Diabetes mellitus MODY: symptoms and methods of treating pathology. What is MODY diabetes? Causes of appearance and possible complications

• MODY diabetes means Maturity-onset diabetes of the young.
• MODY diabetes is a monogenic form of diabetes characterized by
  • early onset
  • autosomal dominant type of inheritance,
  • is based on gene mutation,
    • causing disturbances in the functioning of the islet apparatus of the pancreas.
• The prevalence of MODY diabetes is less than 2% of all cases of diabetes,
  • usually misdiagnosed as type 1 or type 2 diabetes.
• MODY diabetes can only be diagnosed based on the results of a molecular genetic study.
• To date, there are 13 known types of MODY diabetes, to determine which it is necessary to detect mutations in certain genes.
• Correct genetic diagnosis is extremely important because:
  • different types of diabetes require different patient management tactics,
  • Predictive genetic testing of the patient's relatives without signs of diabetes is necessary.

INTRODUCTION

• MODY diabetes was first described by R. Tattersall in 1974 in three families as
  • mild diabetes,
  • with an autosomal dominant type of inheritance,
  • occurring in young people.
• In 1975, R. Tattersall and S. Fajans first introduced the acronym MODY to define mildly progressive diabetes in young people with a hereditary burden.
• It was not until the 1990s that advances in molecular genetics and the availability of large pedigrees helped in identifying the genes responsible for this form of diabetes.
• MODY diabetes is now well described in European and North American populations, but the prevalence in Asian populations is still unknown.

CLASSIFICATION AND PHENOTYPICAL FEATURES OF MODY DIABETES

Genetic heterogeneity of MODY

MODY diabetes is a monogenic form of diabetes that has

• genetic,
• metabolic
• clinical heterogeneity.

Genes currently known to be mutated to cause MODY diabetes:

1. Hepatocyte nuclear factor 4α gene ( HNF4A; MODY1),
2. Glucokinase gene ( GCK; MODY2),
3. Hepatocyte nuclear factor 1α gene ( HNF1A; MODY3),
4. Transcription factor gene PDX1 ( PDX1; MODY4),
5. Transcription factor 2 gene ( TCF2) or hepatocyte nuclear factor 1β ( HNF1B; MODY5),
6. Neurogenic differentiation factor 1 gene ( NEUROD 1; MODY6),
7. Kruppel-like factor gene 11 ( KLF11; MODY7),
8. Carboxyl ether lipase gene ( CEL; MODY8),
9. PAX4 gene ( PAX4; MODY9),
10. Insulin gene ( INS; MODY10),
11. B-lymphocyte kinase ( BLK; MODY11),
12. ATP-binding cassette, sub-family C ( CFTR/MRP), member 8 ( ABCC8; MODY12),
13. Gene KCNJ11(MODY13).

Currently, the 13 known genes do not explain all cases of diagnosed MODY diabetes, implying the presence of as yet unknown gene mutations.

The most common causes of MODY diabetes are mutations in genes:

• G.C.K— 32% of all cases of MODY diabetes in the UK,
• HNF1A - 52%,
• HNF4A— 10%,
• HNF1B - 6%.

In patients from Asian countries, the genes whose mutations lead to MODY diabetes are different:

• In Korea, only 10% of patients with MODY diabetes or early-onset type 2 diabetes mellitus (T2DM) had known MODY gene mutations ( HNF1A 5%, GCK 2.5%, and 2.5% HNF1B),
• in Japan and China - from 10% to 20%.
• This indicates the need to discover new genes whose defects may lead to MODY diabetes in Asian countries.

CLINICAL CHARACTERISTICS OF MODY DIABETES TYPES

GCK-MODY(MODY2)

Glucokinase is a glycolytic enzyme

• catalyzes the conversion of glucose to glucose-6-phosphate,
• controls glucose-mediated insulin release from β-cells.

GCK-MODY, the most common form (approximately 48%) among Caucasians.

• However, only a small proportion (<5%) из выявленных случаев диабета MODY в Корее и Китае были вызваны G.C.K-MODY.

