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Is Type 2 Diabetes Autosomal Dominant

A Gene Conferring Susceptibility To Type 2 Diabetes In Conjunction With Obesity Is Located On Chromosome 18p11

A Gene Conferring Susceptibility To Type 2 Diabetes In Conjunction With Obesity Is Located On Chromosome 18p11

Genome-wide nonparametric linkage analysis of 480 sib-pairs affected with type 2 diabetes revealed linkage to a previously unreported susceptibility locus on chromosome 18p11. This result improved with stringent subphenotyping using age- and sex-adjusted BMI, ultimately reaching a logarithm of odds of 3.82 (allele sharing 0.6654) at a point between markers D18S976 and D18S391 when the most obese 20% of the sample was analyzed. Several genes on chromosome 18 have been suggested as metabolic disease candidates, but none of these colocalize with our linkage result. We conclude that our results provide support for the presence of a currently uncharacterized gene on chromosome 18p, certain alleles of which confer increased susceptibility to type 2 diabetes in conjunction with obesity. We additionally observed moderate evidence for linkage to chromosome 1, near marker D1S3462; chromosome 4, near marker D4S2361; chromosome 5, near marker D5S1505; and chromosome 17, near marker D17S1301. RESEARCH DESIGN AND METHODS We recruited participants from Finland and southern Sweden; no subjects participating in the Botnia type 2 diabetes genome scan (4) were included in this study. Diabetes clinics in Finland and southern Sweden were appointed to participate in the study; after a clinic was appointed, information on all type 2 diabetes patients and their family members was obtained by the clinic’s nurse and verified from clinic records. This strategy differs from that of the ongoing fusion (Finland–United States Investigation of NIDDM Genetics) type 2 diabetes linkage study in that probands for that study have been identified using hospital discharge records and have been recruited only from Finland, rather than both Finland and Sweden. In our study, 617 families characterized by at Continue reading >>

Genes And Pathophysiology Of Type 2 Diabetes: More Than Just The Randle Cycle All Over Again

Genes And Pathophysiology Of Type 2 Diabetes: More Than Just The Randle Cycle All Over Again

Genes and pathophysiology of type 2 diabetes: more than just the Randle cycle all over again Division of Endocrinology, Diabetes and Nutrition, University of Maryland School of Medicine, Baltimore, Maryland, USA. Geriatric Research and Education Clinical Center, Veterans Administration Medical Center, Baltimore, Maryland, USA. Address correspondence to: Alan R. Shuldiner, Division of Endocrinology, Diabetes and Nutrition, University of Maryland School of Medicine, 660 West Redwood Street, Room 494, Baltimore, Maryland 21201, USA. Phone: (410) 706-1623; Fax: (410) 706-1622; E-mail: [email protected] . Author information Copyright and License information Disclaimer Copyright 2004, American Society for Clinical Investigation This article has been cited by other articles in PMC. The Randle cycle, which has been invoked to explain the reciprocal relationship between fatty acid oxidation and glucose oxidation, has long been implicated as a potential mechanism for hyperglycemia and type 2 diabetes mellitus (T2DM). Now genetic, functional genomic, and transgenic approaches have identified PPAR coactivators (PGC-1 and PGC-1) as key regulators of mitochondrial number and function. They regulate adaptive thermogenesis as well as glucose and fat oxidation in muscle and fat tissue, gluconeogenesis in liver, and even glucose-regulated insulin secretion in cells. PGC-1 and PGC-1 mRNA levels and the mitochondrial genes they regulate are decreased in muscle of people with prediabetes and T2DM. A new report indicates that PGC-1 and PGC-1 mRNA levels decrease with age in individuals with a genetic variant in PGC-1, and these decreases correlate with alterations in whole-body glucose and fatty acid oxidation. These findings provide insights into how aging modifies genetic su Continue reading >>

