Insulin excessive production

Manganese is essential fin normal body structure, reproduction, normal functioning of the central nervous system, and activation of numerous en/ymes. An excess of manganese can lead to neural damage and possible impaired insulin production. 

Type II diabetes mellitus Type II diabetes mellitus (age-onset diabetes) is when the pancreas ability to produced insulin is either diminished (age) or is insufficient to metabolize the excess serum glucose (overweight, lack of exercise). Insulin is produced but is not effective. The patient controls Type II diabetes mellitus by diet, exercise, and oral diabetes medication that stimulate insulin production in the pancreas and other organs. This is referred to as non-insulin-dependent diabetes (NIDDM). 

The exact cause of reactive hypoglycemia is difficult to determine, but most researchers believe that the main cause is a shortage of glucagon, resulting in an inability to raise blood glucose levels when necessary. Others speculate that the cause is a hypersensitive response to the release of the normal physiological hormone called epinephrine, a reaction that is the opposite of epinephrine s normal effect on blood sugar, which is to raise it. Still others consider excessive insulin production to be the culprit. 

Disorders of lipoprotein metabolism involve perturbations which cause elevation of triglycerides and/or cholesterol, reduction of HDL-C, or alteration of properties of lipoproteins, such as their size or composition. These perturbations can be genetic (primary) or occur as a result of other diseases, conditions, or drugs (secondary). Some of the most important secondary disorders include hypothyroidism, diabetes mellitus, renal disease, and alcohol use. Hypothyroidism causes elevated LDL-C levels due primarily to downregulation of the LDL receptor. Insulin-resistance and type 2 diabetes mellitus result in impaired capacity to catabolize chylomicrons and VLDL, as well as excess hepatic triglyceride and VLDL production. Chronic kidney disease, including but not limited to end-stage... 

As mentioned above, insulin secretion by p-cells of the pancreatic islets increases in response to increasing glucose concentrations. In the insulin-resistant state, despite insulin concentrations that are increased two- to three-fold, there is an excessive rate of liver-glucose production. In addition, skeletal muscle glucose disposal in response to insulin is markedly decreased. This results in increased glucose concentrations. This inability to control glucose concentrations, is referred to as impaired glucose tolerance and may ultimately lead to type-2 diabetes. 

Insulin also stimulates the storage of excess fuel as fat (Fig. 23-26). In the liver, insulin activates both the oxidation of glucose 6-phosphate to pyruvate via glycolysis and the oxidation of pyruvate to acetyl-CoA. If not oxidized further for energy production, this acetyl-CoA is used for fatty acid synthesis in the liver, and the fatty acids are exported as the TAGs of plasma lipoproteins (VLDLs) to the adipose tissue. Insulin stimulates TAG synthesis in adipocytes, from fatty acids released... 

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