The clinical picture appears as:

• moderate fasting hyperglycemia from birth (from 5.5 to 8.0 mmol/l, glycosylated hemoglobin in the range of 5.8% to 7.6%),
• slight deterioration with age,
• is asymptomatic - often first diagnosed during routine screening or during pregnancy,
• rarely leads to serious complications.

Patients with GCK-MODY do not require treatment outside of pregnancy because:

• hypoglycemic therapy is ineffective,
• there are no late complications.

During pregnancy, insulin therapy may be required to prevent excessive growth of the fetus.

HNF1A-MODY (MODY3)

Heterozygous mutations HNF1A lead to progressive β-cell dysfunction, leading to diabetes in early adult life:

• in 63% of carriers of this gene by the age of 25,
• almost 100% by age 55.

In carriers, glycosuria appears even before the manifestation of diabetes due to reduced renal reabsorption of glucose.

• Hyperglycemia can be severe
• worsens throughout life
• the risks of micro- and macrovascular complications are similar to type 1 diabetes mellitus (T1DM) and type 2 DM.

Careful glycemic control is necessary!

Patients with HNF1A-MODY are sensitive to therapy:

• sulfonylurea drugs (first-line therapy),
• Insulin may be required over time.

HNF4A-MODY (MODY1)

• The first type of diabetes described was MODY.
• HNF4A- a transcription factor found in the liver, intestines, kidneys and pancreas.
  • Participates in the regulation of genes necessary for glucose metabolism and transport.
• HNF4A mutations account for less than 10% of MODY cases in Europe, and more than 103 mutations in 173 families have been identified so far.
• Heterozygous HNF4A mutations lead to
  • significant fetal macrosomia due to increased insulin secretion,
  • development of neonatal hypoglycemia in the fetus.
• Characterized by the absence of glucosuri and low apolipoproteins (apoA11, apoCIII and apoB) HNF4A-MODY.
• Sulfonylureas are the first-line treatment for these patients.

PDX1-MODY (MODY4)

• PDX1 (insulin promoter factor 1 [ IPF1]) - transcription factor,
  • participates in the development of the pancreas and the expression of the insulin gene.
• A homozygous mutation can lead to permanent neonatal diabetes due to underdevelopment of the pancreas.
• Heterozygous mutations PDX1 lead to β-cell and MODY4 dysfunction.
• PDX1— MODY is a very rare cause of MODY diabetes.

HNF1B-MODY (MODY5)

• HNF1B encoded by the gene TCF2,
• expressed in the liver, kidneys, intestines, stomach, lungs, ovaries, β-cells of the pancreas and affects their embryonic development.
• Heterozygous mutation in HNF1B characterized by progressive nondiabetic nephropathy, pancreatic atrophy, and abnormal development of the genital organs.
• Birth weight can be significantly reduced by reducing insulin secretion.
• Half of those who carry the gene develop diabetes.
• Spontaneous De Novo mutations occur relatively frequently, so diagnosis is not always confirmed by family history.
• HNF1B-MODY phenotypes differ from HNF1A-MODY due to the fact that diabetes HNF1B-MODY is developing
  • due to insulin resistance,
  • and a defect in insulin secretion.
• Patients with HNF1B-MODY usually require early initiation of insulin therapy.

NEUROD1-MODY (MODY6)

• NEUROD1 — a transcription factor that regulates the differentiation of pancreatic β-cells and some neurons of the retina, inner ear, cerebellum and hippocampus.
• Heterozygous mutations NEUROD1 can lead to diabetes, both in childhood and in adulthood.
• Mutations in both alleles can lead to neonatal diabetes mellitus with
  • neurological disorders,
  • reduced learning ability.

KLF11-MODY (MODY7)

• KLF11— a transcription factor that regulates pancreatic organogenesis and the activity of insulin-producing β-cells of the adult pancreas.
• Two rare gene variants KLF11 were identified in three French families with early onset type 2 diabetes.