Ask The Diabetes Team

Ask The Diabetes Team

Question: From San Jose, California, USA: Is diabetes recessive or dominant, and how is it inherited? A lot of my ancestors have diabetes and I wanted to know the chance I would get diabetes. Answer: The inheritance of diabetes is rather more complicated than the simple Mendelian concept of dominant and recessive, autosomal or sex-linked. Type 1 Diabetes depends to some extent on the inherited pattern of certain white blood cell surface proteins, usually referred to as HLA types. However, there is an environmental component which is a major factor in deciding whether those who are 'at risk' will develop clinical diabetes. This was realised when it was found that identical twins were discordant for this kind of diabetes. What the factor(s) are is not known: for a number of years early exposure to cow's milk was thought to be one; but this has subsequently been discounted. In adult onsetdiabetes, it is even harder to be precise about the likelihood of developing the condition. In some cases especially amongst Maturity Onset Diabetes of the Young specific chromosomal abnormalities have been defined; but there has not been time to assemble the family trees needed to define the actual mode of inheritance. For the majority of Type 2 Diabetics the mechanisms are not defined in precise molecular or chromosomal terms. Ethnic factors are also important. Finally, there is the factor of stress which may hasten the onset of any form of diabetes and perhaps the commonest of these in later life is age. You write about 'ancestors' which suggest that you have no first degree relatives with any form of diabetes. This in turn would suggest that your chances of getting the disease are no more than for the population as a whole, age adjusted. Continue reading >>

Is Type 2 Diabetes Caused By Genetics?

Is Type 2 Diabetes Caused By Genetics?

Diabetes is a complex condition. Several factors must come together for you to develop type 2 diabetes. For example, obesity and a sedentary lifestyle play a role. Genetics can also influence whether you’ll get this disease. If you’ve been diagnosed with type 2 diabetes, there’s a good chance that you’re not the first person with diabetes in your family. According to the American Diabetes Association, your risk of developing type 2 diabetes is: 1 in 7 if one of your parents was diagnosed before the age of 50 1 in 13 if one of your parents was diagnosed after the age of 50 1 in 2, or 50 percent, if both your parents have diabetes Several gene mutations have been linked to the development of type 2 diabetes. These gene mutations can interact with the environment and each other to further increase your risk. Type 2 diabetes is caused by both genetic and environmental factors. Scientists have linked several gene mutations to a higher diabetes risk. Not everyone who carries a mutation will get diabetes. But many people with diabetes do have one or more of these mutations. It can be difficult to separate genetic risk from environmental risk. The latter is often influenced by your family members. For example, parents with healthy eating habits are likely to pass them on to the next generation. On the other hand, genetics plays a big part in determining weight. Sometimes behaviors can’t take all the blame. Studies of twins suggest that type 2 diabetes might be linked to genetics. These studies were complicated by the environmental influences that also affect type 2 diabetes risk. To date, numerous mutations have been shown to affect type 2 diabetes risk. The contribution of each gene is generally small. However, each additional mutation you have seems to increase your Continue reading >>

Type 2 Diabetes On Chromosome 20q13.1q13.2

Type 2 Diabetes On Chromosome 20q13.1q13.2

We previously reported suggestive linkage between type 2 diabetes and markers in a region on chromosome 20q using data from a collection of 29 Caucasian families in which type 2 diabetes with middle-ageonset was segregated as an autosomal-dominant disorder. To map more precisely the susceptibility locus (or loci) within this broad region, we increased the family collection and genotyped all families for additional markers, both within the critical region and spaced over the rest of chromosome 20. Altogether 526 individuals (including 241 with diabetes) from the total collection of 43 families were included in the study. All individuals were genotyped for 23 highly polymorphic markers. Positive evidence for linkage was found for a 10-cM region on the long arm of chromosome 20q13.1q13.2 between markers D20S119 and D20S428. The strongest evidence in two-point as well as multipoint linkage analysis (P = 1.8 X105) occurred at the position corresponding to marker D20S196. The individuals with diabetes in the seven most strongly linked families had high serum insulin levels during fasting and 2-h postglucose load periods. We did not find any evidence for linkage between type 2 diabetes and any other region on chromosome 20. In conclusion, our larger and more comprehensive study showed very strong evidence for a susceptibility gene for insulin-resistant type 2 diabetes located on the long arm of chromosome 20 around marker D20S196. The development of type 2 diabetes is strongly influenced by genetic factors [ 1 , 2 ]. Recently, genes responsible for several rare forms of autosomal-dominant early-onset type 2 diabetes, also known as maturity-onset diabetes of the young (MODY), have been identified [ 3 , 4 ]. Although mutations in these genes are infrequent, their identification Continue reading >>

