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Ebook `Diabetes mellitus: its history, chemistry, anatomy, pathology, Illustrated with woodcuts, and cases successfully treated: download ebook or read online. EMRO Technical Publications Series Guidelines for the prevention, management and care of diabetes mellitus. Editor. Oussama MN Khatib (MD, PhD, FRCP). "Principles of Diabetes Mellitus, Second Edition" is an important update to the ebooks can be used on all reading devices; Immediate eBook download after.

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which allows users to download, copy and build upon published articles even for commercial Chapter 1 CNS Complications of Diabetes Mellitus Type 1. Buy International Textbook of Diabetes Mellitus: Read Kindle Store Reviews - eBook features: numbers are just like the physical edition; Length: pages; Due to its large file size, this book may take longer to download. The epidemic nature of diabetes mellitus in different regions is reviewed. The Middle East and North Africa region has the highest prevalence of.

The incidence and severity of diabetes mellitus is increasing worldwide, presenting a significant burden to society both in economic terms and overall well-being. Fortunately, time-tested anti-diabetes mellitus plant foods exist that are safe and could be effective in addressing this condition when consumed judiciously with a concomitant change in lifestyle. Plants with Anti-Diabetes Mellitus Properties presents an exhaustive compilation of the anti-diabetes mellitus activities of more than plants occurring worldwide. The author provides a brief botanical description, distribution, pharmacological properties, and phytochemicals, where appropriate. A list of traditional medicinal plants used to treat diabetes, but not tested for anti-diabetic activity, is also given.

This autoimmune type 1 diabetes is characterized by the absence of insulin secretion and is more dominant in children and adolescents. Number of subjects with type 1 diabetes in children years , with diabetes in adults years and with hyperglycemia type 2 or gestational diabetes in pregnancy years. In addition to the importance of genetic predisposition in type 1 diabetes, several environmental factors have been implicated in the etiology of the disease[ 9 , 33 ].

Viral factors include congenital rubella[ 34 , 35 ], viral infection with enterovirus, rotavirus, herpes virus, cytomegalovirus, endogenous retrovirus[ 36 , 37 ] and Ljungan virus. The role of environmental factors remains controversial[ 40 ]. Recent evidence supported the causative effect of viral infections in diabetes[ 41 - 43 ].

Type 1 diabetes often develops suddenly and can produce symptoms such as polydipsia, polyuria, enuresis, lack of energy, extreme tiredness, polyphagia, sudden weight loss, slow-healing wounds, recurrent infections and blurred vision[ 27 ] with severe dehydration and diabetic ketoacidosis in children and adolescents. The symptoms are more severe in children compared to adults. The complete dependence on insulin of type 1 diabetes patients may be interrupted by a honeymoon phase which lasts weeks to months or in some cases years.

In some children, the requirement for insulin therapy may drop to a point where insulin therapy could be withdrawn temporarily without detectable hyperglycemia[ 44 ]. A rare form of type 1 diabetes of unknown origin idiopathic , less severe than autoimmune type 1 diabetes and is not due to autoimmunity has been reported. Most patients with this type are of African or Asian descent and suffer from varying degrees of insulin deficiency and episodic ketoacidosis[ 45 ].

This is a distinct form of type 1 diabetes, first described in the year , and has some common features with idiopathic type 1 diabetes being non-immune mediated[ 46 , 47 ]. Both genetic and environmental factors, especially viral infection, have been implicated in the disease. Anti-viral immune response may trigger the destruction of pancreatic beta cells through the accelerated immune reaction with no detectable autoantibodies against pancreatic beta cells[ 48 , 50 ].

Association of fulminant type 1 diabetes with pregnancy has also been reported[ 51 ]. The global prevalence of diabetes in adults years old according to a report published in by the IDF was 8.

Principles of Diabetes Mellitus | Leonid Poretsky | Springer

With million cases still undiagnosed, the number of people currently suffering from diabetes exceeds half a billion. An additional 21 million women are diagnosed with hyperglycemia during pregnancy.

The Middle East and North Africa region has the highest prevalence of diabetes Despite the fact that adult diabetes patients are mainly type 2 patients, it is not clear whether the reported million adults diagnosed with diabetes also include type 1 diabetes patients.

The number of youth less than 20 years with type 2 diabetes in the United States in the year was 0. The increased incidence of type 2 diabetes in youth is mainly due to the change in the lifestyle of the children in terms of more sedentary life and less healthy food. Obesity is the major reason behind insulin resistance which is mainly responsible for type 2 diabetes[ 52 - 54 ].