CEL-MODY (MODY8)

• CEL expressed in mammary glands and pancreatic acinar cells.
• Heterozygous mutations in the gene CEL lead to:
  • atrophy,
  • fibrosis,
  • pancreatic lipomatosis,
    • which in turn leads to exocrine and endocrine insufficiency and diabetes mellitus.

PAX4-MODY (MODY9)

• PAX4- transcription factor,
• participates in the differentiation of insulin-producing β-cells of the pancreas.
• When this gene is defective, diabetes mellitus often occurs with the development of ketoacidosis.

INS-MODY (MODY10)

• Mutations INS- a common cause of neonatal diabetes,
• but a rare cause of MODY diabetes in childhood or adulthood.
• Heterozygous INS mutations disrupt
  • proinsulin production,
  • may cause apoptosis of β-cells in the endoplasmic reticulum.
• Treatment usually begins with insulin, although some patients can manage with oral glucose-lowering medications.

BLK-MODY (MODY11)

• BLK- through transcription factors PDX1 and NKX6.1 stimulates the synthesis and secretion of insulin in the β-cells of the pancreas.
• Individuals with MODY11 have a higher prevalence of obesity than other MODY types.
• Currently mutations BLK identified in three families.

ABCC8-MODY (MODY12)

• ABCC8 encodes sulfonylurea receptor 1 ( SUR1) subunit of ATP-sensitive potassium channels (K-ATP) in pancreatic β-cells.
• Homo- and heterozygous mutations lead to the development of neonatal diabetes mellitus,
• heterozygous mutations can also cause MODY diabetes, clinically similar to HNF1A/4A-MODY.
• Careful molecular genetic diagnosis is necessary, as it determines the patient’s treatment tactics.
• It is recommended to start therapy with sulfonylurea drugs.

KCNJ11-MODY (MODY13)

• KCNJ11 encodes Kir6.2, part of the K-ATP channel.
• Homozygous mutations lead to neonatal diabetes,
• heterozygous mutations can lead to a wide variety of manifestations of diabetes mellitus.
  • Age at diagnosis ranges from 13 to 59 years.
• Treatment of these patients is carried out depending on the severity of the disease:
  • diet,
  • oral glucose-lowering therapy,
  • insulin.

MODY DIABETES STUDY IN KOREA.

• The prevalence of MODY in Korea is still unknown.
• In a study of a Korean population, only 10% of 40 cases of early-onset MODY diabetes or type 2 diabetes had known MODY gene mutations ( HNF1A 5%, GCK 2.5%, and HNF1B 2,5%).
• These results are similar to those from China and Japan.
• There is a need for studies of MODY diabetes in Asian countries to identify unknown mutations.

DIAGNOSTICS MODY

• The prevalence of MODY diabetes is 1% to 2% of all diabetes cases.
• A correct diagnosis determines the optimal treatment strategy.
  • Patients on insulin therapy due to misdiagnosis of type 1 diabetes
    • may be switched to oral hypoglycemic therapy (sulfonylureas) upon diagnosis HNF1A-MODY or HNF4A- MODY,
    • which will not only improve their quality of life, but also glycemic control.
• Genetic diagnosis of MODY can also affect a patient's prognosis.
  • Patients with mild hyperglycemia in adolescence and diagnosis GCK-MODY, HNF1A-MODY or T1DM requires a different approach to management and therapy.
• Family members of patients with MODY should undergo molecular genetic testing to determine carrier status and likelihood of developing the disease.

According to British diabetologists, 80% of patients with MODY were incorrectly diagnosed with T1DM and T2DM, which resulted in incorrect treatment tactics with a deterioration in the quality of life of patients.

This diagram depicts a diagnostic algorithm for conducting molecular genetic testing to detect MODY diabetes in young people with diabetes.

CONCLUSION

• MODY diabetes is a common cause of monogenic diabetes,
  • accounts for 1% to 2% of all cases of diabetes.
• Despite its low prevalence, identification of MODY genes is important in making a diagnosis.
• The varied clinical presentation of MODY diabetes is explained by genetic heterogeneity.
• Only timely diagnosis of MODY diabetes can ensure correct treatment and management of patients, as well as identification of gene mutations in relatives of patients.
• A nationwide MODY registry and systematic approach are needed to quickly diagnose and guide appropriate management of MODY diabetes.