11111 Fact Sheet 48|diabetes Types 1 And 2 And Inherited Predisposition

11111 Fact Sheet 48|diabetes Types 1 And 2 And Inherited Predisposition

 WHAT IS DIABETES? Diabetes mellitus (commonly known as diabetes) refers to a group of conditions which cause high levels of glucose (a form of sugar) in the blood. Glucose provides the energy that cells need to function. The level of glucose in an individual’s blood is carefully regulated by the hormone insulin. Insulin is produced in the pancreas and its role is to keep the levels of glucose balanced - not too high and not too low - as both extremes are dangerous and can disrupt the body’s chemical processes. There are two major forms of diabetes:  Type 1 (insulin dependent diabetes mellitus: IDDM)  Type 2 (non-insulin dependent diabetes mellitus: NIDDM). There is also another rarer type of diabetes called mature onset diabetes of the young (MODY). All of these forms of diabetes have different symptoms and a different genetic basis. Type 1 diabetes (IDDM) Type 1 diabetes is a chronic autoimmune disease, where the immune system destroys the insulin- producing cells of the pancreas. About 10% to 15% of people with diabetes in Australia have type 1 diabetes. The general population risk for developing type 1 diabetes is around 1 in 1000. The condition is usually first seen in childhood or adolescence and so is sometimes called juvenile diabetes. The risk of type 1 diabetes in 0-14 year olds around 1 in 750. It can, however, occur at any age and onset after the age of 20 years occurs in 50% of cases. Symptoms include:  thirst  frequent urination  weight loss  fatigue  blurred vision  sugar in the urine Insulin medication (usually by injection) is necessary to provide the body with insulin, and thus type 1 diabetes is described as insulin- dependent diabetes (IDDM). In about 90% of cases, individua Continue reading >>

Defining The Genetic Contribution Of Type 2 Diabetes Mellitus

Defining The Genetic Contribution Of Type 2 Diabetes Mellitus

Diabetes mellitus (DM) affects over 150 million people world wide, with a prevalence that varies markedly from population to population.1 Estimates predict that almost 300 million people will suffer from DM by 2025 (fig 1) with the vast majority being cases of diabetes mellitus type 2. Many risk factors have been identified which influence the prevalence (total number of cases as a percentage of the total population) or incidence (total number of new cases per year as a percentage of the total population). Factors of particular importance are a family history of diabetes mellitus, age, overweight, increased abdominal fat, hypertension, lack of physical exercise, and ethnic background. Several biochemical markers have also been identified as risk factors, including fasting hyperinsulinaemia, increased fasting proinsulin, and decreased HDL cholesterol.2 Both diabetes mellitus types 1 and 2 show a familial predisposition, which is a strong indication for the involvement of genes in people's susceptibility to the disease. However, the aetiology underlying types 1 and 2 is different and different genes are likely to be involved in each type of diabetes mellitus. The following discussion focuses on a genetic dissection of type 2 diabetes mellitus. The two most common forms of diabetes mellitus, type 1 and type 2, are both characterised by raised plasma glucose levels. Normal glucose homeostasis depends on the balance between glucose production by the liver and kidneys and glucose uptake by the brain, kidneys, muscles, and adipose tissue. Insulin, the predominant anabolic hormone involved, increases the uptake of glucose from the blood, enhances its conversion to glycogen and triglyceride, and also increases glucose oxidation. Plasma glucose levels are normally kept within a s Continue reading >>

Early-onset Type 2 Diabetes: Metabolic And Genetic Characterization In The Mexican Population

Early-onset Type 2 Diabetes: Metabolic And Genetic Characterization In The Mexican Population

The objective of this study was to investigate possible defects in the insulin sensitivity and/or the acute insulin response in a group of Mexican patients displaying early-onset type 2 diabetes and to evaluate the contribution of mutations in three of the genes linked to maturity-onset diabetes of the young. We studied 40 Mexican patients with an age of diagnosis between 20 and 40 yr in which the insulin sensitivity as well as the insulin secretory response were measured using the minimal model approach. A partial screening for possible mutations in 3 of the 5 genes linked to maturity-onset diabetes of the young was carried out by PCR-single strand conformation polymorphism analysis. A low insulin secretory capacity (AIRg = 68.5 5 U/mLmin) and a near-normal insulin sensitivity (3.43 0.2 min/UmL 104) were found in these patients. Among this group we found two individuals carrying missense mutations in exon 4 of the hepatocyte nuclear factor-1 (HNF-4) gene (Asp126His/Tyr and Arg154Gln, respectively) and one carrying a nonsense mutation in exon 7 of the HNF-1 gene (Gln486stop codon); 7.5% had positive titers for glutamic acid decarboxylase antibodies. Thirty-five percent of cases had insulin resistance; these subjects had the lipid abnormalities seen in the metabolic syndrome. A defect in insulin secretion is the hallmark in Mexican diabetic patients diagnosed between 20 and 40 yr of age. Mutations in either the HNF-1 or the HNF-4 genes are present among the individuals who develop early-onset diabetes in our population. These particular sequence changes have not been previously reported and therefore represent putative new mutations. Even in the absence of endogenous hyperinsulinemia, insulin resistance is associated with an adverse lipid profile. TYPE 2 DIABETES mellit Continue reading >>

