Diabetes mellitus is not a single entity but a heterogeneous group of disorders in which there are distinct genetic patterns as well as other etiologic and pathophysiologic mechanisms that lead to impairment of glucose tolerance.1,7 Box the 1 last update 10 Jul 2020 19-1 outlines an etiologic classification of diabetes mellitus in children, based on the “Report of the Expert Committee on the Classification and Diagnosis of Diabetes Mellitus,” published by the American Diabetes Association in January of 2013.7Diabetes mellitus is not a single entity but a heterogeneous group of disorders in which there are distinct genetic patterns as well as other etiologic and pathophysiologic mechanisms that lead to impairment of glucose tolerance.1,7 Box 19-1 outlines an etiologic classification of diabetes mellitus in children, based on the “Report of the Expert Committee on the Classification and Diagnosis of Diabetes Mellitus,” published by the American Diabetes Association in January of 2013.7
Our classification is modified to reflect more accurately the major categories in childhood, including the emergence of type 2 diabetes mellitus, cystic fibrosis-related diabetes, and drug-induced diabetes—largely from the antirejection agents cyclosporine, sirolimus, and tacrolimus (formerly FK-506). Table 19-1 presents a summary of the classification originally proposed in 1979 but incorporates the newer criteria for blood glucose values used to diagnose diabetes, impaired glucose tolerance, and gestational diabetes.
Among the insulin-dependent forms, severe lack of insulin secretion results most commonly from presumed autoimmune destruction of islets in genetically predisposed hosts. This form is synonymous with type 1a diabetes, formerly called juvenile-onset diabetes.4,5,8,9 Severe insulin-dependent diabetes mellitus, clinically indistinguishable from the autoimmune form, may, however, not have any evidence of autoimmunity and can result from mitochondrial or other gene defects that interfere with normal insulin secretion or rarely from pancreatic agenesis.10-13
The more severe forms of the MODY syndromes, subsequently detailed, also may require insulin.12, the 1 last update 10 Jul 2020 1313 Clinically similar forms of diabetes may occur secondary to cystic fibrosis14,15 from toxic drugs such as the immunosuppressive agents cyclosporine, sirolimus and tacrolimus,16,17 the rodenticide Vacor,18 or streptozotocin as used for certain pancreatic islet cell tumors19; with the hemolytic uremic syndrome20; or after pancreatectomy, such as for persistent hyperinsulinemic hypoglycemia in infancy.21 Childhood insulin-dependent diabetes is generally type 1a diabetes mellitus.
Type 1 diabetes mellitus
This condition is characterized by severe insulinopenia and dependence on exogenous insulin to prevent ketosis and to preserve life. Thus, it was termed insulin-dependent diabetes for 1 last update 10 Jul 2020 mellitusdiabetes mellitus (IDDM). The natural history of this disease indicates that there are preketotic non–insulin-dependent phases before and after the initial diagnosis. Although the onset is predominantly in childhood, the disease may occur at any age.1 Therefore, such names as “juvenile diabetes,” “ketosis-prone diabetes,” and “brittle diabetes” were abandoned in favor of the term type 1 diabetes.
reverses diabetes type 2 reversal (🔥 normal range chart) | reverses diabetes type 2 natural supplementshow to reverses diabetes type 2 for Type 1a diabetes is generally distinct by virtue of its association with certain histocompatibility locus antigens (HLAs) and other genetic markers the majority of which determine the response to self (or exogenous) antigens; by the presence of circulating antibodies to cytoplasmic and cell-surface components of islet cells; of antibodies to insulin in the absence of previous exposure to exogenous injection of insulin, of antibodies to glutamic acid decarboxylase (GAD, the enzyme that converts glutamic acid to γ-aminobutyric acid found abundantly in the innervation of pancreatic islets), of antibodies to IA-2 (an islet cell-associated phosphatase and antibodies to the zinc transporter molecule ZnT8); by lymphocytic infiltration of islets early in the disease; and by coexistence with other autoimmune diseases.4,5 Occasionally, markers of autoimmunity are not found and yet there is profound insulinopenia and dependence on insulin without evidence of a mitochondrial or other genetic defect. In these cases, type 1 diabetes is considered idiopathic (type 1b). With the exceptions noted, diabetes in children is usually insulin dependent and fits the type 1a category. for 1 last update 10 Jul 2020 11
Type 2 diabetes
Persons with this subclass of diabetes (formerly known as “adult-onset diabetes,” “maturity-onset diabetes” [MOD], or “stable diabetes”) may not be permanently insulin dependent and only occasionally develop ketosis. Some may, however, need insulin to correct symptomatic hyperglycemia—and ketosis may develop in some during severe infections or other stress. Therefore, this was previously called non–insulin-dependent diabetes mellitus (NIDDM).1 This form of diabetes is becoming an increasing problem in overweight adolescents, especially those from vulnerable groups such as Africans, Mexicans, Native Indians, and other susceptible ethnic groups.22,23
Type 2 diabetes (T2DM) is not a single entity.1 T2DM may be a primary disorder, with inadequate insulin secretion caused by mutations in one of several genes encoding enzymes or transcription factors important to islet cell development and insulin secretion. Several of these defects are now part of the spectrum of the syndromes commonly associated with maturity onset diabetes of youth (MODY), which has a dominant mode of inheritance.12,13,24 However, some patients with MODY defects, which we term monogenic diabetes of youth, may require insulin from for 1 last update 10 Jul 2020 the outset or as they grow older and become insulin resistant, exceeding their ability to compensate by increasing insulin secretion (see Figure 19-1). A defect in the gene regulating glucose transport into the pancreatic beta cell, the GLUT2 transporter, may be responsible for another form of type 2 diabetes.reverses diabetes type 2 what is it (👍 vitamind3) | reverses diabetes type 2 managementhow to reverses diabetes type 2 for 24
Defects in glycogen synthase have also been implicated.25,26, A primary defect in insulin receptors—often associated with acanthosis nigricans,reverses diabetes type 2 video (🔴 soda) | reverses diabetes type 2 vitamin dhow to reverses diabetes type 2 for 27 postreceptor defects (including Rad [Ras associated with diabetes]),28 and milder mitochondrial gene defects10—also may result in type 2 diabetes. Secondary causes of type 2 diabetes mellitus include excessive counterregulatory hormones, especially pharmacologic doses of glucocorticoids, antibodies to the insulin receptor, and obesity with impaired insulin secretion. the 1 last update 10 Jul 2020 29-4029-40
In type 2 diabetes mellitus, the serum concentration of insulin may be increased, normal, or moderately depressed depending on whether the defect is one of insulin action or secretion.27-40 The onset of type 2 diabetes mellitus occurs in children generally around the time of puberty or shortly thereafter, but it is recognized, that it may occur at any age and is becoming increasingly frequent in childhood and adolescence.22,23 In some instances, there appears to be adequate secretion of insulin but resistance to its actions, and in some individuals it may represent slowly evolving type 1 diabetes mellitus.38 As an initial approach, weight reduction is indicated in children who are obese. In type 2 diabetes, there is no association with specific HLA antigens, autoimmunity, or various islet cell antibodies (ICAs).reverses diabetes type 2 gene (🔴 with keto) | reverses diabetes type 2 oralhow to reverses diabetes type 2 for the 1 last update 10 Jul 2020 4040 However, several genetic abnormalities regulating insulin secretion are increasingly implicated in T2DM.40