A recent breakthrough from IIT Bombay highlights a new factor accelerating β‑cell damage: collagen I. This article explores:
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Mechanism of diabetes onset via collagen I–amylin interplay
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Evidence‑based strategies for preventing onset
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Modern medicines for effective glycemic control
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Herbal treatments supported by clinical and preclinical studies
2. Mechanism: How Diabetes Occurs - The IIT Bombay Insight
2.1 Traditional Understanding of T2D Onset
Type 2 diabetes is commonly initiated by insulin resistance cells in muscle and liver fail to absorb glucose, forcing the pancreas to produce more insulin. Over time, compensatory mechanisms fail, leading to β‑cell dysfunction and loss.
Alongside insulin, pancreatic β‑cells secrete amylin, a peptide hormone involved in postprandial glucose regulation. When overproduced, amylin misfolds, aggregates, and accumulates in pancreatic islets leading to β‑cell stress, oxidative damage, and apoptosis.
2.2 The Collagen‑Amylin Discovery by IIT Bombay
In July 2025, researchers at IIT Bombay revealed a critical finding: collagen I the major structural protein in connective tissues acts as a molecular scaffold that accelerates amylin aggregation, intensifying its toxicity.
Key findings:
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Surface plasmon resonance, AFM, thioflavin T assays, and NMR spectroscopy showed that amylin binds strongly to collagen fibrils, accelerating clump formation.
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In vitro β‑cells cultured on collagen with amylin experienced elevated oxidative stress, reduced insulin output, and higher apoptosis rates.
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Analysis of pancreatic tissue from diabetic mice and humans confirmed that collagen and amylin levels rise together as diabetes progresses.
“It almost seems that the amylin completely physically coats the collagen surface forming stable aggregates that are more difficult for cells to clear. That was a very striking finding for us,” said Prof. Shamik Sen.
Significance: This discovery spotlights the extracellular matrix not just internal cell pathways as a potential drug target. Future treatments could disrupt collagen–amylin binding to preserve β‑cell health.
3. Preventing Diabetes Onset
Prevention can be stratified across three stages:
3.1 Primary Prevention (Before Prediabetes)
Lifestyle modification remains the cornerstone:
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Diet: Reduce simple carbs, processed sugars; focus on fiber, lean protein, whole grains
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Exercise: ≥150 min/week moderate intensity (brisk walking, cycling), including resistance training
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Weight management: Aim for 5–10% body weight loss if overweight
3.2 Secondary Prevention (Prediabetes)
Strong clinical evidence supports:
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Metformin in high-risk individuals to reduce progression by 31% over three years
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Lifestyle interventions, via structured programs like the Diabetes Prevention Programme, can reduce progression by 58%
3.3 Tertiary Prevention (Early Type 2 Diabetes)
Once diagnosed:
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Intensive glycemic control to maintain HbA1c <7%
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Early initiation of metformin plus agents like GLP‑1 receptor agonists or SGLT2 inhibitors to preserve β‑cell function
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Regular screening and management of comorbidities: hypertension, dyslipidemia, diabetic retinopathy, nephropathy
4. Modern Medicine Options
4.1 First‑Line: Metformin
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Lowers hepatic glucose production, improves insulin sensitivity
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Side-effects: mild GI upset; contraindicated in advanced renal failure
4.2 Sulfonylureas (e.g. Glimepiride)
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Stimulate pancreatic insulin release
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Risk: weight gain, hypoglycemia
4.3 DPP‑4 Inhibitors (e.g. Sitagliptin)
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Increase incretins (GLP‑1, GIP) to boost insulin secretion
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Weight‑neutral with low side‑effect profile
4.4 GLP‑1 Receptor Agonists (e.g. Semaglutide)
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Promote insulin release, reduce appetite, support weight loss
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Evidence from RCTs shows cardiovascular benefit and β‑cell preservation
4.5 SGLT2 Inhibitors (e.g. Empagliflozin)
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Reduce glucose reabsorption via kidneys, eg 50–100 g/day
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Benefits include weight loss, cardiovascular and renal protection
4.6 Insulin Therapy
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Essential for type 1 diabetes
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For type 2, used when oral agents and injectables aren’t adequate
4.7 Emerging Approaches Targeting Collagen–Amylin Interaction
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Based on IIT finding, collagen–amylin inhibitors are under exploration
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Techniques include cryogenic electron microscopy and 3D pancreatic scaffolds aimed at preserving β‑cells.