Early-onset Type 2 Diabetes: Metabolic And Genetic Characterization In The Mexican Population

Early-onset Type 2 Diabetes: Metabolic And Genetic Characterization In The Mexican Population

The objective of this study was to investigate possible defects in the insulin sensitivity and/or the acute insulin response in a group of Mexican patients displaying early-onset type 2 diabetes and to evaluate the contribution of mutations in three of the genes linked to maturity-onset diabetes of the young. We studied 40 Mexican patients with an age of diagnosis between 20 and 40 yr in which the insulin sensitivity as well as the insulin secretory response were measured using the minimal model approach. A partial screening for possible mutations in 3 of the 5 genes linked to maturity-onset diabetes of the young was carried out by PCR-single strand conformation polymorphism analysis. A low insulin secretory capacity (AIRg = 68.5 5 U/mLmin) and a near-normal insulin sensitivity (3.43 0.2 min/UmL 104) were found in these patients. Among this group we found two individuals carrying missense mutations in exon 4 of the hepatocyte nuclear factor-1 (HNF-4) gene (Asp126His/Tyr and Arg154Gln, respectively) and one carrying a nonsense mutation in exon 7 of the HNF-1 gene (Gln486stop codon); 7.5% had positive titers for glutamic acid decarboxylase antibodies. Thirty-five percent of cases had insulin resistance; these subjects had the lipid abnormalities seen in the metabolic syndrome. A defect in insulin secretion is the hallmark in Mexican diabetic patients diagnosed between 20 and 40 yr of age. Mutations in either the HNF-1 or the HNF-4 genes are present among the individuals who develop early-onset diabetes in our population. These particular sequence changes have not been previously reported and therefore represent putative new mutations. Even in the absence of endogenous hyperinsulinemia, insulin resistance is associated with an adverse lipid profile. TYPE 2 DIABETES mellit Continue reading >>

Omim Entry - % 601407 - Diabetes Mellitus, Noninsulin-dependent, 2; Niddm2

Omim Entry - % 601407 - Diabetes Mellitus, Noninsulin-dependent, 2; Niddm2

For a phenotypic description and a discussion of genetic heterogeneity of noninsulin-dependent diabetes mellitus (NIDDM), see 125853 . Mahtani et al. (1996) found that, among 26 families enriched for NIDDM ( 125853 ), families with the lowest insulin levels showed significant linkage to chromosome 12 near D12S1349. Lehto et al. (1997) found that NIDDM2, like MODY3 ( 600496 ), is characterized by a reduced insulin secretory response that subsequently progresses to diabetes. By screening over 4,000 individuals from a Swedish-speaking population isolate in the Botnia region of western Finland, Mahtani et al. (1996) identified 26 families (comprising 217 individuals) enriched for NIDDM and performed a genomewide scan using nonparametric linkage analysis. They found no significant evidence for linkage when the families were analyzed together, but strong evidence for linkage when families were classified according to mean insulin levels in affected individuals in oral glucose tolerance tests. Specifically, families with the lowest insulin levels showed significant linkage to chromosome 12 near D12S1349. This region contains the gene causing the rare, dominant, early-onset form of diabetes, designated MODY3. Unlike MODY3 families, the Finnish families with low insulin had an age of onset typical for NIDDM (mean = 58 years). Mahtani et al. (1996) inferred the existence of a gene NIDDM2 causing noninsulin-dependent diabetes mellitus associated with low insulin secretion and suggested that NIDDM2 and MODY3 may represent different alleles of the same gene. Lehto et al. (1997) found that NIDDM2, like MODY3, is characterized by a reduced insulin secretory response that subsequently progresses to diabetes. This, together with the common site of the gene on 12q, suggested to them tha Continue reading >>

What Is Monogenic Diabetes?

What Is Monogenic Diabetes?

