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The Pathophysiology of Type 2 Diabetes and Insulin Resistance

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How do you define Pathophysiology?

The prevalence of Type 2 diabetes increases with age. It is present in 1–2% of those aged 20–40 years but this rises to nearly 20% of those aged over 60 years. Type 2 diabetes is also linked strongly to obesity. The increased prevalence relates principally to decreased levels of physical activity and increased consumption of calorie-dense food. The risk of developing diabetes increases exponentially with body mass index (BMI).

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What is the main cause of insulin resistance?

Type 2 diabetes and other cardiovascular risk factors are particularly closely associated with visceral adiposity (abdominal, upper body, and trunk) as opposed to lower body adiposity. There is therefore a strong correlation with an increased waist:hip ratio. Risk factors for cardiovascular disease are frequently already present when Type 2 diabetes is diagnosed. Hypertension is present in 40% of patients at diagnosis and dyslipidaemia is common. These features are linked by the metabolic defect of insulin resistance. The rate of coronary heart disease, stroke, peripheral vascular disease and heart failure is increased up to fivefold in patients with Type 2 diabetes. When associated with other biochemical and clinical features, Type 2 diabetes forms part of the syndrome of insulin resistance, also known as the metabolic syndrome. The metabolic syndrome consists of a combination of cardiovascular risk factors that include obesity, dyslipidaemia, insulin rsistance, hypertension and an increased tendency to thrombosis.

There are also inherited factors linked to the risk of developing Type 2 diabetes. The lifetime risk of developing Type 2 diabetes is 40% if a single parent is similarly affected. Studies of patients with inherited forms of diabetes (maturity-onset diabetes of the young – MODY) have revealed evidence of single gene defects in these individuals.

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For most cases of Type 2 diabetes, however, there is polygenic inheritance. Genetic risk may not be the sole reason for familial clustering. The fetal origins hypothesis proposes that Type 2 diabetes results in part from intrauterine malnutrition that increases insulin resistance. Population studies have demonstrated a correlation between low birth weight and the development of Type 2 diabetes and other cardiovascular risk factors. It is likely that genes, ethnicity and intrauterine factors all contribute to the familial clustering of Type 2 diabetes.

There are defects in both insulin action and secretion in addition to a complex link with the ‘insulin resistance syndrome’. The main defects in Type 2 diabetes include a marked delay in both first and second phase insulin responses to meals. There are changes in the normal variability of insulin release and an increase in the circulating proinsulin : insulin ratio. Resistance to the effects of insulin has been well documented in Type 2 diabetes. However, although insulin resistance is generally high it is also found in some nondiabetic individuals. It cannot, therefore, be entirely responsible for the development of the condition.

E235 – The Pathophysiology of Type 2 Diabetes and Insulin Resistance –

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