The Link Between Obesety and Type II Diabetes

Diabetes is a devastating and potentially life threatening disease that affects thousands of Americans each year. The fact of the matter is that although it impacts the lives of thousands of people, there still remain questions about the disease that need to be answered. One of the hot topics of today’s scientific research is whether or not there is a link between obesity and type II diabetes. Type II diabetes is a chronic metabolic condition that is caused by defects with the endogenous insulin. Insulin is a hormone produced by the pancreas that carries and transports the glucose from the blood into the cells for energy in amounts that allow the body to function properly (Lebovitz, 1999). This generally occurs because the body is not producing enough insulin to regulate the bloods glucose level (Lebovitz, 1999). Another cause can be that even if the pancreas is producing enough insulin, the cells do not respond properly to the insulin, causing the insulin to be inefficient (Lebovitz, 1999). A major problem of this disease is the resulting high glucose levels, which is a result of the ineffectiveness of the insulin; this may result in hyperglycemia, or high blood pressure, which can cause damage to numerous organs in the body (Lebovitz, 1999).

Type II diabetes has been continuously linked to the rising epidemic of obesity. Recently it has been found that the biggest factor that influences type II diabetes is visceral adipose tissue, which is the fat of the organs, resulting in the bulging of the stomach (Shulman, 2004; Sorisky, 2008). It is found to be that this type of adipose tissue is one of the biggest reasons for insulin resistance; people with Visceral adipose tissue have difficulties storing fat in cells in this area because the tissue can not expand in order to house all the extra calories, the adipogenic capacity with in this adipose tissue weakens which causes hypertrophied (increased) adipocytes (Sorisky, 2008).

This in result causes overproduction of pro-inflammatory adipokines (cell to cell signaling secreted by adipose tissue), causing the shipment of fatty acids to the liver cells, muscle cells, and insulin secreting beta cells (Sorisky, 2008).These tissues of the body become inflamed and dysfunctional causing insulin resistance (Sorisky, 2008). Fat on other parts of the body such as the hip area, does not cause insulin resistance, because the adipocytes here can store the fat and therefore doesn’t need to be sent to liver cells, muscle cells, or beta cells. (Shulman., 2004).

The only cell that is capable of producing insulin is the pancreatic beta-cell, this cell is very important in maintaining glucose homeostasis (Araki et al., 2003). A common theory as to why Type II diabetes occurs is the malfunction of these ОІ-cells. Obesity causes major complications in the Endoplasmic reticulum, when apoptosis (programmed cell death) occurs; it causes death receptors to be activated as well as DNA damage, which causes stress on the endoplasmic reticulum (Araki et al., 2003). This stress leads to restraints on the signaling of insulin receptors which potentially leads to insulin resistance (Araki et al., 2003). The ER is responsible for dealing with proteins and fats, as well synthesizing proteins. Obese individuals are usually consuming more nutrients then their body can handle, as a result the ER is over worked and sends out help signals through out the body. When the cells receive these signals they begin interfering with the insulin receptor, causing the ER to not function properly with insulin. As a result, insulin is suppressed, and interferes with clearing the sugar from the blood stream (Araki et al., 2003).

There are many other factors that seem to influence insulin resistance; these factors have been extensively researched with the use of Magnetic Resonance Spectroscopy (MRS). MRS has been used to study the rate of glucose intake in muscle glycogen; this showed how muscle glycogen synthesis was lower in diabetic patients then normal non-diabetic individuals (Shulman, 2004). Since Muscle glycogen synthesis is one of the major pathways for the breakdown of glucose, its defectiveness has a part in causing insulin resistance in type II diabetic individuals. (Shulman, 2004). Increasing plasma fatty acid concentration also provokes insulin resistance, because it activates serine and theroine, which are also activated by PKC- ОÒ', as well as other kinases, which phosphorilates serine sites on IRS-1 (Shulman, 2004). IRS-1 molecule acts like a connection of proteins between the insulin receptor and many other complex signaling molecules. These phospohorilated serines do not interact with PI3K (this is the enzyme that causes phosphorylation), in result it causes a decrease in the activity of glucose transport, which causes an increase in the fatty acid intermediates of metabolism in muscle and liver cells (Shulman, 2004). In conclusion the build up of intracellular fatty acids has an important function in insulin resistance, which is observed in obese patients, as well as patients with type II diabetes (Shulman, 2004). Last but not least, it is thought that the mitochondria might be correlated to insulin resistance. It has been thought that inherited or acquired defects in mitochondrial function can also lead to an increase in fatty acid, which in result would stop insulin signaling (Shulman., 2004). Insulin resistance in elderly can contribute to an increase of intramyocellular (skeletal muscle) and intrahepatic (with in the liver) lipid, which would cause the activation of the mitochondrial oxidative phosphorylation. (Shulman, 2004). These changes can be a result of a decrease in the mitochondrial content because of a mutation in there mtDNA (mitochondrial DNA) which is thought to be one of the factors of aging, this shows how many genes that seem to regulate proper functioning in the mitochondria also predispose genetically the inheritance of type II diabetes(Shulman, 2004).

Evolution may have also contributed to Insulin Resistance. This resistance

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