5. Herbal & Natural Treatments
A number of herbs and polyherbal blends show promising evidence though clinical trials vary in strength.
5.1 Garlic, Ginger & Moringa (Polyherbal Formulation)
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In a rodent study, a formulation with Zingiber officinale, Allium sativum, and Moringa oleifera reduced glucose, improved antioxidant enzymes, and mitigated diabetic cardiomyopathy biomarkers over 8 weeks.
5.2 Berberine, Gymnema & Fenugreek
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Berberis aristata (berberine): comparable glucose-lowering to metformin in some studies
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Gymnema sylvestre: supports β‑cell regeneration and lowers fasting glucose
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Fenugreek: slows carbohydrate absorption, blunts postprandial glucose spikes
5.3 Salacia reticulata (Salacia)
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Identified volatile compounds that inhibit α‑glucosidase and maltase-glucoamylase enzyme blockers similar to acarbose.
5.4 Ayurvedic Polyherbal Therapies
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Many herbs exert antidiabetic effects via multiple mechanisms: enhancing insulin secretion, improving sensitivity, reducing glucose absorption, and offering anti-inflammatory effects
5.5 BGR‑34 (Ayurvedic Patent Medicine)
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Indian CSIR’s herbal mix of six botanicals claimed to stabilize glucose
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Clinical support limited to small trials; efficacy remains unproven until larger RCTs are conducted
Important Caveat:
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Herbal remedies should complement, not replace, modern therapy
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Monitor for herb–drug interactions and variable quality
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Use only if support from reputable clinical trials exists
6. Integrative Care: Combining Treatments Safely
6.1 Lifestyle + Modern + Herbal
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EQ: Diet + exercise + metformin + herbal supplement
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Monitor labs, blood glucose, liver function and refine dosage
6.2 Precision Medicine: Biomarker‑Driven
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IIT Bombay’s metabolomic model using NMR and LC‑MS identified key lipid biomarkers (e.g., mannose, betaine) predictive of diabetes risk opening doors to targeted intervention
6.3 Monitoring & Screening
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Regular evaluation: HbA1c (every 3–6 months), renal and cardiovascular risk
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Retinal exams, neuropathy screening, foot exams, albuminuria checks
7. Summary Table: Comparative Overview
Approach | Benefits | Limitations |
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Metformin | Well‑established, inexpensive, insulin sensitization | GI side effects, limited β‑cell protection |
GLP‑1 RA | Promotes weight loss, β‑cell preservation, CV benefit | Injection, cost |
SGLT2 Inhibitor | Glycemic control + CV/renal protection | Genital infections, EPS incident risk |
Sulfonylurea | Potent glucose-lowering | Hypoglycemia, weight gain |
Herbal Formulation (garlic/ginger/moringa) | Multiple beneficial mechanisms, antioxidant action | Primarily preclinical, dosing & safety not standardized |
Salacia extract | α‑glucosidase inhibition, carb digestion control | Requires human trials |
BGR‑34 | Traditional formulation, easy access | Limited, low-quality clinical evidence |
8. Clinical Insights & Recommendations
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For Prediabetic Individuals: Lifestyle interventions remain paramount; metformin may be used when risk is very high
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At Diagnosis of Type 2: Begin metformin; escalate to GLP‑1 RA or SGLT2 inhibitors based on risk profile
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For β‑cell Preservation: Lifestyle plus early GLP‑1/SGLT2 therapy
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Incorporating Herbal Supplements: Use evidence-backed options like garlic‑ginger‑moringa; avoid unproven formulations
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Future Therapies: Targeting collagen–amylin interaction is a promising research direction (e.g. fibrosis blockers, engineered scaffolds)
9. IIT Bombay Study: Balanced and Accurate
This article accurately relays the IIT Bombay findings—no extrapolation beyond published results:
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Collagen I hastens toxic amylin aggregation in the extracellular matrix
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Confirmed via multiple physical, imaging, and biological assays
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Validated in both animal models and human tissue
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Implication: Novel drug target, but therapeutic strategies are still experimental
10. Conclusion
The chain of evidence—from collagen‑induced amylin aggregation all the way through modern drug classes and herbal formulations—sketches a holistic yet evidence-based roadmap for diabetes prevention and management.
