Islets Of Langerhans

1045 Words 4 Pages
Core mechanisms
The main organ involved with controlling glucose levels in the body is the pancreas. This organ contains specific areas known as the Islets of Langerhans which contain α cells and β cells. As this essay is focusing on the adverse effects of excess glucose in the body (hyperglycaemia) – the β cells will primary be studied as these act to lower blood glucose within the body. The cells do this by releasing a hormone known as insulin. [10]

Figure 1 – Insulin Secretion [3]
The above image shows insulin secretion stimulated by glucose. There is an uptake of glucose by the carrier protein GLUT2 when glucose levels increase in the blood [4]. GLUT 2 is found within the B-cells of the pancreas. The glucose then goes through
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This condition arises when the pancreas fails to create enough insulin or when the body cannot use the insulin effectively [1].
Diabetes is the main cause of hyperglycaemia and has 2 types. Type 1 diabetes is an autoimmune disease [2] where the immune system targets beta cells in the pancreas. These beta cells are what produce insulin, the key hormone in controlling our blood sugar levels. The beta cells are found within a part of the pancreas known as the islets of Langerhans. Eventually, the immune system attacks the pancreas to the point where it can no longer produce insulin. Consequently, those with type 1 diabetes must inject themselves with insulin as their beta cells can no longer create it. [2]
Type 2 diabetes is a different issue. The body experiences insulin resistance where it can no longer respond properly to the hormone. The body compensates for this issue by producing more insulin than usual in a healthy person. This places a strain on the beta cells, eventually leading to their destruction. When a significant amount of beta cells are destroyed, insulin production is severely diminished [2]. The body’s sensitivity to insulin is highly influenced by excess body weight carried. Carrying too much excess weight can lower insulin sensitivity to a point where glucose levels are not reduced to a healthy level, leading to hyperglycaemia. Because of this, some people with type 2 diabetes must be injected with
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Research shows the formation of advanced glycation end productions (AGEs) is a significant abnormality occurring along with diabetes mellitus and often general inflammation. The diacylglycerol (DAG) protein kinase C (PKC) pathway is thought to have a vital role in mediating AGEs formation. PKC is thought to adversely affect vascular function. It does this by activating superoxide-producing enzymes such as NADPH oxidase and by increasing expression of a dysfunctional, superoxide-producing uncoupled endothelial nitric oxide synthase (NOS III). Studies have shown the PKC-mediated superoxide production may disable NO derived from endothelial NOS III. This may inhibit the activity/expression of soluble guanylyl cyclase, the NO downstream target. The effect AGEs have on vessel wall homeostasis could be the explanation for the swift progressive atherosclerosis that comes with diabetes. Diabetes sufferers experience AGEs forming at much faster degrees than usual. In the wall of the vessel, collagen linked AGEs can trap plasma proteins, reduce NO activity and engage with certain receptors to moderate a great number of cellular properties. AGEs can also initiate oxidative reactions on plasma low density lipoproteins (LDLs) – this promotes the formation of oxidized LDL. When AGEs interact with endothelial cells and other cells within the atherosclerotic

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