ETIOLOGICAL FACTORS AND TREATMENT PRINCIPLES OF DIABETES MELLITUS

Annotasiya

Diabetes mellitus (DM) is a long-standing, complicated, and non-transmissible endocrine ailment that is growing rapidly and has posed clinical challenges globally, often linked with threats related to complicated metabolic development in patients. It is marked by elevated glucose and lipids in the blood as well as oxidative stress, which culminate in chronic complications involving diverse organs, mainly the kidneys, eyes, nerves, and blood vessels, among others, in the body. The article provides a comprehensive overview of the underlying causes and management strategies of diabetes mellitus. It explores both genetic and environmental factors contributing to the development of type 1 and type 2 diabetes, including autoimmune processes, insulin resistance, obesity, and lifestyle influences. The article also outlines current treatment principles, emphasizing individualized care that integrates lifestyle modifications, pharmacological interventions, and patient education. Special attention is given to the role of emerging therapies and the importance of glycemic control in preventing complications. This article is valuable for healthcare professionals and students seeking a foundational understanding of diabetes etiology and evidence-based management.

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Panjiyev, J. (2025). ETIOLOGICAL FACTORS AND TREATMENT PRINCIPLES OF DIABETES MELLITUS. Zamonaviy Fan Va Tadqiqotlar, 4(4). Retrieved from https://inlibrary.uz/index.php/science-research/article/view/82759
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Annotasiya

Diabetes mellitus (DM) is a long-standing, complicated, and non-transmissible endocrine ailment that is growing rapidly and has posed clinical challenges globally, often linked with threats related to complicated metabolic development in patients. It is marked by elevated glucose and lipids in the blood as well as oxidative stress, which culminate in chronic complications involving diverse organs, mainly the kidneys, eyes, nerves, and blood vessels, among others, in the body. The article provides a comprehensive overview of the underlying causes and management strategies of diabetes mellitus. It explores both genetic and environmental factors contributing to the development of type 1 and type 2 diabetes, including autoimmune processes, insulin resistance, obesity, and lifestyle influences. The article also outlines current treatment principles, emphasizing individualized care that integrates lifestyle modifications, pharmacological interventions, and patient education. Special attention is given to the role of emerging therapies and the importance of glycemic control in preventing complications. This article is valuable for healthcare professionals and students seeking a foundational understanding of diabetes etiology and evidence-based management.


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ETIOLOGICAL FACTORS AND TREATMENT PRINCIPLES OF DIABETES

MELLITUS

Panjiyev Jonibek Abdumajidovich

Department of Fundamental Medical Sciences of the Asian International University.

Bukhara, Uzbekistan.

https://doi.org/10.5281/zenodo.15284271

Abstract.

Diabetes mellitus (DM) is a long-standing, complicated, and non-transmissible

endocrine ailment that is growing rapidly and has posed clinical challenges globally, often

linked with threats related to complicated metabolic development in patients. It is marked by

elevated glucose and lipids in the blood as well as oxidative stress, which culminate in chronic

complications involving diverse organs, mainly the kidneys, eyes, nerves, and blood vessels,

among others, in the div. The article provides a comprehensive overview of the underlying

causes and management strategies of diabetes mellitus. It explores both genetic and

environmental factors contributing to the development of type 1 and type 2 diabetes, including

autoimmune processes, insulin resistance, obesity, and lifestyle influences. The article also

outlines current treatment principles, emphasizing individualized care that integrates lifestyle

modifications, pharmacological interventions, and patient education. Special attention is given

to the role of emerging therapies and the importance of glycemic control in preventing

complications. This article is valuable for healthcare professionals and students seeking a

foundational understanding of diabetes etiology and evidence-based management.

Keywords:

hyperglycemia, Diabetes mellitus, insulin, MODY, insulin resistance.

ЭТИОЛОГИЧЕСКИЕ ФАКТОРЫ И ПРИНЦИПЫ ЛЕЧЕНИЯ САХАРНОГО

ДИАБЕТА

Аннотация.

Сахарный диабет (СД) — это хроническое, сложное и

неинфекционное эндокринное заболевание, которое быстро распространяется и

представляет собой клиническую проблему во всём мире. Оно часто связано с рисками,

обусловленными сложными метаболическими нарушениями у пациентов. Заболевание

характеризуется повышенным уровнем глюкозы и липидов в крови, а также

оксидативным стрессом, что приводит к хроническим осложнениям со стороны

различных органов, в первую очередь почек, глаз, нервной системы и кровеносных сосудов.

