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Diabetes mellitus type conversion refers to transition of one diabetic type to another or misdiagnosis of the wrong type, particularly for Latent Autoimmune Diabetes in Adults (LADA) and Maturity-Onset Diabetes of the Young (MODY).[1][2] Studies show misclassification in 5–10% LADA cases and 50–90% of MODY cases.[3][4] Increased misdiagnosis is because of similar clinical features between rarer types and Type 1 diabetes or Type 2 diabetes in early stages.[2]

The universal symbol of diabetes [5]

Accurate diagnosis requires antibody testing for LADA and genetic sequencing for MODY to set the polygenic forms apart.[3][6] Proper management is important since misclassification may lead to inappropriate therapies and negative long-term outcomes.[7][8]

Misdiagnosis is more prominent in low- and middle-income countries, especially LADA and MODY as type 2, due to limited access to testing.[9] After discovery and identification of conditions, research shifted towards precision medicine and analysis, including biomarkers, artificial intelligence and gene therapy to improve management and lower diagnostic errors.[10][11][12]

Classification

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Diabetes mellitus is divided into main categories based on causes (etiology) and impact on body (pathophysiology). According to the American Diabetes Association (ADA) and World Health Organization (WHO), primary categories are:[1][2]

These categories are distinct but features at diagnosis overlap. Misclassification is common between T1D, T2D and other subtypes, especially LADA and MODY. They are frequently mistaken for the more common polygenic forms.[1][2]

Signs and symptoms

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The main symptoms of diabetes

Type 1 diabetes (T1D) and Type 2 diabetes (T2D) are the most common diabetes:[2]

  • T1D: Symptoms appear suddenly, including frequent urination, extreme thirst, unexplained weight loss, fatigue, blurred vision. Emergency signs include nausea, vomiting, and fruity breath.[13]
  • T2D: Symptoms develop gradually or are absent, including increased thirst, pain, fatigue, blurred vision. Many have no symptoms initially, leading to delayed diagnosis.[13]

However, other variants show similar symptoms so they are often misdiagnosed as the above types.[2]

Misdiagnosis

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Correct diagnosis is difficult because all conditions present with hyperglycemia.[14] Despite advances in molecular biology, misclassification as Type 2 diabetes (T2D) is common in adult-onset autoimmune diabetes. 5–10% have Latent Autoimmune Diabetes in Adults (LADA) among presumed T2D[15], while 50-90% of Maturity-Onset Diabetes of the Young (MODY) cases are estimated to be misdiagnosed as Type 1 Diabetes (T1D) or T2D.[16]

Latent Autoimmune Diabetes in Adults (LADA) diagnosis

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The Immunology of Diabetes Society has established three diagnostic criteria: age over 30, presence of islet cell autoantibodies, and no insulin dependence for at least six months after diagnosis.[17] As standards differ across countries, controversies remain on the criteria.[18] Testing for key autoantibodies linked with LADA is more accurate, including GADA, islet antigen-2 (IA-2), pancreatic islet-cell antibodies (ICA), autoantibodies against insulin (IAA), association of zinc transporter-8 autoantibody (ZnT8A).[3] The indicators discriminate LADA from T2D and are better for treatment decisions.[3] While C-peptide concentrations of LADA lie between T1D and T2D (insulin production indicator), C-peptide alone cannot be used for conditions determination and should be confirmed with autoantibody tests.[19]

Misdiagnosis of LADA

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LADA has features of both T1D and T2D.[1][2] Autoimmune destruction of insulin-making beta cells is observed in the pancreas like T1D. LADA individuals usually have islet autoantibodies, the most common is glutamic acid decarboxylase (GAD) antibodies.[20][21]

Beta cell loss in LADA is slower than T1D, and insulin may not be needed for months or years after diagnosis in LADA.[22] The slow progression may mislead towards T2D.[23] Whether LADA is a distinct condition or simply slow-onset type 1 is debatable, but both conditions have different rates of beta cell function decline and specific treatments.[1][2]

Why LADA Is Frequently Misdiagnosed?

