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Type 2 Diabetes Mellitus

  • Unlike type 1 diabetes, people with type 2 diabetes still have some insulin production. Indeed, they may have higher blood levels of insulin than their counterparts without diabetes – albeit in response to higher-than-usual blood glucose concentrations. However,t type 2 diabetes occurs with beta-cell loss.
  • Excess body fat – particularly abdominal or visceral adiposity – is thought to contribute to the insulin insensitivity that is characteristic of this type of diabetes. It has been shown that people who carry excess weight around their abdomen are at higher risk of diabetes.
  • Type 2 diabetes tends to develop slowly such that the symptoms of this condition, and therefore, the diagnosis, are often missed. Longstanding undetected hyperglycaemia – as often precedes the diagnosis of type 2 diabetes – may lead to the development of long-term diabetes complications.
  • Type 2 diabetes is commonly called “adult-onset diabetes”. Type 2 diabetes is the most common form of diabetes – 90% to 95% of people with the condition.The pathogenesis of Type 1 diabetes mellitus underlie as follows:
  • There are multiple genes associated with type 2 diabetes. Some people with the condition may have a single gene defect, while others have multiple gene defects. This may explain why some people’s diabetes is easier to treat than others.
  • Hyperinsulinaemia
  • poor foetal nutrition may cause a decrease in beta-cell formation, provoking diabetes in later life. Poor foetal nutrition is marked by low birth weight
  • Exposure to high glucose levels in utero pre programs the foetus to poor glucose intolerance and diabetes later in life.

      • Pathophysiology of type 2 diabetes


      1. People with type 2 diabetes therefore have a relative – rather than total – insulin deficiency.
      • This results in reduced glucose uptake from muscle tissue and the liver. The breakdown of protein can occur in type 2 diabetes, but is significantly less pronounced than in type 1 diabetes.
      • The liver contributes to the hyperglycaemia seen in people with type 2 diabetes by breaking down and releasing stored glucose (glycolysis) and, to a lesser extent, making new glucose (gluconeogenesis).
      • Some of the excess glucose is taken up by the fat cells ...or taken up by the liver and converted to triglycerides.
      • The storage of these triglycerides in the liver leads to hypertriglyceridemia and the “fatty liver” associated with insulin insensitivity.

      Risk Factors

        Non-modifiable
      • Age > 40
      • Family history and genetic disposition
      • Ethnicity
      • History of impaired glucose tolerance and impaired fasting glucose.
      • Vascular disease
      • History of gestational diabetes or delivery of macrosomic baby.
      • polycystic ovary diseases
      • Schezoprenia
      • hypertension
      • Dyslipidaemia

        • Modifiable
      • Abdominal or central obesity
      • Over weight
      • Physical inactivity
      • Dietary factors

      Signs and Symptoms

      Polyuria
      Polydipsia
      Polyphagia
      Weight loss
      Visual disturbance
      Fatigue
      Infections
      Hunger