Статья предоставляет всесторонний обзор причин возникновения и стратегий

лечения сахарного диабета. Рассматриваются как генетические, так и экологические

факторы, способствующие развитию диабета 1 и 2 типа, включая аутоиммунные

процессы, инсулинорезистентность, ожирение и образ жизни. Также изложены

современные принципы лечения с акцентом на индивидуальный подход, включающий


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изменение образа жизни, медикаментозную терапию и обучение пациентов. Особое

внимание уделено новым методам лечения и значению контроля уровня глюкозы в крови

для предотвращения осложнений. Данная статья будет полезна медицинским

специалистам и студентам, стремящимся получить базовые знания об этиологии

сахарного диабета и его лечении, основанном на доказательной медицине.

Ключевые

слова:

гипергликемия,

сахарный

диабет,

инсулин,

MODY,

инсулинорезистентность

Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the

phenotype of hyperglycemia. Several distinct types of DM are caused by a complex interaction

of genetics and environmental factors. Depending on the etiology of the DM, factors contributing

to hyperglycemia include reduced insulin secretion, decreased glucose utilization, and increased

glucose production. The metabolic dysregulation associated with DM causes secondary

pathophysiologic changes in multiple organ systems that impose a tremendous burden on the

individual with diabetes and on the health care system. It also predisposes to cardiovascular

diseases. With an increasing incidence worldwide, DM will be a leading cause of morbidity and

mortality for the foreseeable future. As reported by World Health Organization (WHO), DM is

an outbreak prone to high malaise and death. Globally, approximately 387 million persons are

affected by this disorder and it is estimated to be more than 640 million by 2040.

Etiologic Classification of Diabetes Mellitus:

I. Type 1 diabetes (beta cell destruction, usually leading to absolute insulin deficiency)

A. Immune mediated

B. Idiopathic

II. Type 2 diabetes (may range from predominantly insulin resistance with relative insulin

deficiency to a predominantly insulin secretory defect with insulin resistance)

III. Other specific types of diabetes

A. Genetic defects of beta cell function characterized by mutations in

1. Hepatocyte nuclear transcription factor (HNF) 4α (MODY 1)

2. Glucokinase (MODY 2)

3. HNF-1α (MODY 3)

4. Insulin promoter factor-1 (IPF-1; MODY 4)

5. HNF-1β (MODY 5)

6. NeuroD1 (MODY 6)

7. Mitochondrial DNA

8. Subunits of ATP-sensitive potassium channel


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9. Proinsulin or insulin

B. Genetic defects in insulin action

1. Type A insulin resistance

2. Leprechaunism

3. Rabson-Mendenhall syndrome

4. Lipodystrophy syndromes

C. Diseases of the exocrine pancreas—pancreatitis, pancreatectomy, neoplasia, cystic

fibrosis, hemochromatosis, fibrocalculous pancreatopathy, mutations in carboxyl ester lipase

D.

Endocrinopathies

acromegaly,

Cushing’s

syndrome,

glucagonoma,

pheochromocytoma, hyperthyroidism, somatostatinoma, aldosteronoma

E. Drug or chemical induced—glucocorticoids, vacor (a rodenticide), pentamidine,

nicotinic acid, diazoxide, β-adrenergic agonists, thiazides, hydantoins, asparaginase, α-

interferon, protease inhibitors, antipsychotics (atypicals and others), epinephrine.

F. Infections—congenital rubella, cytomegalovirus, coxsackievirus.

G. Uncommon forms of immune-mediated diabetes-“stiff-person” syndrome, anti-insulin

receptor antibodies.

H. Other genetic syndromes sometimes associated with diabetes-Wolfram’s syndrome,

Down’s syndrome, Klinefelter’s syndrome, Turner’s syndrome, Friedreich’s ataxia,

Huntington’s chorea, Laurence-Moon-Biedl syndrome, myotonic dystrophy, porphyria, Prader-

Willi syndrome

IV. Gestational diabetes mellitus (GDM)

Other Types of DM:

Other etiologies for DM include specific genetic defects in insulin secretion or action,

metabolic abnormalities that impair insulin secretion, mitochondrial abnormalities, and a host of

conditions that impair glucose tolerance (Table 19-1). Maturity-onset diabetes of the young

(MODY) is a subtype of DM characterized by autosomal dominant inheritance, early onset of

hyperglycemia (usually>25 years), and impairment in insulin secretion (discussed below).

Mutations in the insulin receptor cause a group of rare disorders characterized by severe

insulin resistance. DM can result from pancreatic exocrine disease when the majority of

pancreatic islets are destroyed. Cystic fibrosis–related DM is an important consideration in this

patient population.

