During this 2 ATP and 2 NADH are produced through 10 steps. The first five steps consume ATP whilst the remaining stages release ATP. The regulation of Glycolysis is maintained by steps one, three and ten. In step one, hexokinase is inhibited by C6 preventing any further phosphorylation of Glucose. In step three, the allosteric enzyme Phosphofructokinase in which is inhibited by high levels of ATP and citrate, together this makes phosphofructokinase the regulator of ATP production. In step 10, the enzyme Pyruvate kinase is inhibited by high levels of Acetyl CoA and ATP, this is activated by fructose 1 6-bisphosphate. The product pyruvate is transported from the cytosol to the mitochondrial membranes into the matrix, this process is activated by ADP and AMP. Most pyruvate formed is converted to Acetyl CoA which then enters the Citric Acid Cycle. The citric acid cycle (CAC) takes place in the mitochondrial matrix inside the double mitochondrial membrane. Within this process the acetyl groups are oxidized Thus producing CO2, energy NADH and …show more content…
The cause of diabetes type 1 can be caused by the destruction of islet beta cells, or type 2 diabetes or insulin resistance is linked to the loss of response or the resistance of insulin. This leads to the glucose uptake to muscle and fat cells that is dependent on the activation of GLUT4 receptor by insulin. The insulin-sensing cells no longer register the presence of glucose in the blood, therefore the glucose is not brought into the cell. After this the use of lipids is used as the main energy source through the process of glycolysis. Due to the lack of carbohydrate digestion in this process the fatty acids cannot be used in the citric acid cycle. Therefore, ketogenesis is used instead, however the accumulation of too many ketone bodies can lower the pH of the blood. In Johns case, he is susceptible to type two diabetes because of his excess carbohydrate intake. obesity is strongly linked to diabetes dependant on BMI as this is a sufficient way to analyse diabetes in individuals (Dustan et al 2002) In john’s case as he is 40kgs over recommended weight and can be referred to as developing the disease (Stafford et al. 1482-1490, 2008) “diabesity”. (Stafford et al. 1482-1490, 2008) the major plasma lipid abnormality in obesity is elevated triglycerides (TGs) in the form of VLDL and low HDL cholesterol. Insulin inhibits the production and release of glucose by the liber through blocking gluconeogenesis and