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Home delivered, medically tailored groceries improve diabetes control

A randomized controlled trial published in Circulation found that medically tailored grocery deliveries improved blood sugar control in adults with type 2 diabetes who have public insurance.

The study was conducted by researchers at Kaiser Permanente, Tufts University’s Food is Medicine Institute, and The George Institute for Global Health within Kaiser Permanente Southern California.

Study design:

  • 460 Medicaid-insured patients with persistently elevated blood sugar from 12 medical offices in Southern California
  • Recruited Nov 2021 – July 2022 and followed for 6 months
  • Randomized to usual care or one of two levels of monthly medically tailored groceries (averaging about $135 or $175)
  • The grocery intervention included weekly home deliveries scaled to household size, culturally tailored recipes, and phone-based nutrition counseling

Key findings:

  • Blood sugar: Participants who received groceries had an additional 0.40 point reduction in HbA1c over 6 months compared to usual care
  • Food security: Odds of food security increased by nearly 215% and nutrition security by 365% among those who received groceries
  • Dose: Improvements in blood sugar were similar whether participants received the $135 or $175 level of support

The authors said the results provide RCT-level evidence that integrating Food is Medicine approaches into clinical care can improve both diabetes outcomes and food/nutrition security, particularly for low-income patients facing economic and social barriers. They suggested the findings support incorporating medically tailored grocery programs into Medicaid benefits.

Muscles matter for diabetes risk

A large international study led by Curtin University and published in Diabetes Care tracked nearly 480,000 adults who were diabetes-free at the start for 14 years.

The researchers looked at sarcopenic obesity — having both excess body fat and low muscle mass/strength.

Key findings:

  • Much higher risk: People with sarcopenic obesity were more than 3.5 times as likely to develop type 2 diabetes compared to people with healthy body composition.
  • Worse than obesity alone: They were 19% more likely to develop type 2 diabetes than people with obesity alone, and 91% more likely than people with low muscle mass alone (sarcopenia).
  • Absolute rates: Within 10 years, nearly 15% of people with sarcopenic obesity developed type 2 diabetes, compared to around 11% with obesity alone and just 3% without either condition.
  • Who is most affected: The link was particularly strong among women and adults under 60.

The authors say the results challenge the idea that diabetes risk is driven mainly by weight on the scales. Because muscle uses a lot of glucose and helps regulate insulin resistance, preserving muscle mass and strength through regular physical activity may be just as important as managing weight for prevention.

Lead author was PhD candidate Zhongyang Guan, senior lead Professor Mario Siervo, with comment from Diabetes WA on how physical activity helps use blood glucose and reduce insulin resistance.

GLP-1 agonists may help people with diabetes and long COVID

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.

Gut microbiota can predict risk of type 2 diabetes years before it develops

Researchers at Chalmers University of Technology led a large Swedish study of 4,685 adults and discovered that changes in gut microbiota and metabolism can show up years before type 2 diabetes develops. Participants gave stool samples, and 383 developed diabetes after ∼5 years of follow-up.

Key bacterial links:

  1. 9 specific bacteria were associated with future diabetes risk.
  2. Akkermansia muciniphila – usually seen as beneficial – was high in people who later developed diabetes. Researchers think that with low fiber intake, it eats the gut’s protective mucus instead of fiber, causing inflammation and insulin resistance.
  3. Coprococcus catus – very low levels were linked to diabetes risk, but above a certain level the risk disappeared.
  4. Diet mattered: whether certain gut bacteria were helpful or harmful depended on a person’s eating habits.

Why it matters: The findings suggest gut microbiome changes come before diabetes, not as a result of it. This means stool samples could eventually be used as biomarkers, alongside obesity, genetics, and blood glucose, to identify people at risk earlier and start preventive measures.

Next steps: Results still need validation in larger studies. If confirmed, the microbiome could become a target for personalized prevention through diet and lifestyle, since it can be modified. The study supports current advice to eat fiber-rich foods like fruit, vegetables, legumes, and whole grains.

Hearing loss in diabetes patients a ‘hidden epidemic’

Researchers at University of Queensland are calling hearing loss a “hidden epidemic” in diabetes care, urging that hearing tests be added to routine diabetes check-ups because people with diabetes are more than twice as likely to develop serious hearing loss.

What the research shows

  • Scale: About 1 in 4 adults with diabetes, or roughly 130 million people worldwide, live with serious hearing loss.
  • Who it affects: It often strikes working-age adults in their 40s and 50s, not just those with long-standing diabetes. Even people who have had diabetes for less than 10 years are more than twice as likely to develop significant hearing loss compared to those without diabetes.
  • Evidence base: The call comes from Dr Mehwish Nisar at UQ’s School of Public Health after reviewing 29 studies with over 17,000 people globally, mostly with type 2 diabetes and prediabetes.

Why it matters

  • Daily impact: Hearing loss fuels isolation and creates communication challenges during prime working years.
  • Current gap: While retinopathy, nephropathy, and neuropathy are routinely monitored in diabetes care, hearing impairment is not systematically integrated into protocols despite clear links.
  • Awareness: Most people, including many patients, don’t know diabetes can cause serious hearing loss.

What researchers recommend

  • Add simple hearing tests to every diabetes check-up using low-cost audiometric screening.
  • Detect early: Hearing loss progresses gradually and patients often miss it until advanced. Early detection allows for timely hearing aid support and better glucose management to slow further deterioration.
  • Act sooner: “Waiting for advanced complications before checking hearing is waiting too long,” Dr Nisar said.

Physical exercise may help regulate the immune system in type 1 diabetes

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.

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