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Type 5 diabetes: Recognizing a distinct form of malnutrition-related diabetes in the global health landscape
*Corresponding author: Rahul Garg, Department of Medicine, F H Medical College, Agra, Uttar Pradesh, India. gargrahul27@gmail.com
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Received: ,
Accepted: ,
How to cite this article: Garg R. Type 5 diabetes: Recognizing a distinct form of malnutrition-related diabetes in the global health landscape. Glob J Health Sci Res. 2025;3:71-9. doi: 10.25259/GJHSR_45_2025
Abstract
Diabetes mellitus encompasses a heterogeneous group of metabolic disorders characterized by chronic hyperglycemia. While types 1 and 2 diabetes are well-established, emerging evidence supports the recognition of distinct forms that do not fit these traditional classifications. This comprehensive review examines type 5 diabetes, officially recognized in 2025, which affects an estimated 20–25 million people worldwide, primarily young males with low body mass index in low- and middle-income countries. Unlike other forms of diabetes, type 5 is characterized by insulin secretory defects rather than insulin resistance, preserved but diminished C-peptide response, absence of autoimmune markers, and resistance to ketosis despite significant hyperglycemia. Recent metabolic studies have confirmed its unique pathophysiological profile, demonstrating that affected individuals are relatively insulin sensitive despite high insulin requirements. Evidence suggests type 5 diabetes stems from impaired pancreatic development due to early life malnutrition, highlighting important connections between developmental programming and adult metabolic health. This review synthesizes current knowledge on epidemiology, pathophysiology, clinical presentation, diagnostic approaches, and management strategies for type 5 diabetes while identifying crucial research gaps and public health implications. Recognition of type 5 diabetes as a distinct entity represents a significant advancement in understanding the diverse spectrum of diabetes and has important implications for clinical practice and health policy in regions where this condition is prevalent.
Keywords
Ketosis-resistant diabetes
Low body mass index diabetes
Malnutrition-related diabetes
Type 1 diabetes
Type 2 diabetes
Type 5 diabetes
INTRODUCTION AND HISTORICAL CONTEXT
Type 5 diabetes, also known as malnutrition-related diabetes, represents a significant yet historically underrecognized form of diabetes affecting millions of individuals worldwide, primarily in low- and middle-income countries (LMICs). After decades of being observed but inadequately classified, it was officially designated as “type 5 diabetes” in 2025 by the International Diabetes Federation (IDF) World Diabetes Congress in Bangkok, Thailand.[1]
Diabetes mellitus represents one of the most significant global health challenges of the 21st century, affecting an estimated 589 million adults worldwide, with projections suggesting this number will rise to 853 million by 2050.[2] While the traditional classification of diabetes into types 1 and 2 has provided a useful framework for understanding and treating this condition, it has become increasingly apparent that this binary classification fails to capture the full spectrum of diabetic disorders observed globally.
Malnutrition-related diabetes was first described in Jamaica in 1955 by Hugh-Jones, who encountered a group of patients with diabetes that did not fit the classic descriptions of what we now know as type 1 or type 2 diabetes.[3] Over the following decades, similar cases were documented in various LMICs, including Bangladesh, Nigeria, India, Ethiopia, Korea, Thailand, and Uganda.[4-10]
The World Health Organization (WHO) formally recognized this condition in 1985 as “malnutrition-related diabetes mellitus” (MRDM).[11] However, due to the perceived lack of meaningful evidence demonstrating that malnutrition or protein deficiency directly causes diabetes, the WHO withdrew this category from the classification of diabetes in 1999.[12] This decision left patients with this distinct form of diabetes without a proper diagnostic classification, often leading to inappropriate treatment strategies.
Despite this reclassification, epidemiological data continued to support the existence of this distinct form of diabetes. Estimates of MRDM among patients with diabetes ranged from 5% to 21.4% after excluding those with visible pancreatic pathology.[13-16] In a systematic review of atypical forms of diabetes, Bavuma et al. noted that the prevalence of type 1 diabetes might be overstated among underweight individuals from LMICs, whose clinical features were congruous with the original definition of MRDM.[17] This suggested that many such individuals may be inaccurately treated and highlighted the need for further investigation to characterize diabetes in low-resource settings.
