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66.Kristinsson SY, Thorolfsdottir ET, Talseth B, Steingrimsson E, Thorsson AV, Helgason T, et al. Nearly sixty two million people are affected at present and the number is expected to rise to more than hundred million by 2030. Incidence trends for childhood type 1diabetes in Europe during 1989-2003 and predicted new cases 2005-20: A multicentre prospective registration study. Referral rates for diagnostic testing support an incidence of permanent neonatal diabetes in three European countries of at least 1 in 260,000 live births. Mutations in ATP-sensitive K+channel genes cause transient neonatal diabetes and permanent diabetes in childhood or adulthood. Impaired glucose homeostasis in transgenic mice expressing the human transient neonatal diabetes mellitus locus, TNDM. Pancreatic agenesis attributable to a single nucleotide deletion in the human IPF-1 gene coding sequence. EIF2AK3, encoding translation initiation factor 2-α kinase 3, is mutated in patients with Wolcott-Rallison syndrome. X-linked neonatal diabetes mellitus, enteropathy and endocrinopathy syndrome is the human equivalent of mouse scurfy. Mutations in GLIS3 are responsible for a rare syndrome with neonatal diabetes mellitus and congenital hypothyroidism. Recessive SLC19A2 mutations are a cause of neonatal diabetes mellitus in thiamine-responsive megaloblastic anaemia. Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations.
Effective treatment with oral sulfonylureas in patients with diabetes due to sulfonylurea receptor 1 (SUR1) mutations. Improved motor development and good long-term glycaemic control with sulfonylurea treatment in a patient with the syndrome of intermediate developmental delay, early-onset generalised epilepsy and neonatal diabetes associated with the V59M mutation in the KCNJ11 gene. Incidence, genetics and clinical phenotype of permanent neonatal diabetes mellitus in northwest Saudi Arabia. Permanent neonatal diabetes mellitus due to a C96Y heterozygous mutation in the insulin gene. A difference between the inheritance of classical juvenile-onset and maturity-onset type diabetes of young people. Is maturity onset diabetes at young age (MODY) more common in Europe than previously assumed? Differential effects of HNF-1α mutations associated with familial young-onset diabetes on target gene regulation.
Mutations in the hepatocyte nuclear factor-1alpha gene in maturity-onset diabetes of the young (MODY3).
Mutations in the hepatocyte nuclear factor-1alpha gene are a common cause of maturity-onset diabetes of the young in the U.K. Mutations in the hepatocyte nuclear factor-1alpha gene in MODY and early-onset NIDDM: Evidence for a mutational hotspot in exon 4. Early-onset type II diabetes mellitus in Italian families due to mutations in the genes encoding hepatic nuclear factor-1alpha and glucokinase. Mutations in GCK and HNF-1alpha explain the majority of cases with clinical diagnosis of MODY in Spain.
HNF-1 alpha gene coding regions mutations screening, in a Caucasian population clinically characterized as MODY from Argentina.
Mutations in the hepatocyte nuclear factor-1 alpha gene (MODY3) are not a major cause of early-onset non-insulin-dependent (type 2) diabetes mellitus in Japanese. Low prevalence of MODY2 and MODY3 mutations in Brazilian individuals with clinical MODY phenotype. Clinical characteristics and diagnostic criteria of maturity-onset diabetes of the young (MODY) due to molecular anomalies of the HNF1A gene.
Identification of HNF1A-MODY and HNF4A-MODY in Irish families: Phenotypic characteristics and therapeutic implications.
Mutations in the hepatocyte nuclear factor-4alpha gene in maturity-onset diabetes of the young (MODY1).
Mutations in the genes encoding the transcription factors hepatocyte nuclear factor-1alpha (HNF1A) and 4alpha (HNF4A) in maturity-onset diabetes of the young. Molecular genetics and phenotypic characteristics of MODY caused by hepatocyte nuclear factor-4alpha mutations in a large European collection.
Hepatocyte nuclear factor- 4α gene mutation associated with familial neonatal hyperinsulinism and maturity-onset diabetes of the young. Identification of new mutations in the hepatocyte nuclear factor-4alpha gene among families with early onset Type 2 diabetes mellitus.
Familial young-onset forms of diabetes related to HNF4A and rare HNF1A molecular aetiologies.
Pancreatic agenesis attributable to a single nucleotide deletion in the human IPF1 gene coding sequence.