Source:

1. Kim S-H. Maturity-Onset Diabetes of the Young: What Do Clinicians Need to Know? Diabetes & Metabolism Journal. 2015;39(6):468-477. doi:10.4093/dmj.2015.39.6.468.

One of the atypical forms of diabetes mellitus is Maturity Onset Diabetes of the Young or mature type diabetes in the young. This is a group of similar hereditary diseases that arise due to gene mutations and are not completely curable, only amenable to relief. The disease is characterized by dysfunction of the islet apparatus of the pancreas (PG), slow development, sluggish, asymptomatic and relatively mild course over a long period of time, a unique clinical picture, the severity of diagnosis and requires specific treatment.

Types of pathology

The disease is diagnosed in 5-7% of cases of the total number of people with different types of diabetes, most often manifests itself in children from 10 years of age, adolescents and young people up to 25 years of age, due to pathological changes in metabolism.

There are several types of the disease based on mutated genes. Pathological changes in genes lead to such an anomaly. Patients have different manifestations, the course of the disease, and a variety of therapeutic methods are used. The main types of diabetes mellitus are shown in the table:

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Why is it developing?

MODY diabetes has an autosomal dominant pattern of inheritance. The disease is transmitted in a descending manner in 50% of cases if the pathological gene turns out to be dominant. In this case, the gender of the child does not matter. If defective genes were found in 2 or more generations of the family, this is an increased risk factor for the occurrence of pathology in the child.

Causes of the disease:

• mutations of genes regulating the functioning of the islet apparatus of the pancreas;
• pathological changes in the insulin-secreting activity of endocrine beta cells of the pancreas caused by genetic predisposition.

Mutations occur in 1 of 13 genes, which determines the type of disease, its clinical picture and symptoms:

• HNF4A;
• ABCC8;
• HNF1B;
• KLF11;
• NEUROD1;
• HNF1A;
• KCNJ11;
• IPF1;
• Pax4.

Symptoms of MODI diabetes

Diabetes mellitus MODY type differs from the main forms of the disease in its clinical picture, course and symptoms. MODY diabetes is characterized by specific clinical manifestations, such as:

• maintaining a standard level of C-peptide in the blood;
• there is no need to increase the insulin dose for more than 1 year;
• periodic increase in blood sugar up to 8.0 mmol/l in young children, without any other symptoms;
• impaired carbohydrate tolerance;
• there is no connection with the HLA system;
• long remission period of the disease;
• maintaining normal compensation even with a slight injection of insulin;
• after the diagnosis of type 1 diabetes mellitus, there is no progression of the disease;
• beta cells are also absent;
• the presence of excess glucose in the urine, with its standard amount in the blood;
• absence of decompensation periods;
• adequate functioning of cells that produce glucose;
• ketoacidosis does not appear at presentation (first appearance);
• glycated hemoglobin remains at a level of no more than 8%;
• after diagnosis, type 2 diabetes mellitus is not accompanied by obesity and is diagnosed before the age of 25.

Symptoms of the pathology depend on the type of MODY diabetes and mainly occur at an advanced stage:

• frequent urination;
• systematically occurring dermatological problems;
• anemia;
• disturbances in the functioning of the nervous system;
• long-term non-healing wounds;
• blurry, unclear vision;
• pancreatic insufficiency;
• muscle weakness;
• weight change up or down;
• dehydration;
• problems with the cardiovascular system;
• convulsions;
• recurring yeast infections;
• constant thirst;
• diarrhea;
• kidney and liver dysfunction.

MODI diabetes is one of the most specific types of the presented condition. This form of pathology refers to Maturity Onset Diabetes of the Young, namely mature-type diabetes in young people. Exact data on the prevalence of the disease have not been established; approximately two to five percent of all patients with diabetes are concerned.