With an estimated 20–25 million affected individuals worldwide, primarily in regions such as South-East Asia and Africa, understanding the distinct nature of type 5 diabetes is crucial for developing appropriate treatment strategies, allocating healthcare resources effectively, and implementing targeted prevention programs.[1]
The IDF Diabetes Atlas 11th edition (2025) highlights the particularly concerning diabetes situation in Southeast Asia, where 107 million adults (1 in 10) are living with diabetes, with India accounting for 1 in 7 of all adults living with diabetes worldwide. The number of adults living with diabetes in this region is predicted to increase by 73% to 185 million by 2050. While most of these cases represent type 2 diabetes, a significant proportion is believed to be type 5 diabetes, particularly among lean individuals.[18]
This review examines the historical context, epidemiology, pathophysiology, clinical features, diagnosis, and management of type 5 diabetes, with particular emphasis on its unique metabolic profile that distinguishes it from other forms of diabetes. By synthesizing current knowledge, we seek to increase awareness among healthcare professionals, researchers, and policymakers, particularly in regions where the condition is prevalent but often unrecognized or misclassified.
PATHOPHYSIOLOGY
The classification known as type 5 diabetes represents a distinct metabolic condition characterized by significant insulin secretory deficiency and suboptimal glycemic regulation. This form differs considerably from type 2 diabetes in that its primary etiology appears linked to sustained nutritional inadequacy, particularly during developmental periods of childhood and adolescence. In contrast, type 1 diabetes develops through autoimmune processes targeting insulin-secreting cells, while type 2 diabetes manifests primarily as ineffective utilization of produced insulin. Type 5 diabetes stands apart with its unique pathogenesis, theorized to involve compromised pancreatic development resulting from extended periods of nutritional insufficiency.[1]
Landmark research using state-of-the-art metabolic studies has confirmed its unique metabolic profile.[19]
Key pathophysiological features include:
Insulin secretory defect
Lontchi-Yimagou et al. found that individuals with low body mass index diabetes (LD) have a significantly lower total insulin secretory response compared to lean non-diabetic individuals and those with type 2 diabetes. The first-phase insulin secretion (0–15 min) is particularly blunted, indicating a primary defect in insulin secretion rather than insulin resistance. Beta-cell function is partially preserved, as insulin secretion is still higher than in type 1 diabetes.[19]
Preserved insulin sensitivity
Despite previous assumptions about insulin resistance based on high insulin requirements,[20] sophisticated clamp studies revealed that individuals with type 5 diabetes are relatively insulin sensitive. Endogenous glucose production (a measure of hepatic insulin resistance) is significantly lower in the LD group compared to the type 2 diabetes group. Glucose uptake, reflecting peripheral insulin sensitivity, is significantly higher in the LD group than in the type 2 diabetes group, even after adjustment for lean body mass.[19]
Distinctive body composition
Total lean body mass is significantly lower compared to individuals with type 1 diabetes, type 2 diabetes, and non-diabetic controls. While overall adiposity is low, these individuals show a higher visceral-to-subcutaneous adipose tissue ratio. Hepatocellular lipid content is significantly lower than in type 2 diabetes, consistent with the absence of fatty liver disease.[19]
Early life nutritional programming
This condition seems to be associated with maternal malnutrition, low birth weight, or childhood malnutrition.[21] Animal models show that maternal protein malnutrition leads to lower beta-cell mass and decreased beta-cell regeneration capacity in offspring.[22] Human studies found that small-forgestational-age neonates have smaller fractions of islet cells and less pancreatic vasculature.[21] Early-life malnutrition appears to cause permanent structural and functional changes in the pancreas and adipose tissue distribution.[23]
Figure 1 illustrates the developmental programming pathway leading to type 5 diabetes, highlighting how nutritional deficiencies from pregnancy through childhood can alter metabolism and ultimately manifest as type 5 diabetes in young adulthood.
- Developmental programming pathway of type 5 diabetes. Developmental trajectory showing how early life malnutrition leads to metabolic alterations and ultimately type 5 diabetes in young adulthood. BMI: Body mass index.
CLINICAL FEATURES
Type 5 diabetes has several distinctive clinical features that differentiate it from other types of diabetes: [1,13,15,19,24]
Demographic and anthropometric profile
History of malnutrition in early childhood or in utero
Persistence of low body mass index (BMI) (typically <19 kg/m2) in adulthood
Early onset of diabetes (age <30 years)
Predominantly male prevalence (approximately 85%)
More common in lower socioeconomic groups and rural populations
Higher waist-to-hip ratios compared to BMI-matched control subjects without diabetes.
