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These are forms of type 1 diabetes with no known aetiologies. Some of these patients have permanent insulinopenia and are prone to ketoacidosis, but have no evidence of autoimmunity. Patients with this form of diabetes suffer from episodic ketoacidosis and exhibit varying degrees of insulin deficiency between episodes. This form of diabetes is inherited and has no immunological evidence for β-cell autoimmunity
Type 2 DM or non-insulin-dependent diabetes mellitus, is the much more prevalent type accounting for 90%–95% of the cases in which the body does not produce enough insulin or properly use it (Li et al., 2004) begins with insulin resistance, a condition in which cells fail to respond to insulin properly (WHO, 2013), this may be combined with relatively reduced insulin secretion (Shoback, 2011). Type 2 diabetes is a heterogeneous disorder characterized by insulin resistance coupled with impaired insulin secretion by β-cells in the pancreas (Kahn, 2008). The defective responsiveness of body tissue to insulin is believed to involve the insulin receptor, as the disease progresses a lack of insulin may also develop. This form was previously referred to as “noninsulin-dependent diabetes mellitus” (NIDDM) or “adult-onset diabetes”. It is caused by a combination of resistance to insulin action and an inadequate compensatory insulin secretory response (WHO, 2013). Type 2 diabetes is the most common type (Manohar et al., 2002).
Gestational diabetes occurs when pregnant females without a previous history of diabetes develop high blood-sugar levels (WHO, 2013). GDM is defined as any degree of glucose intolerance with onset or first recognition during pregnancy. Gestational diabetes mellitus (GDM) resembles type 2 DM in several respects, involving a combination of relatively inadequate insulin secretion and responsiveness. It occurs in about 2–10% of all pregnancies and may improve or disappear after delivery (NDIC, 2011). However, after pregnancy approximately 5–10% of females with gestational diabetes are found to have diabetes mellitus, most commonly type 2 later in life (NDIC, 2011), but some usually resolves after the birth of the baby (Cash and Jill, 2014).
The Expert Committee (ECDCDM, 2003) recognized an intermediate group of subjects whose glucose levels, although not meeting criteria for diabetes, are nevertheless too high to be considered normal. This group is defined as having fasting plasma glucose (FPG) levels ≥100 mg/dl (5.6 mmol/l) but <126 mg/dl (7.0 mmol/l) or 2-h values in the oral glucose tolerance test (OGTT) of ≥140 mg/dl (7.8 mmol/l) but <200 mg/dl (11.1 mmol/l).
IFG and IGT are associated with the metabolic syndrome, which includes obesity (especially abdominal or visceral obesity), dyslipidemia of the high-triglyceride and/or low-HDL type, and hypertension Metabolic syndrome (also referred to as syndrome X) This is a set of abnormalities in which insulin-resistant diabetes (type 2 diabetes) is almost always present along with hypertension (high blood pressure), high fat levels in the blood (increased serum lipids, predominant elevation of LDL cholesterol, decreased HDL cholesterol, and elevated triglycerides), central obesity, and abnormalities in blood clotting and inflammatory responses. A high rate of cardiovascular disease is associated with metabolic syndrome.
This indicates a condition that occurs when a patient’s blood glucose level is higher than normal but not high enough for a diagnosis of type 2 DM. Many patients destined to develop type 2 DM spend many years in a state of prediabetes which has been termed America’s largest healthcare epidermic (Handelsman, 2009). Patients with IFG (Impaired fasting glucose) and/or IGT (Impaired glucose tolerance) are now referred to as having “pre-diabetes” indicating the relatively high risk for development of diabetes in these patients. Prediabetes increases the risk of developing type 2 diabetes, heart disease or stroke. Prediabetes can typically be reversed (without insulin or medication) by lifestyle changes, such as losing a modest amount of weight and increasing physical activity levels. Weight loss can prevent, or at least delay the onset of type 2 diabetes.
The term brittle diabetes has been used to refer to patients who have dramatic, recurrent swings in glucose levels, often for no apparent reason. In some patients, counter-regulatory response to hypoglycemia is impaired. Other causes include infection, gastroparesis (which leads to erratic absorption of dietary carbohydrates), and endocrinopathies (eg, Addison disease). Latent autoimmune diabetes of adults (LADA) This is a condition in which type 1 DM develops in adults. Adults with LADA are frequently initially misdiagnosed as having type 2 DM, based on age rather than etiology. Genetic mutations (autosomal or mitochondrial) can lead to defects in beta cell function (Cooke and Plotnick, 2008). Abnormal insulin action may also have been genetically determined in some cases. Any disease that causes extensive damage to the pancreas may lead to diabetes (for example, chronic pancreatitis and cystic fibrosis).
Any process that diffusely injures the pancreas can cause diabetes. Acquired processes include pancreatitis, trauma, infection, pancreatectomy, and pancreatic carcinoma. With the exception of that caused by cancer, damage to the pancreas must be extensive for diabetes to occur; adrenocarcinomas that involve only a small portion of the pancreas have been associated with diabetes. This implies a mechanism other than simple reduction in β-cell mass. If extensive enough, cystic fibrosis and hemochromatosis will also damage β-cells and impair insulin secretion.
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