Main symptoms of MODI diabetes

The first clinical manifestations of MODY diabetes occur in children, adolescents and young adults. 50% of all cases are identified in girls during pregnancy, namely in the form of gestational diabetes.

MODY diabetes is associated with a significant list of symptoms that vary depending on the specific form of the pathology (this will be discussed below). Frequent urination and frequent skin problems occur. There is anemia, minor or more significant disorders associated with the nervous system, and long-term non-healing wounds. Symptoms and signs of the disease may be associated with:

• blurry or unclear vision;
• insufficiency of the pancreas;
• muscle weakness;
• weight changes, both upward and downward;
• dehydration.

In addition, the child may develop problems related to the cardiovascular system and seizures. Occasional yeast infections, constant thirst, and diarrhea are likely. Dysfunctional damage to the kidneys and liver occurs quite often. These symptoms do not occur all at once, and therefore in order to determine which pathology is developing, it is necessary to understand the causes of the disease.

Reasons for the development of the disease

The presented pathological condition is transmitted in a descending manner in 50% of cases if the defective gene turns out to be dominant. At the same time, the gender of the child does not matter. If problematic genes have been previously identified in two or more generations of the family, this should be considered an increased risk factor for the development of the disease in the child.

The causes of the disease are primarily mutations of genes that regulate the activity of the islet apparatus of the pancreas. Another factor should be considered pathological changes associated with the insulin-secreting activity of the beta cells of the gland. Such processes are provoked by hereditary pathologies.

Types of MODY diabetes

The classification of MODY diabetes is quite complex and includes eight types. By frequency of occurrence they are distributed in reverse order:

• MODY-3 - the most common (70% of all cases);
• MODY-2 - formed less frequently;
• MODY-1 is the rarest form of the three presented (up to 1%);
• other types of the disease are formed even less frequently, and therefore have no practical significance.

MODY-3 is characterized by the mildest onset between the ages of 20 and 40, the absence of ketoacidosis, that is, there is no smell of acetone from the mouth, as well as ketone bodies in the urine. Due to a violation of the renal barrier, elevated sugar is often identified in the urine, even with a normal ratio in the blood, and a long (longer than three years) “honeymoon” period is formed (a temporary decrease in the need for insulin).

Subtypes MODY-4, MODY-6, MODY-7 manifest themselves as a form of diabetes mellitus that does not have insulin dependence. However, they are extremely rare, and therefore practicing endocrinologists are not recommended to look for them, and symptomatic treatment is prescribed. Diagnosis of any type of disease must be given special attention before starting a rehabilitation course.

Diagnostic methods

Reliable determination of a specific type of disease is only possible through molecular genetic research. We are talking about PCR, namely the polymerase chain reaction, which confirms the presence of mutations in a gene. The list of examinations includes identification of the ratio of glucose, insulin and C-peptide, glucose tolerance testing.

Diagnosis may involve the detection of autoantibodies to a variety of pancreatic beta cell antigens. You may also need:

• determination of glycosylated hemoglobin to identify the severity and duration of hyperglycemia;
• Ultrasound of the pancreas;
• examination of urine for sugar levels, microalbumin;
• identification of amylase in blood, urine, and fecal trypsin.

The next important diagnostic measure should be the blood lipid spectrum. It is mandatory to consult an ophthalmologist, namely to assess the condition of the fundus, because diabetes is characterized by complications specifically affecting the visual organs. Next, endocrinologists insist on genotyping (PCR) and coprogram. Only after a full diagnosis can we talk about a specific rehabilitation course.

Treatment of adult-onset diabetes in young people

The recovery course depends on the specific form of pathology. Usually, a balanced diet and normalization of metabolism are sufficient measures. Treatment with MODI-2 will not be effective without full physical activity, which has the most positive effect on the functioning of the pancreas.

Diabetes mellitus MODY can be treated by implementing measures such as:

• special yoga for diabetics and other types of breathing exercises;
• introducing into the diet foods that help reduce blood sugar levels;
• use of hypoglycemic medicinal names;
• exclusion from the diet of such types of food as fried, fatty and too salty.