A novel syndrome of diabetes mellitus, renal dysfunction and genital malformation associated with a partial deletion of the pseudo-POU domain of hepatocyte nuclear factor-1beta. MODY in Iceland is associated with mutations in HNF-1alpha and a novel mutation in Neuro-D1. Familial hyperglycemia due to mutations in glucokinase: Definition of a subtype of diabetes. A high prevalence of glucokinase mutations in gestational diabetic subjects selected by clinical criteria. Less frequent causes include pancreatic diabetes, monogenic diabetes and secondary forms of diabetes mellitus. The proportion of young people affected with type 2 diabetes is on the increase which parallels the obesity epidemic worldwide with an impact on developing countries as well. Since diabetes is a silent killer and India being one of the heavily affected countries, more focus needs to be placed on patient care as well as research. A single clinical characteristic or lab finding may not help reach the diagnosis in such cases. Neonatal diabetes mellitus (NNDM) and Maturity onset diabetes of the young (MODY) are the 2 main types of monogenic diabetes that result from β-cell dysfunction.
Other forms of monogenic diabetes result in defective insulin action or insulin receptor dysfunction. Infants born with TNDM harbour a greater risk of developing type 2 diabetes later in the life.

The persistence of the underlying pancreatic defect predisposes to a heightened risk, especially during periods of increased demand like puberty and pregnancy.The genetics of transient neonatal diabetesThe molecular genetic mechanism resulting in TNDM has been elucidated in a majority of cases.
Genomic imprinting is a phenomenon where the phenotypic expression of a particular genetic allele in an individual depends on the parent from which the allele is transmitted.
In other words, the allele from one parent is 'silenced' through epigenetic mechanisms as methylation and histone modification which results in a monoallelic gene expression.
Mutations affecting this single allele have a greater chance of affecting the gene function which results in disease. Abnormalities in the imprinted region of chromosome 6q24 results in the majority of cases of TNDM. Over expression of the paternal allele results from uniparental di-somy or duplication of the 6q24 region of the paternal chromosome. Activation of the maternal allele can occur as a result of hypomethylation of the maternal differentially methylated region (DMR). This results in TNDM as the imprinted region has been shown to contain genes which regulate apoptosis, insulin secretion and foetal growth namely PLAGL1 (Pleomorphic adenoma gene like-1 (also known as ZAC)) and HYMAI- (Hydatidiform mole associated and imprinted).
The ZAC gene is also shown to regulate the imprinted region on chromosome 11p15.5 near the Beckwith-Weidmann syndrome locus and 2 other growth regulatory genes namely igfr2 and igfr2r which possibly explain the sharing of associated features such as macroglossia and umbilical hernia in both conditions. All cases of PNDM result from mutations affecting genes regulating pancreatic development, β-cell function, apoptosis or the insulin molecule as such. The glucose molecule that is transported into the β-cell through the GLUT receptor undergoes hydrolysis after phosphorylation. The pyruvate molecule that is generated is then metabolised inside the mitochondria to CO 2 and H 2 O to generate ATP molecules.
Activating mutations in these genes result in persistent opening of the potassium channels preventing insulin release resulting in impaired glucose sensing and hence diabetes. This explains the occurrence of associated features like developmental delay, epilepsy and muscle weakness (DEND - Developmental delay, Epilepsy and Neonatal Diabetes- syndrome) in infants with NNDM due to these mutations. Homozygous mutations in gene encoding PTF-1α results in PNDM characterised by cerebellar hypoplasia, pancreatic agenesis, intrauterine growth retardation, respiratory distress and microcephaly as described initially in a consanguineous Pakistani family.
Homozygous loss of function mutation in the gene encoding this factor results in PNDM with exocrine deficiency due to pancreatic agenesis. It phosphorylates the glucose molecules entering the cell and initiates subsequent pathways leading to insulin release. Homozygous mutations in the GCK gene results in complete loss of glycolytic activity in the β-cell resulting in PNDM.
In the heterozygous state it results in mild impairment of insulin release manifesting as maturity onset diabetes of the young (MODY2) or as gestational diabetes. The molecular defect is localised to the EIF-2AK3 gene on chromosome 2p12 which regulates protein synthesis and folding. The resultant misfolded proteins increase the stress in the endoplasmic reticulum of various tissues leading to cell death by apoptosis which explains the various phenotypic features. A genetic defect has been identified in the FOXP3 gene on the X chromosome which codes for a forkhead domain-containing protein known as 'scurfin' that is required for immune homeostasis. The diabetes mellitus in this disorder is due to autoimmune destruction of the β-cells as suggested by the presence of a number of islet cell autoantibodies. It ranges from severe early onset neonatal diabetes to a mild form of MODY and gestational diabetes.