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LADA is often misdiagnosed as T2D. Factors include:

  • Age of onset. LADA typically presents in adulthood (usually after age 30), overlapping with T2D.[1][2]
  • Initial presentation. LADA symptoms start slowly or are mild, like tiredness, weight loss, slightly increased thirst and urination. These coincide with T2D rather than classic T1D.[3][4][21]
  • Absence of ketoacidosis. Diabetic ketoacidosis (DKA) is rare in LADA diagnosis, but DKA occurs in 25–50% of classic T1D.[1][2]
  • Initial non-insulin dependence. Many can manage LADA with oral medications or lifestyle changes at early stages, similar to T2D. This temporary response to non-insulin therapies can lead to misdiagnosis.[20][22][24]
  • Body weight. Individuals with LADA are overweight or obese, are also seen in T2D. However, obesity doesn't rule out autoimmunity.[20][21]

Because of overlapping features, LADA individuals are often diagnosed with T2D at onset. Only when autoimmune markers are tested or when the expected outcomes of T2D are not observed in clinical trajectory, individuals may be diagnosed correctly.[1][2][3]

Maturity-Onset Diabetes of the Young (MODY) diagnosis

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The common MODY diagnosis criteria include: diabetes onset before age 25, absence of beta-cells antibodies, sustained insulin secretion with stimulated serum C-peptide level above 200 pmol/l, and presence of hyperglycemia in at least two consecutive generations.[25] But it is not distinct from T2D entirely. Laboratory tests including serum and urine glucose, glycated haemoglobin (HbA1c) should be done with genetic testing and next-generation sequencing.[26]

Unlike LADA which is an autoimmune disease, MODY is caused by a single gene mutation (monogenic) and is an autosomal dominant disease (if one parent has it, each child has a 50% chance of inheriting it.)[6][7]

Over 14 different genes were identified. The most common ones are GCK (MODY 2) (affects how beta cells detect glucose) and HNF1A (MODY 3) (affects insulin secretion).[6][27] Unlike T1D or T2D, MODY does not affected by the environmental and is mostly affected by genetics.[6]

Misdiagnosis of MODY

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MODY can resemble T1D (if diagnosed in a lean young person) or T2D (if diagnosed in adulthood with family history), so it gets misclassified often.[1][2]

Why MODY Is Frequently Misdiagnosed?

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MODY is frequently misclassified as either T1D or T2D.[1][2] The factors are:

  • Age of onset. MODY usually starts in adolescence or early adulthood[1][2], same as type 1 and early-onset type 2. Type 1 is classically diagnosed in youth, but early-onset type 2 is becoming more common in younger people.[6]
  • Absence of obesity. Most people with MODY are lean and don't have insulin resistance.[6][7] Clinicians will be misled to consider as T1D rather than T2D.[1][2]
  • Absence of autoimmunity. MODY is not an autoimmune condition, and people with MODY do not have islet autoantibodies.[6] A young, lean individual without autoantibodies may be misdiagnosed as type 1 because of age and body habitus.[1][2]
  • Variable symptom severity. Some subtypes like GCK-MODY cause stable, mild hyperglycemia (high blood glucose levels) with few or no symptoms thus may not be noticed.[7] Slow-progressing subtype, like HNF1A-MODY, can easily be mistaken for early-onset type 2.[6][27]
  • Family history. There is often a strong family history across multiple generations. But this can be assumed as T2D.[6][7]

As features overlap, people with MODY are often misclassified as T1D or T2D. The correct diagnosis must undergo genetic testing, which may not happen until years after initial diagnosis.[6][7]

Management

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Management should be tailored for each person’s condition with specific glycemic goal to lower blood glucose to target levels. Preservation of beta-cells function to produce insulin, regular monitoring for complications including cardiovascular and metabolic condition are equally essential.[28]

Misdiagnosis of LADA as Type 2 Diabetes

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Misclassification of Latent Autoimmune Diabetes in Adults (LADA) as Type 2 Diabetes (T2D) can have significant impacts due to difference in therapy.[29] Consequences of misclassification are:

  • Delayed insulin initiation. Insulin injection is the most appropriate treatment to address insulin deficiency in autoimmune destruction of pancreatic beta cells in LADA. However, misdiagnosis as T2D may lead to prolonged used of oral medication. It may worsen autoimmune destruction thus speed up beta-cell loss.[20][22][29]
  • Ineffective treatment. Common oral medications used in T2D like sulfonylureas, are discouraged for treatment of LADA. Sulfonylureas may accelerate beta-cell exhaustion, causing earlier insulin dependence, which deteriorates the autoimmune function.[8]
  • Inaccurate risk assessment. The risk of diabetic ketoacidosis is higher in LADA than T2D. Ignoring the condition may cause poorer glycemic control and increased chance of long-term diabetic complications.[1][2][29]

Therefore, early and accurate diagnosis of LADA is crucial. Early insulin therapy protects remaining beta cells and provides more effective glycemic control than standard T2D regimens.[22][6] Apart from metformin, which can be used in medications in both conditions, new drugs including Glucagon-like peptide-1 (GLP 1) receptor agonists and DPP 4 inhibitors can retain C-peptide levels and improve blood glucose management in LADA.[30]

Figure 1: Comparison between two treatment types (LADA and Type 2 Diabetes)[8][30][31][32]
Treatment Type LADA Approach Type 2 Diabetes Approach
Primary Therapy Early Insulin (Long-acting) Lifestyle + Metformin
Metformin Beneficial (for resistance) First-line choice
Sulfonylureas Avoid (accelerates destruction) Common/Effective
GLP-1 RAs Effective (if C-peptide not too low) Common/Effective
DPP-4 Inhibitors Considered useful Common/Effective
Goal Preserve beta-cell function Improve insulin sensitivity

Misdiagnosis of MODY as T1D or T2D

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Misclassification of Maturity-Onset Diabetes of the Young (MODY) as T2D can be severe since management in MODY is specific to each subtype.[27] Consequences of misclassification are:

  • Inappropriate therapy. In GCK-MODY, individuals have mild, stable hyperglycemia and usually do not require pharmacological treatment, except during pregnancy.[33] Some subtypes like HNF1A-MODY and HNF4A-MODY, respond well to low-dose sulfonylurea and does not require insulin. However, many are misclassified and unnecessarily given glucose reducing treatments like insulin injections.[6][7][27][33] On the contrary, HNF1B-MODY individuals with pancreatic developmental defects and kidney abnormalities, require insulin therapy for survival.[33][34]
  • Ineffective or suboptimal oral therapy. If individuals are misclassified as T2D, they may receive medications (such as metformin or other oral agents) that are not specific for MODY, which may lead to poorer glycemic control.[6][27]
  • Missed opportunities for family screening. MODY is an autosomal dominant disease. A genetic diagnosis allows proper screening of potential family members carrying the mutation, then individuals can receive early detection and appropriate management.[7]

Therefore, to prevent incorrect treatments, genetic diagnosis is essential for accurate identification of carriers with family history through screening.[7]

Epidemiology

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Misdiagnosis of diabetes is more prevalent in some regions and types of individuals, especially low- and middle-income countries.[9][35] Studies have shown that limited access to C-peptide and genetic testing increases mislabelling of Latent Autoimmune Diabetes in Adults (LADA) or Maturity-Onset Diabetes of the Young (MODY) as type 2 diabetes or gestational diabetes.[36] LADA is misdiagnosed because clinicians seldom measure islet autoantibodies, a key determining factor of the disease.[37] Additionally, doctors sometimes mistake MODY for gestational diabetes in women who develop high blood sugar early in pregnancy or who have a normal body weight.[38]

History

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In 1977, study showed that a group of individuals initially diagnosed with Type 2 Diabetes (T2D) possessed antibodies characteristic of Type 1 Diabetes (T1D).[39] In 1993, misdiagnosis of T2D was named formally as Latent Autoimmune Diabetes in Adults (LADA), where individuals produced glutamic acid decarboxylase (GAD) autoantibodies, an autoimmune marker of T1D.[10] The term LADA replaced the informal name (Type 1.5 Diabetes) due to symptoms of both diabetic types previously.[40] Since then, LADA represents different levels of insulin resistance.[28] It is characterized by a slower trajectory than classic T1D and an initial appearance as T2D.[22] Although the boundary between T1D, T2D, and LADA is controversial, LADA remains useful in defining the clinical condition.[41]