The ADA recommends screening of overweight children and adolescence to detect type 2 diabetes[ 55 , 56 ]. The prevalence of obesity in children in on the rise[ 6 ] which is probably the main reason for the increased incidence of type 2 diabetes in the young Insulin resistance in type 2 diabetes patients increases the demand for insulin in insulin-target tissues.

Most type 2 diabetes patients are not dependent on insulin where insulin secretion continues and insulin depletion rarely occurs. Dependence on insulin is one of the major differences from type 1 diabetes. Both type 1 and type 2 diabetes have genetic predisposition, however, it is stronger in type 2 but the genes are more characterized in type 1 the TCF7L2 gene is strongly associated with type 2 diabetes [ 58 ].

Due to the mild symptoms of type 2 diabetes in the beginning, its diagnosis is usually delayed for years especially in countries where regular checkup without symptoms is not part of the culture. This delay in diagnosis could increase the incidence of long-term complications in type 2 diabetes patients since hyperglycemia is not treated during this undiagnosed period.

In addition to diabetes, insulin resistance has many manifestations that include obesity, nephropathy, essential hypertension, dyslipidemia hypertriglyceridemia, low HDL, decreased LDL particle diameter, enhanced postprandial lipemia and remnant lipoprotein accumulation , ovarian hyperandrogenism and premature adrenarche, non-alcoholic fatty liver disease and systemic inflammation[ 6 , 54 ].

The presence of type 2 diabetes in children and adolescence who are not obese[ 59 - 61 ], the occasional severe dehydration and the presence of ketoacidosis in some pediatric patients with type 2 diabetes[ 55 ] had led to the misclassification of type 2 to type 1 diabetes. Some patients with many features of type 2 diabetes have some type 1 characteristics including the presence of islet cell autoantibodies or autoantibodies to GAD65 are classified as a distinct type of diabetes called latent autoimmune diabetes in adults LADA [ 62 ].

People diagnosed with LADA do not require insulin treatment. In a recent study, Hawa et al[ 63 ] reported 7. This classification of LADA as a distinct type of diabetes is still controversial[ 6 , 64 - 66 ]. Defects in the insulin-dependent substrate proteins IRS-1 and IRS-2 mediated signaling pathway are implicated in the development of metabolic disorders, mainly diabetes.

In addition, other non-insulin dependent kinases including the AMP-activated protein kinase, c-Jun N-terminal protein kinase and G protein-coupled receptor kinase 2 that are activated under various conditions can phosphorylate the two insulin responsive substrates[ 67 - 71 ].

Disruption in the AKT and PKC kinases is central to the development of diabetes[ 72 ] and is associated with all major features of the disease including hyperinsulinemia, dyslipidemia and insulin resistance[ 73 ]. Replacing the wild type IRS-1 with a mutant version of the protein having alanine instead of tyrosine in three locations using genetic knock-in approach provided evidence to the central role of IRS-1 phosphorylation in the development of insulin resistance[ 74 ].

Using a similar approach to generate IRS-1 mutant with a single mutation involving a specific tyrosine residue, confirmed the role of IRS-1 phosphorylation in the development of insulin resistance pathogenesis[ 75 ]. The large cumulative evidence indicates a complex array of factors including environmental factors[ 76 ] and a wide range of cellular disturbances in glucose and lipid metabolism in various tissues[ 77 ] contribute to the development of insulin resistance.

This condition generates complex cellular metabolic changes in a variety of tissues, mainly liver and muscles, that include the inability of the liver to transport and dispose glucose, control glucose production via gluconeogenesis, impaired storage of glucose as glycogen, de novo lipogenesis and hypertriglyceridemia[ 77 ]. Among the factors implicated in the development of insulin resistance, obesity is the most predominant risk factor leading to insulin insensitivity and diabetes which involves several mechanisms that participate in the pathogenesis of the disease[ 78 ].

Obesity-induced insulin resistance is directly linked to increased nutrient flux and energy accumulation in tissues that directly affect cell responsiveness to insulin[ 77 ]. However, it seems that other insulin-independent mechanisms are involved in the overall metabolic disturbances of glucose homeostasis and diabetes including activities in extra-hepatic tissues in addition to the central role of liver.

Characterization of the genetic etiology of diabetes enables more appropriate treatment, better prognosis, and counseling[ 79 ].