Absence of extrapancreatic features differentiates this disorder from that due to the EIF-2AK3 mutation.GLIS3 - (GLI subfamily of Kruppel-like zinc finger protein-3)Mutations in GLIS3, yet another transcription factor gene, have been shown to be associated with PNDM with multisystem involvement. Neurological deficits, cardiac abnormalities and visual problems are also reported in some of these cases.
Neonatal diabetes due to mutations in the ABCC8 and KCNJ11 genes generally respond well to oral sulfonylureas.
Sulfonylurea therapy has been found to ameliorate the associated neurological dysfunction and hence early initiation of the drug is of utmost importance for an improvement in long term prognosis. Recently a very high incidence of PNDM is reported from Saudi Arabia from a highly consanguineous population (1 in 21, 196 live births). Fourteen out of seventeen PNDM cases had an identifiable genetic aetiology of which 50% were due to the autosomal recessive Wolcott Rallison syndrome. A Neonatal Diabetes Registry has been established in India where facilities are available to sequence KCNJ11, ABCC8 and insulin genes.
Subsequently this group came to be called as maturity onset diabetes of the young and was shown to have an autosomal dominant mode of inheritance. The molecular genetic basis of this condition was unravelled in the 1990's when 5 of the genetic loci were identified and characterised by various investigators. Thereafter, these conditions were referred to as MODY 1-5 based on the sequence of genes identified. Subsequent years have witnessed an explosion of knowledge in this field with 6 more gene loci harbouring mutations resulting in MODY being identified. In addition, mutations in enzymes directly or indirectly involved in glucose sensing of the β-cell have also been shown to result in early onset diabetes. There is wide clinical as well as genetic heterogeneity within and among the different MODY subtypes. The following section gives a brief account of the molecular mechanism and clinical peculiarities of each MODY subtype. It has a crucial role in regulation of transcription of insulin gene in the mature β-cell as well as the glucose transporter GLUT2. Mutations in the HNF-1α gene leads to progressive insulin secretory defect resulting in a severe form of inherited diabetes that is classically termed MODY3.
HNF-1α is also functional in the kidneys in the regulation of proximal renal tubular reabsorption of glucose mediated through sodium glucose transporter-2. MODY3 patients are sensitive to sulfonylureas, though many patients finally require insulin on a long term basis.
Long term microvascular complications occur with the same frequency as in type 2 and type 1 diabetes. 40% of the mutation proven MODY 3 subjects had their age at diagnosis above twenty five years and only about half of these subjects had 3 generations of family history of diabetes. Homozygous mutations in IPF-1 leads to pancreatic agenesis resulting in permanent neonatal diabetes and exocrine pancreatic insufficiency. In the embryonic period HNF-1β is involved in the differentiation of the visceral endoderm.
Apart from its role in pancreatic development, HNF-1β is required for development of the kidneys and the genital tract.

Hence mutations in HNF-1β results in pancreatic insufficiency that includes both exocrine and endocrine dysfunction, cystic renal disease (RCAD-Renal cyst and diabetes syndrome) and anomalies of the vagina and the mullerian structures ranging from uterine aplasia to a bi-cornuate uterus.
Early onset slowly progressive non diabetic renal failure may occur in some affected patients. Mutations in Neuro-D1 results in an autosomal dominant disorder which resembles type 2 diabetes (MODY6). Heterozygous mutations affecting the GCK gene results in mild fasting hyperglycemia that has been demonstrable from birth but is non progressive .[67] The Glucokinase enzyme is also functional in the liver.
As a result of the molecular defect, there is reduced hepatic glucose sensing especially after a meal resulting in reduced glycogen synthesis and stimulation of hepatic gluconeogensis manifesting as postprandial hyperglycemia. However due to a milder degree of hyperglycemia, long term microvascular complications rarely occur in MODY2 compared to other forms of diabetes. GCK mutations have been shown to be responsible for gestational diabetes mellitus in 80% of Caucasian pregnant women when strict clinical criteria were applied for patient selection. However an unaffected foetus can develop macrosomia under the effect of maternal hyperglycemia.
Genome wide screen detected mutations in the carboxy ester lipase (CEL) gene to be a rare cause for diabetes and exocrine pancreatic insufficiency. In 2007 two novel mutations in the Pax 4 gene were identified in 2 patients from a Thai population as the cause for diabetes (now termed MODY9).