Maturity-onset diabetes of the young (MODY) was outlined in 1974 and 1975 in multi-generational families study. individuals with mild hyperglycemia were diagnosed before age 25 and varied from traditional diabetes forms. individuals were found to be autosomal-dominant inheritance due to family history (50% chance of inheriting if parents have it).[11] In the 1990s, with the help of molecular genetics and genetics analysis, key mutations in genetic markers including GCK (MODY2) and HNF1A (MODY3) were identified. Results has shown that it is a monogenic beta-cell disorder, a single gene mutation which affects insulin secretion.[42]  

Research directions

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Current research emphasises on precision diagnostics like tailored genetic tests based on metabolic and genomic data, better biomarkers uses and individual tests.[12] For Latent Autoimmune Diabetes in Adults, clinical trials should focus on beta-cell protective therapies to reverse diabetes, immune modulation and validating key predictors to lower misdiagnosis.[43] Maturity-onset diabetes of the young research should focus on identifying rare subtypes, disease modelling via stem cells and gene therapy like AAV vectors.[7] Artificial Intelligence and Machine learning will be useful in accurate diagnosis, optimising diabetes management and reducing cardiovascular complication.[44]

References

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  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 American Diabetes Association Professional Practice Committee; ElSayed, Nuha A.; McCoy, Rozalina G.; Aleppo, Grazia; Balapattabi, Kirthikaa; Beverly, Elizabeth A.; Briggs Early, Kathaleen; Bruemmer, Dennis; Ebekozien, Osagie; Echouffo-Tcheugui, Justin B.; Ekhlaspour, Laya; Gaglia, Jason L.; Garg, Rajesh; Khunti, Kamlesh; Lal, Rayhan (2025-01-01). "2. Diagnosis and Classification of Diabetes: Standards of Care in Diabetes—2025". Diabetes Care. 48 (Supplement_1): S27–S49. doi:10.2337/dc25-S002. ISSN 0149-5992. PMC 11635041. PMID 39651986.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 American Diabetes Association Professional Practice Committee for Diabetes*; Bajaj, Mandeep; McCoy, Rozalina G.; Balapattabi, Kirthikaa; Bannuru, Raveendhara R.; Bellini, Natalie J.; Bennett, Allison K.; Beverly, Elizabeth A.; Briggs Early, Kathaleen; ChallaSivaKanaka, Sathyavathi; Echouffo-Tcheugui, Justin B.; Everett, Brendan M.; Garg, Rajesh; Laffel, Lori M.; Lal, Rayhan (2026-01-01). "2. Diagnosis and Classification of Diabetes: Standards of Care in Diabetes—2026". Diabetes Care. 49 (Supplement_1): S27–S49. doi:10.2337/dc26-S002. ISSN 0149-5992. PMC 12690183. PMID 41358893.
  3. 1 2 3 4 5 6 Ravikumar, Vijay; Ahmed, Ariba; Anjankar, Ashish; Ravikumar, Vijay; Ahmed, Ariba; Anjankar, Ashish (2023-10-29). "A Review on Latent Autoimmune Diabetes in Adults". Cureus. 15 (10). doi:10.7759/cureus.47915. ISSN 2168-8184. PMC 10683931. PMID 38034250.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. 1 2 Ramu, Deepika; Ramaswamy, Selvaraj; Rao, Suresh; Paul, Solomon F. D. (2023-10-01). "The worldwide prevalence of latent autoimmune diabetes of adults among adult-onset diabetic individuals: a systematic review and meta-analysis". Endocrine. 82 (1): 28–41. doi:10.1007/s12020-023-03424-5. ISSN 1559-0100.