Note: This article is part of our library of resources for Forms of Diabetes. Monogenic diabetes is a rare type of diabetes thats caused by a single gene mutation.It accounts for about 1-2% of all diabetes cases, though its prevalence may actually be up to 5%.It has characteristics of both Type 1 and Type 2, and is often misdiagnosed as one of those more common types. Treatment can vary, depending on the particular gene involved and the way the diabetes presents in each individual. Some manage their diabetes with diet and exercise, and some use oral medications or insulin.People with this rare form of diabetesare usually very insulin sensitive and use smaller than typical doses of insulin. Their bodies make insulin, but not enough and not always at the right time. There are two main forms of Monogenic diabetes (with subtypes in each): Neonatal diabetes is usually diagnosed in infants from birth to 6 months, though diagnosis may occur later in some cases. MODY (Maturity Onset Diabetes of the Young)is usually diagnosed in late childhood to adulthood. Monogenic diabetes is usually passed on in an autosomal dominant gene, (a sex independentgene thats inherited from one of the parents). This means only one copy of the mutation is needed to develop diabetes. There is usually a strong family history of diabetes and in multiple generations, (although its possible for someone to have a spontaneous mutation). Diagnosis, therefore, involves genetic testing for these diabetes-causing gene mutations that disrupt insulin production. Monogenic diabetes patients are also usually antibody negative, (though there are cases where low levels of antibodies have been detected). Once treatment for the diabetes begins, the antibodies usually resolve. In addition to blood sugar issues, some of Continue reading >>

Genetic Causes Of Diabetes Mellitus Type 2

Genetic Causes Of Diabetes Mellitus Type 2

Most cases of diabetes mellitus type 2 involved many genes contributing small amount to the overall condition.[1] As of 2011 more than 36 genes have been found that contribute to the risk of type 2 diabetes.[2] All of these genes together still only account for 10% of the total genetic component of the disease.[2] There are a number of rare cases of diabetes that arise due to an abnormality in a single gene (known as monogenic forms of diabetes).[1] These include maturity onset diabetes of the young (MODY), Donohue syndrome, and Rabson–Mendenhall syndrome, among others.[1] Maturity onset diabetes of the young constitute 1–5% of all cases of diabetes in young people.[3] Polygenic[edit] Genetic cause and mechanism of type 2 diabetes is largely unknown. However, single nucleotide polymorphism (SNP) is one of many mechanisms that leads to increased risk for type 2 diabetes. To locate genes and loci that are responsible for the risk of type 2 diabetes, genome wide association studies (GWAS) was utilized to compare the genomes of diabetic patient group and the non-diabetic control group.[4] The diabetic patients’ genome sequences differ from the controls' genome in specific loci along and around numerous genes, and these differences in the nucleotide sequences alter phenotypic traits that exhibit increased susceptibility to the diabetes. GWAS has revealed 65 different loci (where single nucleotide sequences differ from the patient and control group's genomes), and genes associated with type 2 diabetes, including TCF7L2, PPARG, FTO, KCNJ11,NOTCH2, WFS1, IGF2BP2, SLC30A8, JAZF1, HHEX, DGKB, CDKN2A, CDKN2B, KCNQ1, HNF1A, HNF1B MC4R, GIPR, HNF4A, MTNR1B, PARG6, ZBED3, SLC30A8, CDKAL1, GLIS3, GCKR, among others.[4][5][6][7]KCNJ11 (potassium inwardly rectifying channel, subfa Continue reading >>

Diabetes Mellitus Type 1 Inheritance

Diabetes Mellitus Type 1 Inheritance

Type 1 diabetes is an inherited condition and individuals with a first degree relative who has the condition are at an increased risk of developing the condition. Details regarding the risk of inheriting type 1 diabetes are given below: In men with type 1 diabetes, the risk of their child also developing the condition is one in 17. In women with type 1 diabetes who have their baby before the age of 25, the risk of the child developing the condition is one in 25. If she has her baby after the age of 25, the risk falls to 1 in 100. If both parents have type 1 diabetes, the risk of the condition developing in offspring varies between 1 in 4 and 1 in 10. The risks are somewhat increased if one of the parents developed type 1 diabetes before the age of 11. Around 1 in 7 people with type 1 diabetes suffer from a condition called type 2 polyglandular autoimmune syndrome and these individuals have parathyroid and adrenal gland disorders in addition to type 1 diabetes. If one of the parents has type 2 polyglandular autoimmune syndrome, the risk that the child will inherit the condition, including type 1 diabetes, is 50%. Genes associated with type 1 diabetes Some genes have repeatedly been identified in people with type 1 diabetes. Among white individuals, examples of such genes include the HLA-DR3 or HLA-DR4 genes. Carrying these genes raises the risk that offspring will inherit type 1 diabetes. Children born with the HLADR3/4-DQ8 genotype make up nearly 50% of all children who develop type 1 diabetes before they are 5 years of age. Some studies on other ethnic groups have shown that similar risks are associated with the HLA-DR7 genotype among African Americans and with the HLA-DR9 gene among Japanese individuals. Genetic studies have also located HLA class II genes at 6p21 and Continue reading >>