The search for a genetic cause for diabetes in children with type 1 diabetes with negative autoantibodies identified mutations in the insulin gene as a rare cause for MODY (MODY10). Mutations in BLK gene result in β-cell dysfunction and have been shown to be associated with early onset diabetes (MODY11). Hyperglycemia due to mutations in HNF-1α has been found to be well controlled with Sulfonylureas for a number of years. Especially in a developing country like India, where there is lack of awareness for a genetic diagnosis of MODY, the probability of MODY being falsely diagnosed as either type 1 or type 2 diabetes is rather high. This may result in patients receiving inappropriate therapy with suboptimal glycaemic control.
An alarming proportion (28%) of adolescents and young adults from Southern India were detected to have impaired fasting glucose during a search for metabolic abnormalities and their anthropometric correlates.
Even though one can diagnostically suspect MODY based on the phenotypical features we have mentioned earlier, one cannot treat the patient without knowing the specific genotype.
The specific management protocols for each genetic subtype mandates genetic analysis in patients with clinical suspicion of MODY.3.
Avoiding insulin therapy Given the fact that MODY is misdiagnosed as either type 1 or type 2 diabetes, many patients end up receiving insulin, along with the complications of insulin therapy and manage to achieve only suboptimal glycaemic control.
Understanding the relationship between MODY mutations and birth weight It has been proven beyond doubt that a strong relationship exists between maternal malnutrition, low-birth weight and the predisposition to metabolic and cardiovascular disease in later life. Overfeeding of these infants in the postnatal period results in the onset of metabolic disease in the early years of life.
Such rats also developed diabetes at seventeen months of age showing continued repression of the gene throughout the ageing process.
Genome-wide association scans have further proven the genetic association between low birth weight and type 2 diabetes in early adulthood.
Genetic variants in the ADCY5 (Adenylate Cyclase 5) and CCNL1 (Cyclin L1) gene loci have been shown to be associated with low birth weight in Europeans.
Identifying the effect of consanguinity on the frequency of MODY The 1992-1993 National Family Health Survey had shown high frequency of consanguinity and co-efficient of inbreeding in Southern Indian states of Tamil Nadu, Karnataka and Andhra Pradesh.
It is likely that MODY is an under diagnosed subset of diabetes in our country than is thought of.6.
Unravelling the impact of variations in the susceptibility genes on MODY Genome-wide association studies have identified several susceptibility genes for developing type 2 diabetes. It would be interesting to investigate this possible interaction through genetic studies.What is the status of monogenic diabetes worldwide?Significant progress in molecular research is taking place worldwide. At the time of writing this paper eleven genes have been identified to harbour MODY related mutations.
Epidemiological studies from different ethnic groups have shown varying frequencies of prevalence of these mutations. Additionally some of them have established monogenic diabetes registries.Molecular diagnostic platform used in MODYSanger sequencing is a widely used genetic diagnostic platform for identifying MODY and is the gold standard sequencing platform to test single-gene genetic disorders. This sequencing technique has been reported to be >99% sensitive to detect a heterozygous base substitution in MODY genes.
The turn around time for the genetic diagnosis of MODY for sequencing these 3 genes is around fourty working days for unknown mutations and twenty working days for known mutations.Based on the 2008 best practice guidelines for genetic diagnosis of MODY, it has been recommended that genetic testing should be performed only for subjects who fit into the clinical criteria of MODY. The genetic diagnosis of MODY has been recommended by a clinician only when he considers that a genetic diagnosis may make a difference in the clinical management of the patient.
Furthermore, owing to issues of affordability, there is a delay from the time of diagnosis of diabetes to the definitive genetic diagnosis of MODY. At present due to limitations in throughput and scalability of the present Sanger sequencing, there are limitations to genetically characterizing patients with MODY, in a fast, comprehensive and cost-efficient manner.Status of MODY genetics in IndiaIndia is making rapid advances in the field of molecular genetics and its application in the field of health and disease. However, few groups of investigators have embarked on the molecular genetic studies in diabetes particularly MODY. The performed studies have been centred on mutations on very few genes which were reported to be relatively common in the western population. The same polymorphism was associated with earlier age of diabetes onset in type 2 diabetes. They also observed co-segregation with diabetes of the Arg263His coding region mutation in eight members of one MODY family.
In this study, mutations in only 1 gene that was implicated in MODY was looked for, while there are more than ten genes on the list currently. In addition, they also reported single nucleotide polymorphisms of HNF-4α that are both susceptible to and protective against MODY and early onset T2DM. A comprehensive genetic service for the diabetic population particularly for the younger age group may benefit in the long run in terms of treatment as well as genetic counselling. The complexities of the molecular genetic techniques as well the financial requirements for the sophisticated instruments and reagents and the need for expert manpower limits the widespread availability of such a facility in our country at present, however steps in this direction are in the phase of evolution.

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