  5. ↑ "Diabetes Blue Circle Symbol". www.diabetesbluecircle.org. Archived from the original on 2008-04-24. Retrieved 2026-03-24.
  6. 1 2 3 4 5 6 7 8 9 10 11 12 13 Zečević, Ksenija; Volčanšek, Špela; Katsiki, Niki; Rizzo, Manfredi; Milardović, Tanja Miličević; Stoian, Anca Pantea; Banach, Maciej; Muzurović, Emir (2024-07-01). "Maturity-onset diabetes of the young (MODY) - in search of ideal diagnostic criteria and precise treatment". Progress in Cardiovascular Diseases. Assorted Topics 2024. 85: 14–25. doi:10.1016/j.pcad.2024.03.004. ISSN 0033-0620.
  7. 1 2 3 4 5 6 7 8 9 10 Kant, Ravi; Davis, Amanda; Verma, Vipin (2022-02-01). "Maturity-Onset Diabetes of the Young: Rapid Evidence Review". American Family Physician. 105 (2): 162–167. ISSN 1532-0650.
  8. 1 2 3 Cabrera-Rode, Eduardo; Perich, Pedro; Diaz-Horta, Oscar; Tiberti, Claudio; Molina, Gisela; Arranz, Celeste; Martin, Juana M.; Licea, Manuel; De Leiva, Alberto; Puig-Domingo, Manuel; Dimario, Umberto (2002-11-15). "Slowly Progressing Type 1 Diabetes: Persistence of Islet Cell Autoantibodies is Related to Glibenclamide Treatment". Autoimmunity. 35 (7): 469–474. doi:10.1080/0891693021000050574. ISSN 0891-6934.
  9. 1 2 Flood, David; Seiglie, Jacqueline A.; Dunn, Matthew; Tschida, Scott; Theilmann, Michaela; Marcus, Maja E.; Brian, Garry; Norov, Bolormaa; Mayige, Mary T.; Gurung, Mongal Singh; Aryal, Krishna K.; Labadarios, Demetre; Dorobantu, Maria; Silver, Bahendeka K.; Bovet, Pascal (2021-06-01). "The state of diabetes treatment coverage in 55 low-income and middle-income countries: a cross-sectional study of nationally representative, individual-level data in 680 102 adults". The Lancet Healthy Longevity. 2 (6): e340–e351. doi:10.1016/S2666-7568(21)00089-1. ISSN 2666-7568. PMC 8865379. PMID 35211689.
  10. 1 2 Tuomi, Tiinamaija; Groop, Leif C; Zimmet, Paul Z; Rowley, Merrill J; Knowles, William; Mackay, Ian R (1993-02-01). "Antibodies to Glutamic Acid Decarboxylase Reveal Latent Autoimmune Diabetes Mellitus in Adults With a Non—Insulin-Dependent Onset of Disease". Diabetes. 42 (2): 359–362. doi:10.2337/diab.42.2.359. ISSN 0012-1797.
  11. 1 2 Tattersall, R. (2004-07-19). "Maturity-onset diabetes of the young: a clinical history". Diabetic Medicine. 15 (1): 11–14. doi:10.1002/(SICI)1096-9136(199801)15:1<11::AID-DIA561>3.0.CO;2-0. ISSN 0742-3071.
  12. 1 2 Stone, Stephen I.; Balasubramanyam, Ashok; Posey, Jennifer E. (2024-05-01). "Atypical Diabetes: What Have We Learned and What Does the Future Hold?". Diabetes Care. 47 (5): 770–781. doi:10.2337/dci23-0038. ISSN 0149-5992. PMC 11043229. PMID 38329838.
  13. 1 2 "Symptoms & Causes of Diabetes - NIDDK". National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved 2026-04-09.
  14. ↑ American Diabetes Association (2009-01-01). "Diagnosis and Classification of Diabetes Mellitus". Diabetes Care. 32 (Supplement_1): S62–S67. doi:10.2337/dc09-S062. ISSN 0149-5992.
