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This type of diabetes mellitus is generally considered rare in children and adolescents. The incidence of type 2 diabetes has increased dramatically in the past decade in some ethnic groups. This increased incidence of youth-onset non-insulin dependent diabetes mellitus (NIDDM-Y) has corresponded temporally to an unprecedented increase in body weight and prevalence of obesity in youth in various ethnic populations. Maturity-onset diabetes of the young (MODY), another type of non-insulin-dependent diabetes mellitus, is characterized by an early onset and autosomal dominant inheritance. MODY blood glucose is primarily due to beta-cell defects resulting in inadequate insulin secretion for a given level. In contrast to NIDDM-Y there is no significant increase in insulin resistance.
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PMID:[Non-insulin dependent diabetes mellitus during development in the population ]. 1143 86

Right classification of diabetes is important clinical issue. The aim of present study was to compare clinical, biochemical and immunological features, to analyze their practical use and to establish new decision tree which make the distinction between diabetes type 1, LADA, diabetes type 2 and MODY. We studied 97 not obese (mean BMI 26.3 +/- 4.9 kg/m2) patients aged 14 to 70 years, mean age 43 +/- 11.7 years, 53 women, 44 men. Mean duration of diabetes--2.3 +/- 4.3 years. We measured basal and stimulated C-peptide (6 minutes after 1 mg i.v. glucagon) (ELISA) and antibodies titers to glutamic acid decarboxylase--antiGAD65, tyrosine phosphatase-like molecule--IA2 and insulin--IAA (RIA). Autoimmune diabetes (LADA, type 1) was diagnosed with presence of one or more islet antigen antibodies. The highest frequencies had anti-GAD antibodies 33/97 (34%). The most complicated was to sort out group of patients with LADA. Comparison between this group and patients with diabetes type 2 have shown that BMI, co-existence of autoimmune disease, autoimmune markers and basal and stimulated C-peptide level measured at entry for the classification were useful in differentiation. Moreover we observed significantly lower C-peptide basal, stimulated and over basal level in group with MODY diabetes in comparison to diabetes type 2 patients. In the studied group were 5 patients with diabetes type 2 and obesity, in relatively young age. At the end there was one case of ADM (atypical diabetes mellitus). Clinical criteria for the classification of diabetes not always correlated with diagnosis. Autoimmune markers, basal and stimulated C-peptide were useful specially in differentiation between LADA and diabetes type 2 or diabetes type 1. Autoimmune diabetes co-existe with autoimmune disease. Proposed diagnostic scheme take for consideration presence of autoantibodies as well as C-peptide criteria.
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PMID:[Clinical, biochemical and immunological characteristic of diabetes type I, LADA, diabetes type II, and MODY patients]. 1268 30

The spectrum of diabetes in the young has widened; it now includes monogenic diseases, for example the various forms of permanent and transient neonatal diabetes and MODY as well as the emerging obesity-associated Type 2 diabetes in late childhood, but the main form is still Type 1 diabetes. Age-related major medical, physiological, social and emotional problems make the clinical management of diabetes in children and adolescents a difficult task for the physician and the family. Overall glycaemic control remains moderate or poor despite a treatment schedule, which interferes with several elements of "normal" childhood. There is an up to tenfold geographical variation in the incidence of childhood Type 1 diabetes within Europe with relatively stable incidence rates in some countries (mainly northern), but dynamic increases in incidence in other countries (mainly central European).A number of nongenetic (environmental) factors have been associated with the risk of Type 1 diabetes. Among these, perinatal factors, early nutrition, growth and vaccinations, atopic diseases and vitamin D are discussed in detail. The important interplay between genes, organism and environment is illustrated with new genetic data supporting the importance of environmental pressures in the evolution of this major disease.Although Type 1 diabetes usually accounts for only a minority of the total impact of diabetes in a population, it is the predominant form of the disease in younger age-groups in most developed countries. It is estimated that on an annual basis almost 100 000 children younger than 15 years of age develop Type 1 diabetes worldwide. The autoimmune destruction of the pancreatic beta cells in Type 1 diabetes leads to absolute insulin dependence and a high rate of complications typically occurring at a relatively young age. Therefore, Type 1 diabetes places a particularly heavy burden on the individual, the family and health services.
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PMID:Diabetes in the young: a paediatric and epidemiological perspective. 1269 Apr 39