Hormones that antagonize insulin action can also lead to DM. Thus, DM is often a feature

of endocrinopathies such as acromegaly and Cushing’s disease. Viral infections have been

implicated in pancreatic islet destruction but are an extremely rare cause of DM.


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A form of acute onset of type 1 diabetes, termed fulminant diabetes, has been noted in

Japan and may be related to viral infection of islets.

In addition, There are several risk factors associated with diabetes. These risk factors

contribute significantly to the progression of diabetes. They include but not limited to age;

weight; family history of diabetes; smoking and race/ethnicity (Asiimwe et al., 2020; Noh et al.,

2018). While T1DM is mostly found in the young, T2DM is an adult-related condition. The risk

of T2DM increases with age which is due to the deficiency of insulin secretion which develops

with age, and growing insulin resistance caused by a change in div composition. Increase in

div weight which leads to obesity is closely associated with diabetes in a condition termed

diabesity.

This is because increase in div weight leads to increased insulin resistance.

According to the FDA, smokers are 30 to 40% more likely to come down with T2DM

than nonsmokers. Smoking can also increase insulin resistance which makes the patients require

more insulin for the control of their sugar level [19]. Diabetes is hereditary. Those with the

family history are advised to adhere to lifestyles that reduce the risk of developing diabetes.

Treatment:

The treatment principles of diabetes mellitus (DM) aim to achieve and maintain optimal

blood glucose levels, prevent complications, and enhance the quality of life. The approach

depends on the type of diabetes and the individual patient’s needs. Below are the core principles:

1. Lifestyle Modifications

Dietary Management:

-Emphasize a balanced diet with controlled carbohydrate intake.

-Focus on high-fiber foods, lean proteins, healthy fats, and low glycemic index foods.

-Avoid sugary beverages and processed foods.

Physical Activity:

-Regular exercise (e.g., 150 minutes of moderate aerobic activity per week) improves

insulin sensitivity and helps manage weight.

Weight Management:

-Encourage weight loss in overweight or obese patients to improve glycemic control.

2. Pharmacologic Therapy

Type 1 Diabetes Mellitus (T1DM):

Insulin therapy is mandatory:

-Basal-bolus insulin regimen or insulin pumps.

-Regular monitoring of blood glucose levels.

Type 2 Diabetes Mellitus (T2DM):


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Oral or injectable antihyperglycemic agents are often the first-line therapy:

-Metformin: First-line medication for most patients.

-Other options: SGLT2 inhibitors, GLP-1 receptor agonists, DPP-4 inhibitors, or

sulfonylureas.

-Insulin therapy may be required in advanced stages or during acute illness.

Gestational Diabetes:

-Lifestyle changes and, if needed, insulin or metformin.

3. Monitoring and Glycemic Targets

Self-Monitoring of Blood Glucose (SMBG):

-Frequent monitoring to assess glucose control, especially for those on insulin.

HbA1c Testing:

-Target levels: <7% for most patients, but individualized based on age, comorbidities, and

risk of hypoglycemia.

Continuous glucose monitoring (CGM) may be beneficial for some patients.

4. Management of Comorbidities

Hypertension: ACE inhibitors or ARBs are commonly used.

Dyslipidemia: Statins are often recommended.

Obesity: GLP-1 receptor agonists or bariatric surgery in selected cases.

Prevention of Complications:

-Regular screening for retinopathy, nephropathy, and neuropathy.

-Foot care to prevent ulcers and infections.

5. Patient Education and Support

Provide comprehensive education on disease management.

Psychological support to address stress, anxiety, or depression.

Encourage active participation in care and goal setting.

6. Prevention of Acute and Chronic Complications

Acute Complications:

-Prevent hypoglycemia with proper dosing and meal planning.

-Manage diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS)

promptly.

Chronic Complications:

-Control glucose, blood pressure, and lipids to reduce risks of cardiovascular disease,

kidney disease, and nerve damage.

7. Regular Follow-Up


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Routine visits to monitor progress, adjust treatment plans, and address new issues.

Coordination with a multidisciplinary team, including endocrinologists, dietitians, and

diabetes educators.

Effective diabetes management relies on a tailored approach that considers the patient’s

age, type of diabetes, lifestyle, comorbid conditions, and preferences.