  15. ↑ Saiprasad, Saraswathi; Swamy, Narayana; Saiprasad, Saraswathi; Swamy, Narayana (2026-02-04). "When Type 2 Diabetes Isn't Type 2: Latent Autoimmune Diabetes in a Lean, Highly Physically Active Adult". Cureus. 18 (2). doi:10.7759/cureus.102964. ISSN 2168-8184. PMC 12965300. PMID 41798410.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  16. ↑ Tosur, Mustafa; Philipson, Louis H (2022-05-31). "Precision diabetes: Lessons learned from maturity‐onset diabetes of the young (MODY)". Journal of Diabetes Investigation. 13 (9): 1465–1471. doi:10.1111/jdi.13860. ISSN 2040-1116. PMC 9434589. PMID 35638342.
  17. ↑ Fourlanos, S.; Dotta, F.; Greenbaum, C. J.; Palmer, J. P.; Rolandsson, O.; Colman, P. G.; Harrison, L. C. (2005-11-01). "Latent autoimmune diabetes in adults (LADA) should be less latent". Diabetologia. 48 (11): 2206–2212. doi:10.1007/s00125-005-1960-7. ISSN 1432-0428.
  18. ↑ Luo, Shuo-Ming; Liu, Bing-Wen; Yin, Wen-Feng; Li, Xia; Zhou, Zhi-Guang (2021-01-05). "A long and winding road to understand latent autoimmune diabetes in adults". Chinese Medical Journal. 134 (01): 1–4. doi:10.1097/CM9.0000000000001321. PMC 7862824. PMID 33395070.
  19. ↑ Maddaloni E, Bolli GB, Frier BM (2022). "C-peptide determination in the diagnosis of type of diabetes and its management: A clinical perspective". Diabetes, Obesity and Metabolism. doi:10.1111/dom.14785. PMC 9543865. PMID 35676794. Retrieved 2026-03-24.{{cite web}}: CS1 maint: multiple names: authors list (link)
  20. 1 2 3 4 Buzzetti, Raffaella; Tuomi, Tiinamaija; Mauricio, Didac; Pietropaolo, Massimo; Zhou, Zhiguang; Pozzilli, Paolo; Leslie, Richard David (2020-10-01). "Management of Latent Autoimmune Diabetes in Adults: A Consensus Statement From an International Expert Panel". Diabetes. 69 (10): 2037–2047. doi:10.2337/dbi20-0017. ISSN 0012-1797. PMC 7809717. PMID 32847960.
  21. 1 2 3 Jones, Angus G.; McDonald, Timothy J.; Shields, Beverley M.; Hagopian, William; Hattersley, Andrew T. (2021-06-01). "Latent Autoimmune Diabetes of Adults (LADA) Is Likely to Represent a Mixed Population of Autoimmune (Type 1) and Nonautoimmune (Type 2) Diabetes". Diabetes Care. 44 (6): 1243–1251. doi:10.2337/dc20-2834. ISSN 0149-5992. PMC 8247509. PMID 34016607.
  22. 1 2 3 4 5 Maddaloni, Ernesto; Moretti, Chiara; Mignogna, Carmen; Buzzetti, Raffaella (2020-04-30). "Adult-onset autoimmune diabetes in 2020: An update". Maturitas. 137: 37–44. doi:10.1016/j.maturitas.2020.04.014. ISSN 0378-5122.
  23. ↑ Lundholm, Michelle D.; Zhou, Keren (2025-12-01). "Latent autoimmune diabetes in adults: Not type 1, not type 2, a little of both". Cleveland Clinic Journal of Medicine. 92 (12): 757–763. doi:10.3949/ccjm.92a.25069. ISSN 0891-1150. PMID 41326180.
  24. ↑ Hu, Jingyi; Zhang, Rong; Zou, Hailan; Xie, Lingxiang; Zhou, Zhiguang; Xiao, Yang (2022-07-21). "Latent Autoimmune Diabetes in Adults (LADA): From Immunopathogenesis to Immunotherapy". Frontiers in Endocrinology. 13. doi:10.3389/fendo.2022.917169. ISSN 1664-2392. PMC 9350734. PMID 35937817.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  25. ↑ Zečević, Ksenija; Volčanšek, Špela; Katsiki, Niki; Rizzo, Manfredi; Milardović, Tanja Miličević; Stoian, Anca Pantea; Banach, Maciej; Muzurović, Emir (2024-07-01). "Maturity-onset diabetes of the young (MODY) - in search of ideal diagnostic criteria and precise treatment". Progress in Cardiovascular Diseases. Assorted Topics 2024. 85: 14–25. doi:10.1016/j.pcad.2024.03.004. ISSN 0033-0620.
