This slow in others, mainly adults, and rapid in

This form of diabetes, formerly called insulin-dependent diabetes mellitus
(IDDM) or juvenile-onset diabetes, results from a cellular-mediated autoimmune
destruction of the ?-cells of the pancreas. Onset most often appears in childhood,
but it can also develop in adults in their late 30s and early 40s (ADA,
2014). The mechanisms that lead to ?-cell destruction are still not completely
understood but it is more accepted that the selective destruction of ?-cell is interposed
by cytotoxic T-cells and by certain cytokines (Graham et al., 2012).

 

     In this type of diabetes, the rate of ?-cell destruction is widely
variable, being slow in others, mainly adults, and rapid in some individuals, mainly
infants and children (ADA, 2014). Patients with this form often become relied on insulin for survival
and are at risk for ketoacidosis (Willis et al., 1996).

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Type 2 Diabetes Mellitus (T2DM):

     This type of diabetes, formerly
known as non-insulin-dependent diabetes mellitus (NIDDM), is an expression used
for persons who have insulin resistance and usually have relative insulin insufficiency.
It usually exists in individuals over 40 and is called adult onset diabetes
mellitus. T2DM frequently goes not diagnosed for many years since the
hyperglycemia appears gradually and at earlier stages is often not severe
enough for the patient to notice any of the classic symptoms of diabetes (ADA, 2014).

 

 

     The risk of developing this
type of diabetes increases with obesity, age, and lack of physical activity and
it exists more frequently in individuals with hypertension or dyslipidemia and
in women with prior gestational diabetes mellitus (GDM) (ADA, 2014). T2DM also requires continuous medical care
and multifactorial risk reduction strategies to normalize blood glucose levels
and prevent or minimize acute and long-term microvascular or macrovascular complica­tions
(DeFronzo et al., 2015).

 

     Many T2DM individuals need
exogenous insulin in the later stages of the disease since endogenous insulin secretion
becomes insufficient to maintain acceptable levels of glycemia despite ongoing
therapy with other anti-diabetic agents (Ma et al., 2012).

 

     Although insulin resistance
is considered the initiating event in the pathogenesis of T2DM, pancreatic ?-cell
dysfunction is an indispensable condition for the development of the disease
and hyperglycemia does not become apparent until there is severe ?-cell
dysfunction (Tripathy and Chavez, 2010). Several factors contribute to ??cell dysfunction, including ageing,
genetic abnormali­ties, lipotoxicity, glucotoxicity, insu­lin resistance
leading to ??cell stress and reactive oxygen stress (DeFronzo et al.,
2015).