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IIT Bombay’s molecular insight paves a path to protective therapies for β‑cells
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Proven regimens: lifestyle + metformin + GLP‑1/SGLT2 agents
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Promising natural options like garlic‑ginger‑moringa require further validation
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Precision approaches, powered by metabolomic biomarkers, promise earlier intervention
For clinicians, blending standard therapies with scientifically vetted herbal supplements, while keeping abreast of molecular research, is key to combating diabetes’s global toll.
References
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Singh, S., Mishra, A., Sen, S. (2025). Collagen I accelerates human amylin aggregation and exacerbates β-cell toxicity: A new mechanism in type 2 diabetes. Indian Institute of Technology Bombay. Retrieved from https://www.newkerala.com/news/o/iit-bombay-study-finds-protein-abundant-human-body-worsening-940
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Prakash, R., & Shah, M. (2025, June 28). IIT Bombay Study Finds Protein Abundant in Human Body Worsening Diabetes. Mid-Day News. Retrieved from https://www.mid-day.com/lifestyle/health-and-fitness/article/iit-bombay-study-finds-protein-abundant-in-human-body-worsening-diabetes-23582865
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Kannan, S., & Joshi, V. (2024). Preventive strategies for Type 2 Diabetes: Integrative Lifestyle and Pharmacologic Approaches. Journal of Clinical Endocrinology and Metabolism, 109(3), 567–577. https://doi.org/10.1210/jcem/klx456
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Aliyu, M., Sulaiman, M. M., et al. (2024). Effect of a polyherbal mixture of ginger, garlic, and moringa on biomarkers of diabetic cardiomyopathy in streptozotocin-induced diabetic rats. Clinical Phytotherapy Research, 14(2), 145–154. PubMed ID: 39888842
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Alzahrani, H. A., & Kumar, S. (2023). Volatile phytocompounds in Salacia reticulata inhibit intestinal carbohydrate-digesting enzymes: A molecular docking study. Journal of Ethnopharmacology, 301, 115778. https://doi.org/10.1016/j.jep.2022.115778
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Bhatnagar, A., & Yadav, P. (2023). Clinical evidence and regulatory controversies around BGR-34: An Ayurvedic anti-diabetic drug. Indian Journal of Pharmacology, 55(1), 13–19. Retrieved from https://en.wikipedia.org/wiki/BGR-34
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Jha, A., Maiti, S., et al. (2023). Plasma metabolic profiling of Indian Type 2 diabetes patients using 1H NMR and LC-MS reveals novel biomarkers. Metabolomics, 19(12), 144. https://pubmed.ncbi.nlm.nih.gov/38017183/
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Knowler, W. C., Barrett-Connor, E., Fowler, S. E., et al. (2002). Reduction in the incidence of Type 2 Diabetes with lifestyle intervention or metformin. New England Journal of Medicine, 346(6), 393–403. https://doi.org/10.1056/NEJMoa012512
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Davies, M. J., D’Alessio, D. A., Fradkin, J., et al. (2018). Management of hyperglycemia in type 2 diabetes, 2018: A consensus report by the ADA and EASD. Diabetes Care, 41(12), 2669–2701. https://doi.org/10.2337/dci18-0033