Clinical presentation
Absence of ketonuria or ketosis despite uncontrolled blood glucose levels (fasting plasma glucose >200 mg/dL)
High insulin requirements (>60 IU/day or 2.0 units/kg/day)
Increased risk of diabetes complications
Often misdiagnosed as type 1 diabetes, though without developing ketosis despite high blood glucose.
Laboratory findings
Preserved C-peptide response (>0.5 ng/mL) to standard mixed-meal tolerance test
Negative for glutamic acid decarboxylase 65 (GAD-65) and islet antigen-2 (IA-2) antibodies (autoimmune markers typical in type 1 diabetes)
No significant micro- or macrovascular complications at diagnosis
Negative for mutations in candidate genes for MODY and lipodystrophy
Lower blood corpuscular volume and hemoglobin levels
Higher triglyceride levels compared to lean subjects without diabetes
Significantly lower protein and calcium levels compared to lean non-diabetic individuals.
Table 1 summarizes the key differences between type 1, type 2, and type 5 diabetes, highlighting the unique clinical and pathophysiological characteristics of each type.
| Characteristic | Type 1 diabetes | Type 2 diabetes | Type 5 diabetes |
|---|---|---|---|
| Primary pathophysiology | Autoimmune destruction of beta cells | Insulin resistance with progressive beta cell dysfunction | Insulin secretory defect due to malnutrition |
| Age of onset | Usually childhood/adolescence | Usually over 30 years | Under 30 years |
| Body composition | Usually normal weight | Often overweight/obese | Low BMI (<19 kg/m2) |
| Gender predilection | Equal gender distribution | Equal gender distribution | Predominantly male (85%) |
| Endogenous insulin | Absent/very low | Present (initially) | Diminished but present |
| Autoimmune markers | Positive (GAD-65, IA-2, etc.) | Negative | Negative |
| C-peptide | Absent/Low | Normal/High | Reduced but present |
| Insulin sensitivity | Present | Reduced | Relatively preserved |
| Ketosis tendency | High | Low | Resistant despite hyperglycemia |
| Primary risk factors | Genetic susceptibility to environmental triggers | Obesity, sedentary lifestyle, obesity, age | Malnutrition in early life low birth weight |
| Primary treatment | Insulin replacement | Lifestyle modification, oral medications, insulin | Insulin or oral medications, nutritional rehabilitation |
GAD-65: Glutamic acid decarboxylase 65, IA-2: Islet antigen-2, BMI: Body mass index
DIAGNOSTIC APPROACH
The diagnosis of type 5 diabetes requires careful consideration of clinical characteristics, laboratory findings, and exclusion of other types of diabetes. The IDF working group is currently developing formal diagnostic criteria.[1]
To facilitate clinical implementation, particularly in resource-limited settings, I present a simplified diagnostic framework.
Essential clinical features (All must be present):
Low BMI (<19 kg/m2), age of onset <30 years, male gender (85% of cases), and absence of ketosis despite severe hyperglycemia (>200 mg/dL).
Supporting historical features:
History of malnutrition in early childhood or low birth weight, rural or low socioeconomic background, and no family history of diabetes.
Laboratory requirements:
Fasting plasma glucose >126 mg/dL or 2-hour glucose ≥200 mg/dL, detectable C-peptide levels (>0.5 ng/mL after stimulation), and negative autoimmune markers (GAD-65, IA-2 antibodies).
The diagnostic approach should be comprehensive, including detailed history taking, physical examination, laboratory investigations, and possibly genetic testing to exclude other forms of diabetes. Given the resource limitations in regions where type 5 diabetes is prevalent, the development of cost-effective diagnostic algorithms is essential. Figures 2 and 3 provide a diagnostic algorithm for differentiating type 5 diabetes from other forms of diabetes in well-resourced settings and low-resource settings, respectively.
- Diagnostic algorithm for type 5 diabetes in well-resourced settings. Clinical decision pathway for identifying type 5 diabetes, emphasizing age of onset, absence of autoantibodies, C-peptide levels, ketosis resistance, low BMI, and malnutrition history. BMI: Body mass index, GAD-65: Glutamic acid decarboxylase 65, IA-2: Islet antigen-2, MODY: Maturity-onset diabetes of the young.