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Conventionally, monogenic diabetes is classified according to the age of onset as neonatal diabetes before the age of six months or Maturity Onset Diabetes of the Young MODY before the age of 25 years.

However, certain familial defects are manifested in neonatal diabetes, MODY or adult onset diabetes[ 2 , 9 , 80 ]. Others believe that classification of diabetes as MODY and neonatal diabetes is obsolete and monogenic diabetes is currently used relating specific genetic etiologies with their specific treatment implications[ 79 ]. Beta cell differentiation depends on the expression of the homeodomain transcription factor PDX1 where mutation in the gene results in early onset diabetes MODY and its expression decreases before the onset of diabetes[ 81 ].

Mitochondrial diabetes is due to a point mutation in the mitochondrial DNA associated with deafness and maternal transmission of the mutant DNA can result in maternally-inherited diabetes[ 1 , 83 ]. Mutations that result in mutant insulin or the inability to convert proinsulin to insulin result in glucose intolerance in some of these cases.

Genetic defects in the insulin receptor or in the signal transduction pathway of insulin have been demonstrated to result in hyperinsulinemia and modest hyperglycemia to severe diabetes[ 1 ]. This damage could be due to pancreatic carcinoma, pancreatitis, infection, pancreatectomy, and trauma[ 1 ].

In most cases, extensive damage of the pancreas is required before diabetes occurs and the exocrine function of the pancreas is decreased in these patients[ 86 ]. Cirrhosis in cystic fibrosis may contribute to insulin resistance and diabetes[ 2 ].

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Some of these hormones are used as drugs such as glucocorticoids to suppress the immune system and in chemotherapy and growth hormone to treat children with stunted growth.

Diabetes has been detected in patients with various genetic syndromes such as Down syndrome, Klinefelter syndrome, Turner syndrome and Wolfram syndrome[ 1 ]. Individuals with prediabetes do not meet the criteria of having diabetes but are at high risk to develop type 2 diabetes in the future. Prediabetes has been shown to correlate with increased cardiovascular mortality[ 87 , 88 ] and cancer[ 89 ]. The definition of prediabetes with the indicated cut off values is misleading since lower levels of glucose in the normal range are still correlated with cardiovascular disease in a continuous glycemic risk perspective[ 90 ].

According to a report in by the Center for Disease Control and Prevention, 86 million Americans 1 out of 3 have prediabetes[ 92 ]. The number of people diagnosed with prediabetes is different according to the method and criteria used to diagnose prediabetes. Individuals with an HbA1c of 6. In addition to monitor the treatment of diabetes, HbA1c has been recommended to diagnose diabetes by the International Expert Committee in [ ] and endorsed by ADA[ ], the Endocrine Society, the WHO[ ] and many scientists and related organizations all over the world.

The advantages and disadvantages of the different tests used to diagnose diabetes have been reviewed by Sacks et al[ ]. It is recommended to repeat the HbA1c test in asymptomatic patients within two weeks to reaffirm a single apparently diagnostic result[ ]. Cut-off values of 5. The Australians recommended the use of two cut-off values: Variations in the prevalence of diabetes[ 94 , - ] and prediabetes[ ] due to ethnicity have been documented.

Yet, other studies reported more subjects diagnosed with diabetes using HbA1c[ 96 , - ]. Hyperglycemia in pregnancy whether in the form of type 2 diabetes diagnosed before or during pregnancy or in the form gestational diabetes has an increased risk of adverse maternal, fetal and neonatal outcome. Mothers with gestational diabetes and babies born to such mothers have increased risk of developing diabetes later in life. Risk factors for gestational diabetes include obesity, personal history of gestational diabetes, family history of diabetes, maternal age, polycystic ovary syndrome, sedentary life, and exposure to toxic factors[ 3 ].

Diagnosis of type 2 diabetes before or during pregnancy is based on criteria mentioned before. However, gestational diabetes has been diagnosed at wk of gestation in women not previously diagnosed with diabetes using two approaches: This criteria is derived from the Hyperglycemia and Adverse Pregnancy Outcome HAPO study[ ] even though the HAPO study showed a continuous relationship between hyperglycemia and adverse short-term pregnancy outcome with no threshold reported[ ].

The diagnosis of gestational diabetes is made when at least two of the four plasma glucose levels are met. A strategy of using fasting plasma glucose as a screening test and to determine the need for OGTT is valid[ , ]. According to Sacks[ ], correlation of glucose concentrations and the risk of subsequent complications will eventually lead to universal guidelines.