  26. ↑ Ruiz-Urbaez, Rossana; Males-Maldonado, David; Villagómez-Estrada, Mariela Viviana; Reyes-Silva, Carlos; Salazar-Vega, Jorge; Jaramillo-Koupermann, Gabriela; Sosa-Copa, Diana; Gea-Izquierdo, Enrique (2025-09-12). "Case Report: Misdiagnosis of Maturity-Onset Diabetes of the Young as type 1, type 2 or gestational diabetes: insights from a Latin American tertiary center". Frontiers in Medicine. 12. doi:10.3389/fmed.2025.1613877. ISSN 2296-858X. PMC 12463888. PMID 41020216.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  27. 1 2 3 4 5 Delvecchio, Maurizio; Pastore, Carmela; Giordano, Paola (2020-08-01). "Treatment Options for MODY Patients: A Systematic Review of Literature". Diabetes Therapy. 11 (8): 1667–1685. doi:10.1007/s13300-020-00864-4. ISSN 1869-6961. PMC 7376807. PMID 32583173.
  28. 1 2 Rajkumar, Venkatraman; Levine, Steven N. (2026), "Latent Autoimmune Diabetes", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 32491820, retrieved 2026-03-24
  29. 1 2 3 Pieralice, Silvia; Pozzilli, Paolo (2018-12-17). "Latent Autoimmune Diabetes in Adults: A Review on Clinical Implications and Management". Diabetes & Metabolism Journal. 42 (6): 451–464. doi:10.4093/dmj.2018.0190. ISSN 2233-6079. PMC 6300440. PMID 30565440.
  30. 1 2 Poudel, ReshamR (2012). "Latent autoimmune diabetes of adults: From oral hypoglycemic agents to early insulin". Indian Journal of Endocrinology and Metabolism. 16 (7): 41. doi:10.4103/2230-8210.94257. ISSN 2230-8210. PMC 3354922. PMID 22701843.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  31. ↑ Hoogwerf, Byron J. (2025-12-01). "LADA: A case for starting insulin therapy at diagnosis". Cleveland Clinic Journal of Medicine. 92 (12): 764–766. doi:10.3949/ccjm.92a.25084. ISSN 0891-1150. PMID 41326194.
  32. ↑ Zhao, Yunjuan; Yang, Lin; Xiang, Yufei; Liu, Lingjiao; Huang, Gan; Long, Zhaofeng; Li, Xia; Leslie, R. David; Wang, Xiangbing; Zhou, Zhiguang (2014-05-01). "Dipeptidyl Peptidase 4 Inhibitor Sitagliptin Maintains β-Cell Function in Patients With Recent-Onset Latent Autoimmune Diabetes in Adults: One Year Prospective Study". The Journal of Clinical Endocrinology & Metabolism. 99 (5): E876–E880. doi:10.1210/jc.2013-3633. ISSN 0021-972X.
  33. 1 2 3 Tosur, Mustafa; Philipson, Louis H (2022-05-31). "Precision diabetes: Lessons learned from maturity‐onset diabetes of the young (MODY)". Journal of Diabetes Investigation. 13 (9): 1465–1471. doi:10.1111/jdi.13860. ISSN 2040-1116. PMC 9434589. PMID 35638342.