- Diagnostic algorithm for type 5 diabetes in low-resource settings. Simplified clinical decision pathway for identifying type 5 diabetes in resource-limited settings, emphasizing readily available clinical criteria and basic laboratory tests when C-peptide testing is unavailable. BMI: Body mass index.
Lontchi-Yimagou et al. used rigorous criteria in their study, screening 272 individuals to identify 20 with low BMI diabetes who met the criteria. They excluded type 1 diabetes based on C-peptide responses, absence of ketoacidosis history, and negative autoantibody status. They also performed genetic screening to exclude MODY and lipodystrophy, finding that patients with low BMI diabetes were negative for pathogenic mutations in 13 genes for MODY and 6 genes for lipodystrophy.[19]
MANAGEMENT
The management of type 5 diabetes requires a tailored approach that addresses its unique pathophysiology. The current evidence suggests that these patients are insulin deficient but not insulin resistant, with implications for treatment strategies.[1,19] Treatment decisions should be stratified based on clinical features and available resources.
Group A: Candidates for oral medication
Patient profile
C-peptide >1.0 ng/mL (after stimulation)
Recent diagnosis (<2 years)
Absence of severe hyperglycemia (hemoglobin A1C [HbA1c] <10%)
No history of diabetic ketoacidosis.
Treatment strategy
-
First-line: Sulfonylureas (glimepiride 1–4 mg daily or gliclazide 30–120 mg daily)
Rationale: Addresses primary insulin secretory defect
Monitor for hypoglycemia, especially with food insecurity.
-
Second-line: Add metformin 500–1,000 mg twice daily
Provides additional glycemic benefit and potential cardiovascular protection.
Monitoring: Monthly glucose monitoring for the first 3 months, then quarterly.
Group B: Requires insulin therapy
Patient profile
C-peptide >0.5 ng/mL (after stimulation)
Severe hyperglycemia (HbA1c >10%)
Long-standing diabetes (>5 years)
Failed oral medication trial.
Treatment strategy
Initial: NPH insulin 0.3–0.5 units/kg/day, divided twice daily
Alternative: Long-acting insulin analogs if available
Adjustment: Increase by 10–20% weekly until target glucose achieved
Target: Fasting glucose 80–130 mg/dL, post-meal <180 mg/dL.
Group C: Combination therapy
Patient profile
C-peptide 0.5–1.0 ng/mL (after stimulation)
Partial response to oral medications
HbA1c 7–10% on oral therapy.
Treatment strategy
Continue oral medications
Add basal insulin 10–15 units daily or 0.1–0.2 units/kg
Titrate insulin based on fasting glucose levels.
Nutritional support
Immediate priorities
Protein intake: 1.0–1.2 g/kg body weight daily
Caloric adequacy: 25–30 kcal/kg for weight maintenance
Micronutrient supplementation: Iron, B vitamins, zinc.
Long-term strategy
Regular nutritional assessment every 6 months
Family-based dietary counseling
Community nutrition education programs.
IMPLEMENTATION BARRIERS AND SOLUTIONS
Key implementation challenges in LMICs
Diagnostic barriers
Challenge 1: Limited laboratory access
C-peptide testing unavailable in many rural settings
Autoantibody testing is expensive and rarely available
Solutions
Develop clinical scoring systems based on readily available parameters
Train healthcare workers on clinical recognition patterns
Establish regional reference laboratories for confirmation testing
Implement point-of-care C-peptide testing where feasible.
Challenge 2: Misdiagnosis as type 1 diabetes
Default insulin prescription for young, lean diabetics
Lack of awareness about type 5 diabetes among healthcare providers.
Solutions
Develop simplified diagnostic flowcharts for primary care
Implement continuing medical education programs
Create mobile health applications for diagnostic support
Establish telemedicine consultation networks.
Treatment barriers
Challenge 3: Insulin access and affordability
High cost of insulin relative to income
Cold chain storage requirements
Limited availability in rural areas.
Solutions
Prioritize oral medications where appropriate (reduces insulin demand by ~30–40%)
Negotiate bulk purchasing agreements for essential medicines
Develop insulin access programs for severe cases
Train patients and families on proper insulin storage and administration.
Challenge 4: Healthcare provider training
Limited knowledge of type 5 diabetes management
Unclear treatment protocols.
Solutions
Develop context-specific treatment guidelines
Create training modules for different healthcare levels
Establish mentor-mentee programs with diabetes specialists
Implement regular case-based learning sessions.