Conclusion:

Diabetes mellitus remains a major global health concern with multifactorial

etiology and complex pathophysiology. Understanding the diverse causes—from genetic

predispositions to lifestyle and environmental triggers—is essential for effective prevention and

early diagnosis. While treatment strategies continue to evolve, a patient-centered approach that

combines lifestyle modifications, pharmacological therapy, and continuous monitoring remains

the cornerstone of management. Advances in research and technology hold promise for more

personalized and effective interventions, but prevention through public awareness and early

intervention remains key. A comprehensive understanding of both the etiological factors and

treatment principles is critical for reducing the burden of diabetes and improving long-term

outcomes.

REFERENCES

1.

Rajaei E, Jalali MT, Shahrabi S, Asnafi AA, Pezeshki SMS. HLAs in Autoimmune

Diseases: Dependable Diagnostic Biomarkers? Curr Rheumatol Rev. 2019;15(4):269-

276. [

PubMed

]

2.

Klein BE, Klein R, Moss SE, Cruickshanks KJ. Parental history of diabetes in a

population-based study. Diabetes Care. 1996 Aug;19(8):827-30. [

PubMed

]

3.

Barnett AH, Eff C, Leslie RD, Pyke DA. Diabetes in identical twins. A study of 200

pairs. Diabetologia. 1981 Feb;20(2):87-93. [

PubMed

]

4.

Diabetes Genetics Initiative of Broad Institute of Harvard and MIT, Lund University, and

Novartis Institutes of BioMedical Research. Saxena R, Voight BF, Lyssenko V, Burtt NP,

de Bakker PI, Chen H, Roix JJ, Kathiresan S, Hirschhorn JN, Daly MJ, Hughes TE,

Groop L, Altshuler D, Almgren P, Florez JC, Meyer J, Ardlie K, Bengtsson Boström K,

Isomaa B, Lettre G, Lindblad U, Lyon HN, Melander O, Newton-Cheh C, Nilsson P,

Orho-Melander M, Råstam L, Speliotes EK, Taskinen MR, Tuomi T, Guiducci C,

Berglund A, Carlson J, Gianniny L, Hackett R, Hall L, Holmkvist J, Laurila E, Sjögren M,

Sterner M, Surti A, Svensson M, Svensson M, Tewhey R, Blumenstiel B, Parkin M,

Defelice M, Barry R, Brodeur W, Camarata J, Chia N, Fava M, Gibbons J, Handsaker B,

Healy C, Nguyen K, Gates C, Sougnez C, Gage D, Nizzari M, Gabriel SB, Chirn GW, Ma

Q, Parikh H, Richardson D, Ricke D, Purcell S. Genome-wide association analysis


background image

1794

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identifies loci for type 2 diabetes and triglyceride levels. Science. 2007 Jun

01;316(5829):1331-6. [

PubMed

]

5.

Fajans SS, Bell GI, Polonsky KS. Molecular mechanisms and clinical pathophysiology of

maturity-onset diabetes of the young. N Engl J Med. 2001 Sep 27;345(13):971-

80. [

PubMed

]

6.

Felner EI, Klitz W, Ham M, Lazaro AM, Stastny P, Dupont B, White PC. Genetic

interaction among three genomic regions creates distinct contributions to early- and late-

onset type 1 diabetes mellitus. Pediatr Diabetes. 2005 Dec;6(4):213-20. [

PubMed

]

7.

Writing Group for the SEARCH for Diabetes in Youth Study Group. Dabelea D, Bell RA,

D'Agostino RB, Imperatore G, Johansen JM, Linder B, Liu LL, Loots B, Marcovina S,

Mayer-Davis EJ, Pettitt DJ, Waitzfelder B. Incidence of diabetes in youth in the United

States. JAMA. 2007 Jun 27;297(24):2716-24. [

PubMed

]

8.

Patterson CC, Dahlquist GG, Gyürüs E, Green A, Soltész G., EURODIAB Study Group.

Incidence trends for childhood type 1 diabetes in Europe during 1989-2003 and predicted

new cases 2005-20: a multicentre prospective registration study. Lancet. 2009 Jun

13;373(9680):2027-33. [

PubMed

]

9.

Zheng Y, Ley SH, Hu FB. Global aetiology and epidemiology of type 2 diabetes mellitus

and its complications. Nat Rev Endocrinol. 2018 Feb;14(2):88-98. [

PubMed

]

10.

American Diabetes Association. Standards of medical care in diabetes--2012. Diabetes

Care. 2012 Jan;35 Suppl 1(Suppl 1):S11-63. [

PMC free article

] [

PubMed

]

11.