  34. ↑ Skoczek, Dawid; Dulak, Józef; Kachamakova-Trojanowska, Neli (2021-07-14). "Maturity Onset Diabetes of the Young—New Approaches for Disease Modelling". International Journal of Molecular Sciences. 22 (14): 7553. doi:10.3390/ijms22147553. ISSN 1422-0067. PMC 8303136. PMID 34299172.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  35. ↑ Wu, Hongjiang; Meng, Xiangrui; Wild, Sarah H.; Gasevic, Danijela; Jackson, Caroline A. (2017-06-18). "Socioeconomic status and prevalence of type 2 diabetes in mainland China, Hong Kong and Taiwan: a systematic review". Journal of Global Health. 7 (1): 011103. doi:10.7189/jogh.07.011103. ISSN 2047-2986. PMC 5481892. PMID 28702177.{{cite journal}}: CS1 maint: article number as page number (link)
  36. ↑ Alemán-Contreras, Ricardo; Gómez-Díaz, Rita A.; Noyola-García, Maura E.; Mondragón-González, Rafael; Wacher, Niels; Ferreira-Hermosillo, Aldo (2024-04-25). "Utility of Fasting C-Peptide for the Diagnostic Differentiation of Patients with Type 1, Type 2 Diabetes, MODY, and LADA". Life. 14 (5): 550. doi:10.3390/life14050550. ISSN 2075-1729. PMC 11122504. PMID 38792571.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  37. ↑ Stone, Stephen I.; Balasubramanyam, Ashok; Posey, Jennifer E. (2024-05-01). "Atypical Diabetes: What Have We Learned and What Does the Future Hold?". Diabetes Care. 47 (5): 770–781. doi:10.2337/dci23-0038. ISSN 0149-5992. PMC 11043229. PMID 38329838.
  38. ↑ Majewska, Agata; Stanirowski, Paweł; Wielgoś, Mirosław; Bomba-Opoń, Dorota. "Maturity-onset Diabetes of the Young (MODY) in Pregnancy: A Review". Current Diabetes Reviews. 19 (1): 28–32. doi:10.2174/1573399818666220128124043.
  39. ↑ Irvine, W.J; Gray, R.S; Mccallum, C.J; Duncan, L.J.P (1977-05-14). "CLINICAL AND PATHOGENIC SIGNIFICANCE OF PANCREATIC-ISLET-CELL ANTIBODIES IN DIABETICS TREATED WITH ORAL HYPOGLYCÆMIC AGENTS". The Lancet. 309 (8020): 1025–1027. doi:10.1016/s0140-6736(77)91258-2. ISSN 0140-6736.
  40. ↑ Lundholm, Michelle D.; Zhou, Keren (2025-12-01). "Latent autoimmune diabetes in adults: Not type 1, not type 2, a little of both". Cleveland Clinic Journal of Medicine. 92 (12): 757–763. doi:10.3949/ccjm.92a.25069. ISSN 0891-1150. PMID 41326180.
  41. ↑ Buzzetti, Raffaella; Zampetti, Simona; Maddaloni, Ernesto (2017-09-08). "Adult-onset autoimmune diabetes: current knowledge and implications for management". Nature Reviews Endocrinology. 13 (11): 674–686. doi:10.1038/nrendo.2017.99. ISSN 1759-5037.
  42. ↑ Naylor, Rochelle; Knight Johnson, Amy; del Gaudio, Daniela (1993), Adam, Margaret P.; Bick, Sarah; Mirzaa, Ghayda M.; Pagon, Roberta A. (eds.), "Maturity-Onset Diabetes of the Young Overview", GeneReviews®, Seattle (WA): University of Washington, Seattle, PMID 29792621, retrieved 2026-03-24
  43. ↑ Yin, Wenfeng; Luo, Shuoming; Xiao, Zilin; Zhang, Ziwei; Liu, Bingwen; Zhou, Zhiguang (2022-08-05). "Latent autoimmune diabetes in adults: a focus on β-cell protection and therapy". Frontiers in Endocrinology. 13. doi:10.3389/fendo.2022.959011. ISSN 1664-2392. PMC 9389314. PMID 35992113.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  44. ↑ Oikonomou, Evangelos K.; Khera, Rohan (2023-09-25). "Machine learning in precision diabetes care and cardiovascular risk prediction". Cardiovascular Diabetology. 22 (1): 259. doi:10.1186/s12933-023-01985-3. ISSN 1475-2840. PMC 10521578. PMID 37749579.{{cite journal}}: CS1 maint: unflagged free DOI (link)
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