An important therapeutic and preventive measure is the abstinence of alcoholic beverages and the use of folk remedies, if they have been approved by an endocrinologist. For any type of diabetes, it is extremely important to evaluate the patient as early as possible. Such patients should visit an endocrinologist on a regular basis and also be registered with him, especially when it comes to children.

Our ways are inscrutable; often a person cannot even imagine what will be interesting to him in 5-10 years. If you are reading our pages, then the concept modi diabetes You are not unfamiliar with and are seriously interested in the disease itself and how to cure it.

Among the many mysteries of nature, the human body interests scientists the most. The troubles associated with the severe course of almost all chronic diseases force doctors to look for new ways of therapy and make the most accurate diagnoses.

More recently, any young patient who came to the doctors with serious glycemic disorders received an unambiguous diagnosis of type 1 diabetes. Sometimes even insulin therapy was strictly of an order nature, since not a single doctor simply dared to suggest otherwise.

Today, knowledge about the problem has greatly expanded. Modern doctors know very well that in nature there is a specific form that is found among very young patients. This pathology is also called modi diabetes.

Diagnostics

This disease is hereditary in nature and is associated with a breakdown in genes. Official statistics classify this type of diabetes as quite rare. But doctors say that the percentage of its spread in reality is quite high (about 12%-17%). Sometimes it can be called type 2 diabetes in children, but, nevertheless, it is a slightly different disease. Unlike typical diabetes, type 2 diabetes can occur in young people with low or normal body weight.

Highlight 6 mody subtypes. Each of them has its own specifics, requires a separate patient management regimen, and is easy or relatively difficult to correct. Often the development of the disease is sluggish, without sudden surges, against the background of good compensation.

Mody occurs more often than impaired glycemia in men. Specific characteristics of the body + strong nervous tension are the main culprits of the current trend. It is generally accepted that the course of the disease itself in representatives of the stronger sex is milder than in women.

The widespread opinion of many parents is that the child got sick because he ate a lot of sweets incorrectly. Genetic predisposition + trigger moment – ​​these are the reasons for the rapid development of pathology. A healthy child can eat as much sweets as he wants and it is unlikely that his normoglycemia will be disrupted. Although such food really cannot be called healthy.

Diabetes treatment mody

At first. Diagnosis and treatment of diabetes is not very difficult. Blood sugar is easily controlled with a strict diet and organized physical activity. Moreover, it is the 2nd point that gives excellent results. Sometimes regular exercise therapy is quite enough even with a relatively mild diet.

To correct blood glucose levels, various sugar-lowering methods are actively used: traditional treatment of diabetes, breathing exercises, consumption of sugar-lowering foods (jerusalem artichoke, green beans, vegetable fiber, bran).

Gradually the condition worsens. Usually during this period, in addition to diet and exercise, glucose-lowering tablets are prescribed. Over time, their action also ceases to bring a noticeable effect, then traditional insulin therapy is added. The management regimen for such patients is constantly being adjusted, so particularly careful monitoring is required on the part of medical personnel and those around the diabetic.

Children and adolescents who develop diabetes at a young age are at greatest risk of developing severe complications. The sharp transition from good compensation without medications to the use of insulin in most cases occurs during puberty. This feature is associated, first of all, with changes in the hormonal status of the body.

Remember, any methods of therapy for endocrine pathologies can only be used after agreement with the attending physician! The information provided is for informational purposes only. Self-medication can be dangerous.

Determining the type of diabetes mellitus is not always easy, since there are variations of the disease, the symptoms of which can be attributed to both the first and second types. A persistent increase in glucose at a young age, as in type 1, with a mild course characteristic of type 2, was called Modi diabetes.

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MODY is an abbreviation for “maturity onset diabetes of the young,” which can be translated as “adult diabetes in the young.” The age at which the disease debuts does not exceed 25 years. Modi diabetes has several forms. Some of them have obvious signs of high sugar - thirst and increased urine volume, but most are asymptomatic and are detected only during medical examination.