Further investigation is required in light of recent reports on HbA1c in combination with OGTT and its usefulness to predict adverse effect of gestational diabetes or obviate the use OGTT in all women with gestational diabetes[ - ].

Diabetes is a complex disease that involves a wide range of genetic and environmental factors. Over the past several years, many studies have focused on the elucidation of the wide spectrum of genes that played a role in the molecular mechanism of diabetes development[ - ].

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However, despite the vast flow of genetic information including the identification of many gene mutations and a large array of single nucleotide polymorphisms SNPs in many genes involved in the metabolic pathways that affect blood glucose levels, the exact genetic mechanism of diabetes remains elusive[ , ]. Evidently, a major complication is the fact that a single gene mutation or polymorphism will not impose the same effect among different individuals within a population or different populations.

This variation is directly or indirectly affected by the overall genetic background at the individual, family or population levels that are potentially further complicated by interaction with highly variable environmental modifier factors[ , ].

One of the major focuses of biomedical research is to delineate the collective and broad genetic variants in the human genome that are involved in the development of diabetes. This major effort will potentially provide the necessary information to understand the molecular genetics of the different forms of diabetes including type 1, type 2 and monogenic neonatal diabetes among individuals of all populations and ethnic groups.

Despite the fact that linkage and association studies allowed the identification and characterization of many candidate genes that are associated with type 2 diabetes[ , , ], however, not all of these genes showed consistent and reproducible association with the disease[ ]. Genome wide association studies GWAS in various populations identified 70 loci associated with type 2 diabetes and revealed positive linkage of many mutations and SNPs that influence the expression and physiological impact of the related proteins and risk to develop type 2 diabetes.

Two similar studies from the Finns and Swedish populations and the United States resulted in the identification of similar single nucleotide variants[ ] that are linked to the risk of acquiring type 2 diabetes[ , ]. The study in the United States population included in addition to type 2 diabetes, the association of the identified SNPs with the level of triglycerides in the tested subjects[ ].

Other GWAS analysis studies were performed in the Chinese, Malays, and Asian-Indian populations which are distinct from the European and United States populations in addition to meta-analysis of data from other populations in the region revealed relevant findings among patients with European ancestry[ ].

These results provide strong evidence of common genetic determinants including common specific genes that are linked to diabetes. A small list of specific genetic markers seem strongly associated with the risk of developing type 2 diabetes including the TCF7L2 [ ] and CAPN10 [ , ] genes which also play a significant role in the risk and pathogenesis of the disease[ , ]. The association of TCF7L2 gene variants with type 2 diabetes and its mechanism of action received special attention by several investigators[ , ].

Over expression of the protein was shown to decrease the sensitivity of beta islet cells to secrete insulin[ , ] and was more precisely involved in the regulation of secretary granule fusion that constitute a late event in insulin secretion pathway[ ]. The role of TCF7L2 in insulin secretion was partially clarified[ ] that involves modifying the effect of incretins on insulin secretion by lowering the sensitivity of beta cells to incretins.

Several other genes have been found to be significantly associated with the risk of developing type 2 diabetes including a specific SNP in a hematopoietically-expressed homeobox HHEX gene[ ]. The islet zinc transporter protein SLC30A8 [ ] showed positive correlation with the risk of developing type 2 diabetes where variant mutations in this gene seem protective against the disease which provides a potential tool for therapy[ ].

More recently, a low frequency variant of the HNF1A identified by whole exome sequencing was associated with the risk of developing type 2 diabetes among the Latino population and potentially may serve as a screening tool[ ]. In a study involving the hormone sensitive lipase responsible for lipolysis in adipose tissues, a deletion null mutation, which resulted in the absence of the protein from adipocytes, was reported to be associated with diabetes[ ].

Nine specific rare variants in the peroxisome proliferator-activated receptor gamma PPARG gene that resulted in loss of the function of the protein in adipocytes differentiation, were significantly associated with the risk of developing type 2 diabetes[ ].

In addition, certain SNPs in the alpha 2A adrenergic receptor ADRA2A gene, involved in the sympathetic nervous system control of insulin secretion and lipolysis, were found to be associated with obesity and type 2 diabetes[ ]. Link analysis between the melatonin MT2 receptor MTNR1B gene, a G-protein coupled receptor, identified 14 mutant variants from 40 known variants revealed by exome sequencing, to be positively linked with type 2 diabetes[ ].