Sade Pblica - The Burden Of Gestational Diabetes Mellitus In Jamaican Women With A Family History Of Autosomal Dominant Type 2 Diabetes The Burden Of Gestational Diabetes Mellitus In Jamaican Women With A Family History Of Autosomal Dominant Type 2 Diabetes

Sade Pblica - The Burden Of Gestational Diabetes Mellitus In Jamaican Women With A Family History Of Autosomal Dominant Type 2 Diabetes The Burden Of Gestational Diabetes Mellitus In Jamaican Women With A Family History Of Autosomal Dominant Type 2 Diabetes

The burden of gestational diabetes mellitus in Jamaican women with a family history of autosomal dominant type 2 diabetes La carga de la diabetes mellitus gestacional en mujeres de Jamaica con antecedentes familiares de diabetes autosmica dominante tipo 2 Rachael R. IrvingI, * ; James L. MillsI; Eric G. Choo-KangII; Errol Y. MorrisonI; Santosh KulkarniIII; Rosemarie Wright-PascoeIV; Wayne MclaughlinI IDepartment of Basic Medical Sciences, University of the West Indies, Kingston, Jamaica IIDepartment of Pathology, University of the West Indies, Kingston, Jamaica IIIDepartment of Gynaecology, Obstetrics and Child Health, University of the West Indies, Kingston, Jamaica IVDepartment of Medicine, University of the West Indies, Kingston, Jamaica OBJECTIVES:To determine if Jamaican women of African descent with a family history of early onset autosomal dominant type 2 diabetes have greater odds of developing gestational diabetes mellitus (GDM) than those without a family history of the disease. METHODS:A comparative study was conducted of two groups of pregnant Jamaican women: the first with a family history of early onset autosomal dominant type 2 diabetes; the second with no history of the disease. Incidence, odds for developing GDM, and metabolic profiles in first and second trimesters were assessed using SPSS 11.5 (SPSS Inc., Chicago, Illinois, United States). RESULTS: The incidence of GDM was 12.0 % in women with a family history of early onset autosomal dominant type 2 diabetes and 1.5% in women without a family history of the disease (P < 0.05). Women with a family history were nine times more likely to develop GDM than those without a family history of diabetes (95% confidence interval: 5.0016.38, P < 0.0001). CONCLUSION:Family history of early onset autosomal domina Continue reading >>

Genetic Diabetes

Genetic Diabetes

Many people wonder, is type 1 diabetes genetic, and is type 2 diabetes genetic? The common types of diabetes tend to run in families. However, neither type 1 diabetes (thin diabetes) nor type 2 diabetes (fat diabetes) is truly a genetic disease. It is possible for one member of a pair of identical twins to have thin or fat diabetes, while the other twin remains healthy. It is even possible for a person with fat diabetes to recover from their diabetes, by losing weight. Nevertheless, there are a few rare forms of diabetes that truly are genetic diseases. These conditions are sometimes called monogenic diabetes because they result from a mutation in a single gene. By the 1970s, it was clear that some cases of diabetes did not fit neatly into either of the main types of diabetes mellitus. In particular, there were some cases that were relatively mild (like type 2 diabetes) but occurred in young, thin children (like type 1 diabetes). In these cases, the doctors suspected that they had spotted an early case of type 1 diabetes, but the problem never seemed to progress. Eventually, doctors realized that this problem ran in families. This condition was eventually called maturity-​onset diabetes of the young (MODY). Several forms of MODY have been identified. Each is associated with one particular gene mutation. MODY is an autosomal dominant trait. You need only one copy of the defective gene in order to have the problem. Cases of MODY tend to be mild. In many cases, the person seems healthy. The only evidence of disease may be a high blood sugar reading during routine bloodwork. Many cases are discovered only after relatives of someone with a diagnosed case of MODY go in for testing. The treatment for MODY varies, depending on the particular gene mutation involved. Many cases Continue reading >>

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