A Closer Look at Type 2 Diabetes (Part 1)

What’s going on in that picture? The insulin hormone binds to a receptor in the cell wall. When this happens, it signals a transporter molecule, called the GLUT4 pathway molecule, to open up and allow glucose(sugar) into the cell. When the cell-receptor for insulin is defective, insulin cannot bind to the receptor, and therefore cannot signal the GLUT4 pathway to activate, and so glucose is not shuttled through the cell wall from the blood. This image is the comparison of two cells. One is a normal cell, the other is an insulin resistant cell. The insulin resistant cell is a representation of a typical fat or muscle cell in a type 2 diabetic’s body. The normal cell has regular function of its insulin cell-receptors and therefore allows for the cell’s uptake of glucose from the blood to make cellular energy (ATP). The insulin resistant cell exhibits defects in most of its insulin cell-receptors, and therefore cannot take up as much glucose into the cell (and so it cannot make as much ATP) resulting in it slowly starving.

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An Overview of the Condition: 

Diabetes mellitus is a serious medical condition with increasing prevalence in modern society. Worldwide 90-95 percent cases of diagnosed diabetes are type 2. Currently, Diabetes is one of the top five leading causes of death in US. Most cases diagnosed are in the adult population, but recently type 2 Diabetes Mellitus (DMII) has had increasing frequency in children and adolescents. Unlike type 1 diabetes, type 2 diabetics can produce insulin. But due to the regular bodily bombardment of a high sugar diet, their tissues have become insulin resistant. This causes increased insulin needs, and consequently, the pancreas ramps up production. Eventually, due to the regular stress of increased insulin production, the pancreas becomes fatigued and slowly loses its ability to produce insulin levels to meet the body’s increased demand. Type 2 diabetics can therefore be both insulin resistant and relatively insulin deficient at the same time.

Insulin resistance in the body’s tissues happens gradually, developing for many years before the onset of diabetes. Insulin resistance and defective insulin secretion faced by diabetics vary in severity on an individual basis. Insulin resistance is a condition faced by all diabetics and is caused by a cell-receptor defect resulting in the body’s inability to use insulin (as explained above). To summarize, because of this cell-receptor defect, cells cannot respond to insulin, and therefore cannot take up glucose from the blood for fuel. So essentially, cells are starving in a sea of glucose that they just cannot get a hold of. Moreover, because cells cannot take glucose out of the blood, blood sugar levels remain dangerously high and uncontrolled.

Insulin production occurs in the pancreas and acts as a control for sugar (glucose) levels in the body. It inhibits glycogenolosis, the conversion of glycogen into glucose, and gluconeogenesis, the making of glucose from non-carbohydrate sources, when blood glucose is high. In other words, the body, mainly the liver, can synthesize glucose from other molecules when it needs it (if glucose levels in the blood are low). So after a big slice of cake, and subsequent blood sugar spike, insulin tells the body to stop making glucose because it has enough, and cells start taking glucose out of the blood to use or store. When tissues are insulin resistant and if insulin secretion is low (due to pancreatic fatigue), the body has gotten all of that sugar from the cake, but insulin cannot tell the other organs about it. So the liver keeps producing sugar (even though you just ate a ton), and the cells do not efficiently take the sugar out of the blood to use. Therefore the body becomes hyperglycemic, meaning blood sugar levels remain high and out of control, resulting in many dangerous short and long-term complications.

References:

Mateljan, George. World’s Healthiest Foods. Washington; 2007

Murray, Michael, Pizzorno, Joseph, Pizzorno L. The Encyclopedia of Healing Foods. New York; 2005

Nelm, M., Sucher, K. P., & Lacey, K. Nutrition Therapy and Pathophysiology (2nd ed.). : Brooks/Cole Cengage Learning; 2011 +image: pcos.com