The authors suggested that mutations in the MT2 gene could provide a tool with other related genes in modifying therapy for type 2 diabetes patients based on their specific genetic background to formulate personalized therapies which potentially may ensures the optimum response.

Interestingly, mutations in the clock[ , ] and Bmal1 [ ] transcription factor genes which are involved in beta cells biological clock affecting growth, survival and synaptic vesicle assembly in these cells, resulted in reduced insulin secretion and diabetes.

Evidently, prominent metabolic functions involve the production of specific reactive metabolites, leading to oxidative stress, which affect lipids, proteins and other biological compounds leading to serious damage in various tissues and organs. Mutations and SNPs in the antioxidant genes, including superoxide dismutase, catalase and glutathione peroxidase, that decrease their activity are implicated in the risk and pathogenesis of type 2 diabetes[ ].

The metabolic syndrome was shown to be associated with the development of type 2 diabetes in a population that is described as highly endogenous especially in individuals over 45 years of age[ ]. Since consanguinity marriages is high in this population, screening for this syndrome among families could provide an informative marker on the risk of developing type 2 diabetes[ ]. Even though type 1 diabetes is basically described as an autoimmune disease that results in the destruction of pancreatic beta cells, however, single gene mutations and SNPs have been found to be associated with the susceptibility to this type of diabetes.

Initially, two gene mutations were linked to the development of type 1 diabetes including the autoimmune regulator AIRE gene which affect the immune tolerance to self antigens leading to autoimmunity[ ] and the FOXP3 gene which results in defective regulatory T cells[ ].

In addition, a mutation in the histone deacetylase SIRTI gene predominantly expressed in beta cells involved in the regulation of insulin secretion[ ] and played a role in modulating the sensitivity of peripheral tissues to insulin[ ] was detected in type 1 diabetes patients[ ]. Two specific polymorphisms in the promoter region of a transmembrane protein DC-SIGN gene expressed in macrophages and played an important role of T- cell activation and inflammation were found to be protective against type 1 diabetes[ ].

An innovative non-parametric SNP enrichment tool using summary GWAS DATA allowed the identification of association between several transcription factors and type 1 diabetes and are located in a type 1 diabetes susceptibility region[ ].

Nine SNP variants in several genes associated with type 1 diabetes, not including the major histocompatibility gene region, were identified using extensive GWAS analysis[ ]. Furthermore, several novel SNPs in a region in chromosome 16 located in the CLEC16A gene were shown to be associated with type 1 diabetes and seem to function through the reduced expression of DEX1 in B lymphoblastoid cells[ ].

Since more than 40 regions in the human genome were identified to be associated with the susceptibility to type 1 diabetes[ - ], a weighted risk model was developed utilizing selected genes SNPs could be used for testing infants for these genetic markers that could provide insights in the susceptibility to type 1 diabetes development or safe prevention of the disease among young children[ ].

Monogenic diabetes results primarily from gene defects that lead to a decrease in beta cell number or function. Monogenic diabetes genes were identified using linkage studies or code for proteins that directly affected glucose homeostasis. The majority of genes responsible for monogenetic diabetes code for either transcription factors that participate in the control of nuclear gene expression or proteins that are located on the cell membrane, cytoplasm and endoplasmic reticulum, proteins involved in insulin synthesis and secretion, exocrine pancreatic proteins and autoimmune diabetes proteins[ 80 ].

The collective function of these proteins is their participation in glucose metabolism at different levels. Evidently, the hierarchy of a specific gene in the overall glucose metabolism pathway determines the onset of diabetes in the patient and whether it is neonataly expressed or have late onset expression adulthood.

Consequently, molecular defects in the structure and function of these genes lead to the disturbance of plasma glucose level, the primary pathological sign of diabetes. The molecular mechanism of permanent neonatal diabetes mellitus PNDP in addition to MODY explains the observed phenotype of monogenetic diabetes that involves loss of function of the expressed mutant protein.

The first gene implicated in monogenic diabetes was the glucokinase GCK gene[ ] which functions as a pancreatic sensor for blood glucose where more than 70 mutations in the gene were identified that affected its activity[ ]. A recent study on GCK gene mutations causing neonatal and childhood diabetes showed that the majority of mutations resulted in the loss of the enzyme function primarily due to protein instability[ , ]. Definitely, a whole list of other genes involved in monogenic diabetes are either overlooked or included in the genetic determinants of type 1 and type 2 diabetes which will be identified and clarified through more careful future studies.

