data: Trained on genomes from 20,000+ people with T1D and ∼800,000 without, all of European ancestry. Confirmed 79 known loci and found 13 new loci tied to immune function, gene regulation, and blood sugar control.

4 T1D subtypes identified

T1GRS groups people by the genetic features driving their score, each with distinct clinical patterns:

  1. MHC-driven – Known high-risk MHC variants; earliest childhood onset.
  2. MHC-enriched – Mix of MHC and non-MHC variants; slightly later onset, intermediate severity.
  3. T-cell-enriched – Non-MHC variants affecting adaptive immune response; intermediate onset age.
  4. Pancreas-enriched – Non-MHC variants impacting pancreatic beta cells; later onset but highest rates of complications like kidney disease, nerve damage, heart problems.

How well it works

  • Validated externally: Tested on NIH All of Us and nPOD biobank data. Despite smaller samples, it still predicted risk with 87% accuracy.
  • Works beyond Europeans: Even though developed on European-ancestry data, it performed well in non-European populations too.

Clinical impact

  • Better screening: Captures at-risk people missed by current tools, enabling closer monitoring to reduce complications like diabetic ketoacidosis at diagnosis.
  • Personalized prevention: Helps identify candidates for preventive therapies such as teplizumab before T1D fully develops.

Lifestyle changes don’t help everyone equally with diabetes risk

A new study from the German Center for Diabetes Research (DZD), University Hospital Tübingen, and Helmholtz Munich found that long-term weight loss and lifestyle changes don’t prevent type 2 diabetes for all high-risk groups.

Key findings:

The study background

  • Researchers previously identified 6 distinct risk clusters for type 2 diabetes. Clusters 3 and 5 have especially high diabetes risk.
  • This study looked at whether lifestyle interventions work equally well across those clusters. It used data from the Tübingen Lifestyle Intervention Program (TULIP), where high-risk participants did a 2-year lifestyle program and were tracked for ∼9 years total.

What happened to Cluster 5

  • Participants in risk cluster 5 achieved substantial, sustained weight loss of 8% over 9 years.
  • Despite this, they still showed:
    • Rising blood glucose levels
    • Declining insulin secretion
    • Persistently high diabetes risk
  • This surprised researchers, since weight loss + diet + exercise usually prevent type 2 diabetes effectively.

Why Cluster 5 is different

  • The likely cause: pronounced fatty liver disease and insulin resistance
  • These factors appear to impair insulin secretion from pancreatic beta cells, driving blood glucose up even when weight stays down.
  • Cluster 5 has previously been linked to higher susceptibility to both type 2 diabetes and cardiovascular disease.

What this means

  • Standard lifestyle interventions may not be enough for people in risk cluster 5.
  • If confirmed in future studies, precision prevention strategies will be needed. High-risk groups like cluster 5 may require more intensive or targeted interventions beyond typical diet and exercise programs.

The research was published in the journal Diabetes and led by Professor Norbert Stefan.

Major trial shows continuous glucose monitoring improves blood sugar control in people with type 2 diabetes

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.

Keto diet may improve beta cell function in people with type 2 diabetes

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.

Progress in stem cell therapy for type 1 diabetes

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

One in 10 people may have resistance to GLP-1 diabetes drugs

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

New cause for diabetes in babies found in non-coding genes

Scientists at the University of Exeter have identified DNA changes in two non-coding genes, RNU4ATAC and RNU6ATAC, as a cause of autoimmune neonatal diabetes in 19 babies.

Key findings

  • First time non-coding genes linked to neonatal diabetes: Unlike most genetic research that focuses on protein-coding genes, this study found mutations in genes that produce functional RNA molecules instead of proteins. These RNA molecules help regulate other genes and how genetic information is interpreted.
  • How it was discovered: Using genome sequencing of children worldwide through Exeter’s free genetic testing program for suspected genetic diabetes, researchers found mutations in these two genes disrupted ∼800 other genes, many tied to immune function.
  • Disease mechanism: All 19 children had an autoimmune form of diabetes where the immune system attacks insulin-producing beta cells, similar to type 1 diabetes. The mutations appear to disrupt immune pathways.

Why it matters

  1. Diagnosis: Up to half of people with rare diseases lack a diagnosis. Exploring non-coding DNA could provide answers for more families.
  2. Treatment potential: Understanding the cause opens possibilities for new treatments and better care for neonatal diabetes.
  3. Broader implications: One or more of the 800 disrupted genes may play a central role in autoimmune diabetes, potentially revealing new biology and drug targets for the more common type 1 diabetes.

Study details

  • Lead: Associate Professor Elisa De Franco, University of Exeter Medical School
  • Support: NIHR Exeter Biomedical Research Centre and Exeter NIHR Clinical Research Facility
  • Publication: Peer-reviewed, announced April 9, 2026

Dr De Franco noted this shows “the importance of non-protein coding genes and their potential to cause disease in humans.” Dr Matthew Johnson added that while this condition is rare, it gives researchers “a window into the ways type 1 diabetes can develop.

Women with diabetes less likely to receive preventive care and some screenings

A new UCLA-led study, published in the Journal of General Internal Medicine, found that women with diabetes are less likely to receive crucial preventive care and certain cancer screenings compared to women without diabetes.

Summary:

  • Preventive Care Gaps: The study, which analyzed over 40 previous studies, highlighted that physicians often overlook services like conception counseling and some cancer screenings for women (ages 15-49) with diabetes.
  • Specific Findings: For women with diabetes, contraceptive services were received by 48% (vs. 62% for those without), cervical cancer screening rates ranged from 38-79% (vs. 46-86%), breast cancer screenings were 38-69% (vs. 54-82%), and pre-conception counseling was only given to just over 1% of those planning pregnancy (vs. 46% for women without diabetes).
  • Need for Coordinated Care: The researchers emphasized that robust, coordinated care teams involving endocrinology, primary care, and other specialists could significantly improve access to these services.
  • Limitations & Future Research: The review was limited by a small number of studies, some relying on patient recall, and many with small sample sizes. Future research should focus on how health systems can leverage electronic health records and improve care coordination to address these gaps.

New study demonstrates feasibility and safety of deprescribing diabetes medications when lifestyle medicine is integrated into primary care

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

Implantable islet cells could control diabetes without insulin injections

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

Widespread temptations bad news for people with a high risk of diabetes

A new NTNU study finds that people with a high genetic predisposition to type 2 diabetes are developing the disease much more often now than they did in the 1980s — and the researchers link the rise to today’s environment of easy-access calories and sedentary leisure.

What the study did
• Analyzed data from over 86,000 participants with nearly 200,000 measurements from the HUNT Study (Trøndelag Health Study, running since 1984).
• Published in The Lancet Diabetes & Endocrinology by PhD fellow Vera Vik Bjarkø and colleagues.

What they found
• The gap in type 2 diabetes prevalence between people with high versus low genetic risk widened from the 1980s to the 2010s.
• For people with low genetic risk, prevalence stayed low throughout the period.

Why this matters
• Researchers suggest modern “temptations” — abundant cheap snacks, sweets available any day (not just weekends), plus more sedentary activities like multiple TV channels, phones, and tablets — amplify genetic vulnerability.
• In other words, people with high genetic risk appear especially susceptible in a society that encourages unhealthy eating and inactivity, while those with low genetic risk seem to have protective factors that buffer these exposures.