Karagiannis T, Bekiari E, Manolopoulos K, Paletas K, Tsapas A. Gestational diabetes

mellitus: why screen and how to diagnose. Hippokratia. 2010 Jul;14(3):151-4. [

PMC free

article

] [

PubMed

]

12.

Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA,

Nathan DM., Diabetes Prevention Program Research Group. Reduction in the incidence of

type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002 Feb

07;346(6):393-403. [

PMC free article

] [

PubMed

]

Bibliografik manbalar

Rajaei E, Jalali MT, Shahrabi S, Asnafi AA, Pezeshki SMS. HLAs in Autoimmune Diseases: Dependable Diagnostic Biomarkers? Curr Rheumatol Rev. 2019;15(4):269-276. [PubMed]

Klein BE, Klein R, Moss SE, Cruickshanks KJ. Parental history of diabetes in a population-based study. Diabetes Care. 1996 Aug;19(8):827-30. [PubMed]

Barnett AH, Eff C, Leslie RD, Pyke DA. Diabetes in identical twins. A study of 200 pairs. Diabetologia. 1981 Feb;20(2):87-93. [PubMed]

Diabetes Genetics Initiative of Broad Institute of Harvard and MIT, Lund University, and Novartis Institutes of BioMedical Research. Saxena R, Voight BF, Lyssenko V, Burtt NP, de Bakker PI, Chen H, Roix JJ, Kathiresan S, Hirschhorn JN, Daly MJ, Hughes TE, Groop L, Altshuler D, Almgren P, Florez JC, Meyer J, Ardlie K, Bengtsson Boström K, Isomaa B, Lettre G, Lindblad U, Lyon HN, Melander O, Newton-Cheh C, Nilsson P, Orho-Melander M, Råstam L, Speliotes EK, Taskinen MR, Tuomi T, Guiducci C, Berglund A, Carlson J, Gianniny L, Hackett R, Hall L, Holmkvist J, Laurila E, Sjögren M, Sterner M, Surti A, Svensson M, Svensson M, Tewhey R, Blumenstiel B, Parkin M, Defelice M, Barry R, Brodeur W, Camarata J, Chia N, Fava M, Gibbons J, Handsaker B, Healy C, Nguyen K, Gates C, Sougnez C, Gage D, Nizzari M, Gabriel SB, Chirn GW, Ma Q, Parikh H, Richardson D, Ricke D, Purcell S. Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels. Science. 2007 Jun 01;316(5829):1331-6. [PubMed]

Fajans SS, Bell GI, Polonsky KS. Molecular mechanisms and clinical pathophysiology of maturity-onset diabetes of the young. N Engl J Med. 2001 Sep 27;345(13):971-80. [PubMed]

Felner EI, Klitz W, Ham M, Lazaro AM, Stastny P, Dupont B, White PC. Genetic interaction among three genomic regions creates distinct contributions to early- and late-onset type 1 diabetes mellitus. Pediatr Diabetes. 2005 Dec;6(4):213-20. [PubMed]

Writing Group for the SEARCH for Diabetes in Youth Study Group. Dabelea D, Bell RA, D'Agostino RB, Imperatore G, Johansen JM, Linder B, Liu LL, Loots B, Marcovina S, Mayer-Davis EJ, Pettitt DJ, Waitzfelder B. Incidence of diabetes in youth in the United States. JAMA. 2007 Jun 27;297(24):2716-24. [PubMed]

Patterson CC, Dahlquist GG, Gyürüs E, Green A, Soltész G., EURODIAB Study Group. Incidence trends for childhood type 1 diabetes in Europe during 1989-2003 and predicted new cases 2005-20: a multicentre prospective registration study. Lancet. 2009 Jun 13;373(9680):2027-33. [PubMed]

Zheng Y, Ley SH, Hu FB. Global aetiology and epidemiology of type 2 diabetes mellitus and its complications. Nat Rev Endocrinol. 2018 Feb;14(2):88-98. [PubMed]

American Diabetes Association. Standards of medical care in diabetes--2012. Diabetes Care. 2012 Jan;35 Suppl 1(Suppl 1):S11-63. [PMC free article] [PubMed]

Karagiannis T, Bekiari E, Manolopoulos K, Paletas K, Tsapas A. Gestational diabetes mellitus: why screen and how to diagnose. Hippokratia. 2010 Jul;14(3):151-4. [PMC free article] [PubMed]

Knowler WC, Barrett-Connor E, Fowler SE, Hamman RF, Lachin JM, Walker EA, Nathan DM., Diabetes Prevention Program Research Group. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002 Feb 07;346(6):393-403. [PMC free article] [PubMed]