In addition to the genetic determinants of diabetes, several gene mutations and polymorphisms have been associated with the clinical complications of diabetes. The cumulative data on diabetes patients with a variety of micro- and macrovascular complications support the presence of strong genetic factors involved in the development of various complications[ ].

A study on Chinese patients revealed a single SNP in the promoter region of the smooth muscle actin ACTA2 gene correlates with the degree of coronary artery stenosis in type 2 diabetes patients[ ]. Furthermore, the alpha kinase 1 gene ALPK1 identified as a susceptibility gene for chronic kidney disease by GWAS[ ], was demonstrated in type 2 diabetes patients[ ].

Three additional genes have been strongly correlated with this risk of diabetic retinopathy DR including the vascular endothelial growth receptor, aldose reductase and the receptor for advanced glycation products genes[ ] where specific polymorphisms in these genes seem to increase the risk of DR development in diabetes patients[ ].

A significant differential proteome involving 56 out of proteins is evident that characterizes vitreous samples obtained from diabetes patients with the complication in comparison to diabetes patients without the complication and control individuals[ ]. Interestingly, a large portion of these proteins 30 proteins belong to the kallikrein-kinin, coagulation and complement systems including complement C3, complement factor 1, prothrombin, alphaantitrypsin and antithrombin III that are elevated in diabetic patients with retinopathy[ ].

In addition, 2 single nucleotides polymorphisms in the human related B7-I gene seem to mediate podocyte injury in diabetic nephropathy[ ]. Furthermore, increased concentration of the ligand of B correlates with the progression of end-stage renal disease ESRD in diabetes patients[ ].

Recently, it was shown that direct correlation is evident between circulating levels of tumor necrosis factors 1 and 2 and increased risk of ESRD in American Indian patients[ ]. The link between diabetes and proper bone development and health is evident. Studies using animal models with major significant reduction in insulin receptor IR in osteoprogenitor cells resulted in thin and rod-like weak bones with high risk of fractures[ ].

Similar findings were observed in animal models with bone-specific IR knockdown animals which points to the central role of IR in the proper development of bones[ ]. Type 2 diabetes is also associated with mitochondrial dysfunction in adipose tissues. Using knockout animal models of specific mitochondrial genes led to significant reduction in key electron transport complexes expression and eventually adipocytes death[ ]. These animals exhibited Insulin resistance in addition to other complications that can potentially lead to cardiovascular disease[ ].

Diabetes mellitus is the epidemic of the century and without effective diagnostic methods at an early stage, diabetes will continue to rise.

This review focuses on the types of diabetes and the effective diagnostic methods and criteria to be used for diagnosis of diabetes and prediabetes. Evidently, diabetes is a complex disease with a large pool of genes that are involved in its development.

The precise identification of the genetic bases of diabetes potentially provides an essential tool to improve diagnoses, therapy more towards individualized patient targeted therapy and better effective genetic counseling. The authors declare that there is no conflict of interest associated with this manuscript.

This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. Peer-review started: November 23, First decision: February 7, Article in press: April 14, P- Reviewer: Gong XM L- Editor: A E- Editor: Wang CH.

National Center for Biotechnology Information , U. Journal List World J Diabetes v. World J Diabetes. Published online Jun Author information Article notes Copyright and License information Disclaimer.

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Author contributions: Kharroubi AT and Darwish HM contributed equally to the writing of the review article; Kharroubi AT wrote the classification, diagnosis, and etiology of diabetes; Darwish HM wrote the molecular genetics of diabetes. Published by Baishideng Publishing Group Inc. All rights reserved. This article has been cited by other articles in PMC. Abstract The epidemic nature of diabetes mellitus in different regions is reviewed.

Table 1 Number of subjects with type 1 diabetes in children years , with diabetes in adults years and with hyperglycemia type 2 or gestational diabetes in pregnancy years. Region Type 1 diabetes in children yr Diabetes in adults yr Hyperglycemia in pregnancy yr Number in thousands Newly diagnosed in thousands Number in millions Comparative prevalence Number in millions Comparative prevalence Cases in live births in millions Comparative prevalence Africa Open in a separate window.

Idiopathic type 1 diabetes A rare form of type 1 diabetes of unknown origin idiopathic , less severe than autoimmune type 1 diabetes and is not due to autoimmunity has been reported. Read more Read less. Kindle Cloud Reader Read instantly in your browser. Customers who viewed this item also viewed.

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