The pathogenesis of type 2 diabetes is complex, with two distinct mechanisms: insulin resistance (decrease of insulin action on peripheral tissues) and insulin deficiency (impaired insulin secretion by pancreatic beta-cells). These abnormalities are due to genetic and environmental factors. Type 2 diabetes is a heterogeneous disease: besides the common form with obesity, monogenic forms (such as MODY) exist. Knowledge of these forms has permit a better understanding of the genetic factors involved in diabetes, and of their relationship with insulin resistance. In this review, we discuss the main data available on genetics of type 2 diabetes, as well as the various research approaches. Today, the genetic determinism of functional abnormalities of pancreatic beta-cell is no longer discussed. However, it is also clearly established that acquired metabolic factors may contribute to pancreatic beta-cell failure. Hyperglycaemia, even moderate, induces a reduced insulin biosynthesis potential (glucotoxicity), and the increased free fatty acid flux accelerates pancreatic beta-cell apoptosis (lipotoxicity). The role of these metabolic abnormalities in the development of type 2 diabetes is briefly described.
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PMID:[Physiological basis of insulin secretion abnormalities]. 1270 60

As clinicians, we are faced to difficult situations in young diabetic patients. The prevalence of type 2 diabetes increases in these patients due to a rising incidence of obesity. We present two clinical observations which both illustrate the insufficiencies of the present classifications. Modern tools are now available for diagnosis such as anti-GAD65 and IA-2 antibodies, genetic tools to investigate for specific mutations, but quantitative means of beta cell mass are lacking. Clinical examination is still accurate to identify type 1 or type 2 diabetes, MODY and mitochondrial diabetes. Weight curve, lesions of acanthosis nigricans, criteria of metabolic syndrome, history of diabetes are critical factors. This problematic has important consequences in our daily practice: the right choice for rapid and good metabolic control.
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PMID:Classification of diabetes in young adults: new concepts for an old disease. 1635 9

Differentiation of the various forms of diabetes is necessary for therapeutic reasons. Typical signs of type 2 diabetes are age over 40, obesity, and other markers for metabolic syndrome, a positive famitory, gradual development of the classical symptoms, and no evidence of ketosis. It is important to distinguish this from LADA (latent autoimmune diabetes of adulthood), a form of type 1 diabetes mellitus. To establish this differential diagnosis antibody testing is employed. Antibody tests in patients with newly manifest diabetes make good sense when the clinical diagnosis is not unequivocal, that is, to distinguish it from type 2 diabetes, MODY diabetes, hereditary and secondary forms. At present, immunodiagnosis is used too often in unambiguous cases of type 1 diabetes, but too rarely in supposed type 2 diabetes. As a rule, LADA patients are GADA-positive. If MODY diabetes is suspected, a genetic examination is indicated. In patients with GDM, antibody testing with GADA makes sense, in particular in slim patients receiving insulin treatment, since these patients have a high risk for developing a postpartum diabetes already in the first years.
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PMID:[Diabetes mellitus--differential diagnosis]. 1680 91

About 2-5% of all pregnant women develop gestational diabetes mellitus (GDM) during their pregnancies and the prevalence has increased considerably during the last decade. GDM is a heterogeneous disorder that is defined as carbohydrate intolerance with onset or first recognition during pregnancy. It is manifested when pancreatic beta cells are no longer able to compensate for the increased insulin resistance during pregnancy, but the pathogenesis of the disease is still largely unknown. GDM is considered to result from interaction between genetic and environmental risk factors. Genetic predisposition to GDM has been suggested since GDM clusters in families. Also, women with mutations in MODY (Maturity onset diabetes of the young) genes often present with GDM. In addition, common variants in several candidate genes (e.g. potassium inwardly rectifying channel subfamily J, member 11 [KCNJ11], Glucokinase [GCK], Hepatocyte nuclear factor-1alpha [HNF1A] etc.) have been demonstrated to increase the risk of GDM. Old age, obesity and high fat diet represent some important non-genetic factors. There are several approaches to search for genes predisposing to a polygenic disease like GDM including linkage and association studies, expression profiling and animal models. A combination of several methods is usually necessary. Identification of the underlying genetic causes of GDM will eventually give a better view of the mechanisms that contribute to the pathophysiology of the disease. Furthermore, it may improve options to possibly prevent GDM and complications for the mother and her child. This review focuses on the genetics of GDM and possible implications in clinical practice.
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PMID:Genetics of gestational diabetes mellitus. 1734 48