Differences between Modi diabetes and other types

Modi diabetes is a fairly rare disease. According to various estimates, the proportion of patients ranges from 2 to 5% of all diabetics. The cause of the disease is a gene mutation, as a result of which the functioning of the islets of Langerhans is disrupted. These are clusters of special cells in the pancreas that produce insulin.

Mody diabetes is transmitted in an autosomal dominant manner. If a child received at least one defective gene from his parents, he will develop the disease in 95% of cases. The probability of gene transfer is 50%. A patient in previous generations must have direct relatives with Modi diabetes; their diagnosis may sound like type 1 or 2 diabetes if genetic diagnosis has not been carried out.

Mody diabetes can be suspected if blood glucose rises sporadically, this increase remains at the same level for a long time, and does not cause severe ketoacidosis. A characteristic feature is the reaction to: the honeymoon after its onset does not last 1-3 months, as with type 1 diabetes, but much longer. Insulin drugs, even with the correct dosage calculation, regularly cause unpredictable symptoms.

Diagnostic criteria to distinguish Modi diabetes from more common types of the disease:

Table No. 2

Types of Modi Diabetes

The disease is classified depending on the mutated gene. In total, 13 possible mutations that increase blood glucose have been identified so far, and the same number of types of Modi-diabetes. All cases of diabetes with a non-standard course do not fall under them, so research is constantly being conducted to find new defective genes. Gradually, the number of known forms of the disease will increase.

Type statistics for the Caucasian race:

• Modi-3 - 52% of cases;
• Modi-2 – 32%;
• Modi-1 – 10%;
• Modi-5 – 5%.

Approximate frequency in Asians:

• Modi-3 - 5% of cases;
• Modi-2 – 2.5%;
• Modi-5 – 2.5%.

It is now possible to classify diabetes of this type in only 10% of patients of the Mongoloid race, so research to find new genes is being conducted specifically in this group of the population.

Characteristics of the most common types:

What are the signs to suspect

It is quite difficult to recognize Mody diabetes at the onset of the disease, since most often the disorders begin gradually, and obvious symptoms are completely absent. Nonspecific signs may include vision problems (temporary blurred vision, difficulty focusing on an object). The risk of fungal infections increases; women are characterized by frequent relapses of thrush.

As blood sugar rises, the usual symptoms of diabetes begin:

• thirst;
• frequent urination;
• increased appetite;
• weakened immune system;
• poorly healing skin lesions;
• weight change, depending on the form of Mody diabetes, the patient can either lose weight or gain weight.

It is worth getting tested for Modi diabetes if a child or young person has a blood glucose level above 5.6 mmol/l several times, but there are no symptoms of diabetes. A warning sign is a sugar level greater than 7.8 mmol/L at the end of glucose tolerance testing. In children, Mody diabetes is also indicated by the lack of weight loss at the onset of the disease and glucose levels after meals are not higher than 10 units.

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Laboratory confirmation of Modi diabetes

Despite the complexity of laboratory confirmation of Mody diabetes, genetic studies are very important, as they allow us to determine the correct treatment tactics not only for the patient, but also for his older relatives.

A full examination includes:

• blood sugar;
• sugar and protein in urine;
• C-peptide;
• glucose tolerance test;
• autoimmune antibodies to insulin;
• glycated hemoglobin;
• blood lipids;
• Ultrasound of the pancreas;
• blood and urine amylase;
• fecal trypsin;
• molecular genetic research.

The first 10 tests can be taken at your place of residence. The latest study allows you to determine the type of Modi diabetes, it is being done only in Moscow and Novosibirsk. Diagnostics are carried out on the basis of endocrinological research centers. For the study, they take blood, extract DNA from the cell, break it into sections and examine the fragments in which defects are most likely.

Treatment

The drugs prescribed depend on the typeMody-diabetes:

Treatment is more effective if you are not overweight. Therefore, obese patients are prescribed an additional calorie-restricted diet.

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