System-level barriers
Challenge 5: Healthcare infrastructure
Limited specialist availability
Inadequate follow-up systems
Poor integration between healthcare levels.
Solutions
Task-shifting to trained nurses and community health workers
Implement structured diabetes care protocols
Develop patient tracking and reminder systems
Create hub-and-spoke models with specialist support.
Resource-stratified implementation framework
Minimal resource settings
Focus on clinical diagnosis using simplified criteria
Prioritize sulfonylureas as first-line therapy
Implement basic nutritional counseling
Establish referral pathways for complex cases.
Moderate resource settings
Add C-peptide testing capability
Include metformin in treatment algorithms
Provide structured diabetes education
Implement basic complication screening.
Well-resourced settings
Full diagnostic capabilities including autoantibodies
Access to insulin analogs and advanced therapies
Comprehensive diabetes care teams
Regular monitoring and complication management.
Policy recommendations
Include type 5 diabetes in national diabetes guidelines
Ensure essential medications (sulfonylureas and metformin) are on essential medicine lists
Develop diabetes care pathways that recognize different diabetes types
Implement nutrition programs targeting vulnerable populations
Establish diabetes registries to track prevalence and outcomes.
Cost-effectiveness considerations
Appropriate diagnosis and treatment of type 5 diabetes can reduce healthcare costs by 25–40% compared to inappropriate insulin therapy
Early nutritional interventions may prevent development in high-risk children
Oral medication management reduces the need for specialized diabetes care
Community-based approaches can reach larger populations at a lower cost.
PUBLIC HEALTH IMPLICATIONS
The recognition of type 5 diabetes as a distinct entity has important public health implications, particularly for LMICs:
Disease burden
With an estimated 20–25 million affected individuals worldwide, type 5 diabetes contributes significantly to the global diabetes burden, particularly in South-East Asia and Africa.[1] The IDF Diabetes Atlas 11th edition (2025) indicates that in South-East Asia alone, 107 million adults have diabetes, with a projected increase to 185 million by 2050.[18]
Resource allocation
Understanding the unique nature of type 5 diabetes allows for more targeted allocation of healthcare resources, potentially reducing the unnecessary use of insulin in settings where it is scarce and expensive.
Prevention strategies
Recognition of the link between early life malnutrition and later development of type 5 diabetes emphasizes the importance of maternal and child nutrition programs as potential diabetes prevention strategies.
Health system adaptation
Healthcare systems in affected regions need to adapt to recognize and appropriately manage this form of diabetes, including training healthcare providers and developing context-appropriate guidelines.
FUTURE RESEARCH DIRECTIONS
Several important research questions remain to be addressed regarding type 5 diabetes:
Genetic factors
While environmental factors, particularly malnutrition, play a crucial role, genetic susceptibility factors have not been well characterized. Genome-wide association studies in affected populations could provide insights into genetic contributors.
Developmental programming
Further research into the mechanisms by which early-life malnutrition affects pancreatic development and function could identify potential intervention targets.
Treatment optimization
Clinical trials comparing different treatment strategies (oral medications versus insulin) are needed to develop evidence-based management guidelines.
Epidemiological studies
More comprehensive epidemiological studies are required to better understand the true prevalence, geographic distribution, and natural history of type 5 diabetes.
Prevention strategies
Research into effective prevention strategies, particularly focusing on maternal and child nutrition, could reduce the incidence of type 5 diabetes in vulnerable populations. The establishment of a global research registry by the IDF working group will be an important step in facilitating these research efforts.
CONCLUSION
The official recognition of type 5 diabetes represents a significant advancement in understanding the diverse spectrum of diabetes. This distinct form, affecting an estimated 20–25 million people worldwide, is characterized by insulin secretory defects rather than insulin resistance, and has strong associations with early-life malnutrition. Its unique pathophysiological profile has important implications for treatment approaches, suggesting some patients may be managed with oral medications rather than insulin. As diabetes prevalence continues to rise globally, particularly in LMICs, recognizing and appropriately managing type 5 diabetes become increasingly crucial. This highlights the lasting impact of early nutrition on lifelong metabolic health and the potential for preventive interventions.
Ethical approval:
Institutional Review Board approval is not required.
Declaration of patient consent:
Patient’s consent not required as there are no patients in this study.
Conflicts of interest:
There are no conflicts of interest.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The author confirms that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.
Financial support and sponsorship: Nil.
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