Gestational diabetes mellitus (GDM) is defined as glucose intolerance with onset or first recognition during pregnancy. Data from Western countries suggest that the prevalence of GDM is increasing, being almost 10% of pregnancies and probably reflecting the global obesity epidemic. The majority of women with GDM seem to have beta-cell dysfunction that appears on a background of chronic insulin resistance already present before pregnancy. In less than 10% of GDM patients, defects of beta-cell function can be due to autoimmune destruction of pancreatic beta-cells, as in type 1 diabetes, or caused by monogenic mutations, as in several MODY subtypes. Diagnostic criteria for GDM vary worldwide and there are no clear-cut plasma glucose cut-off values for identifying women at a higher risk of developing macrosomia or other fetal complications. Because the oral glucose tolerance test (OGTT) is restricted to high risk individuals, 40% of GDM cases are left undiagnosed. Therefore, in high risk populations almost universal screening is recommended; only women considered to have very low risk do not need screening. Diet and exercise are the key elements in the treatment of GDM. If necessary, either insulin, certain oral hypoglycemic agents or combinations can be used to achieve normoglycemia. After delivery, women with GDM and their offspring have an increased risk for developing the metabolic syndrome and type 2 diabetes. Thus, pregnancy may act as a "stress test", revealing a woman's predisposition to T2D and providing opportunities for focused prevention of important chronic diseases.
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PMID:Gestational diabetes: pathogenesis and consequences to mother and offspring. 1929 Mar 80

We studied the genetic and clinical features of diabetic subjects in a 5-generation Michigan-Kentucky pedigree ascertained through a proband with pancreatic agenesis and homozygous for the IPF1 mutation Pro63fsx60. Diabetic and nondiabetic family members were genotyped and phenotyped. We also carried out genetic studies to determine the history of the IPF1 mutation in the Michigan-Kentucky family and a Virginia family with the same mutation. We identified 110 individuals; 34 are currently being treated for diabetes and 10 of these are Pro63fsX60 carriers (ie, MODY4). Subjects with MODY as well as those with type 2 diabetes are characterized by obesity and hyperinsulinemia. Genetic studies suggest that the IPF1 mutation was inherited from an ancestor common to both the Michigan-Kentucky and Virginia families. MODY4 and type 2 diabetes in the Michigan-Kentucky pedigree are associated with obesity and hyperinsulinemia. Obesity and hyperinsulinemia have been observed occasionally in other subtypes of MODY, which suggests that hyperinsulinemia may be a general phenomenon when obesity occurs in MODY subjects. Hypoinsulinemia in nonobese MODY subjects seems to be caused by a functional defect in the beta cell. Genetic testing should be considered in multigenerational obese diabetic subjects, particularly when such families contain young diabetic members.
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PMID:Obesity and hyperinsulinemia in a family with pancreatic agenesis and MODY caused by the IPF1 mutation Pro63fsX60. 2062 Oct 32

Type 2 diabetes mellitus (T2D) is no longer a disease only of adults. In some American locations and populations, incidence and prevalence of T2D are much higher than those of type 1 diabetes, because of increased calorie and fat intake, and decreased exercise. The increasing prevalence of T2D in the United States has closely paralleled the increase in childhood obesity noted there, but now across the Western world. Besides obesity, the other youth risk factors for T2D are: ethnicity, family history, puberty, female, metabolic syndrome, acanthosis nigricans and polycystic ovary syndrome. Any feature or condition associated with insulin resistance/hyperinsulinemia should alert to screen youth at increased risk for (pre)T2D. T2D should be differenciated from monogenic diabetes (Maturity Onset Diabetes of the Young or MODY). Treatment goals are to decrease weight and increase exercise, to normalize insulinemia, glycemia and HbA1c, to control hypertension and hyperlipidemia. The aim of the pharmacological therapy is to decrease insulin resistance, namely by metformin. Sometimes, insulin therapy is necessary.
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PMID:[(Pre)type 2 diabetes and MODY: pediatric diabetology future]. 2181 23


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