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Type II Diabetes

Thomas Rocco

Introduction

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“Where’s the beef”, “I’m loving it” and “live mas” are some of the fast food restaurant slogans that many people recognize. More people are eating out than cooking for themselves. One study revealed that 59% of men and 32% of women don’t spend any time a day meal prepping (Jawoska, Blackham, Davies, and Stevenson 2013).  Especially with the cost of feeding a family, it’s easier and allows everyone what they want to eat. Fast food has double the calories than a recommended energy density of a healthy diet (Prentice and Jebb 2003).  Besides just eating more people are living sedentary lifestyles from working long hours to being exhausted and wanting to sit and relax. One’s lifestyle can have a major impact on a person health and can have lasting consequences.

 

One of the changes that has occurred is a rise in obesity that can be linked to other diseases. Obesity is one factor for people who are considered type 2 diabetic. According to the Center for Disease Control (CDC), type 2 diabetic is on the rise for children because of the increase in childhood obesity (“Type 2 Daibetes” n.d.).

 

There is no cure for type 2 diabetes. However, you can reduce your risk of getting type 2 diabetes and treat the symptoms. Some ways to reduce the risk of getting type 2 diabetes is eating healthy, working out and reducing your weight (“Type 2 Diabetes”,2017). Eating healthy and being more active can cut your risk of type 2 diabetes in half (“Diabetes Home” 2019).

 

Type 2 diabetes is a serious disease and can lead to death they do not take monitor their blood sugar level and regulate their insulin level. This causes the blood glucose levels to increase and can cause other complications for the individual. Type 2 diabetes can cause different issue including heart disease and stroke, nerve damage, kidney disease and gum disease.  In 2015, diabetes was ranked the seventh leading cause of death (“Statistics About Diabetes”, 2018).

 

Type 2 diabetes is a hormone disease. Insulin, a hormone, is produced in the pancreases. Type 2 diabetes is considered a resistance to insulin. The body is unable to take in glucose in the cell because the cell receptor doesn’t respond to insulin. As a result, the amount of glucose doesn’t decrease and so the pancreas creates more insulin.  As a result, the pancreas is unable to make enough insulin to accommodate the amount of glucose in the blood. The high blood sugar can damage to tissue and organs.

 

Type 2 diabetes differs from type 1 diabetes by how the body responds to the cells. Type 1 diabetes is classified as an autoimmune disease where the body attacks its beta cells. However, in type 2 diabetes the cells are unable to respond to insulin signaling.  In addition, type 1 diabetes is predominately diagnosed in adolescents while type 2 diabetes is usually diagnosed in adults around the age of 30. Type 1 diabetes is usually treated with insulin while type 2 diabetes is either not treated by medication or in some cases treated with tablets. Type 2 diabetes is associated with high blood pressure and cholesterol level compared to type 1 diabetes having normal levels (“Difference Between Type 1 and Type 2 Diabetes”).

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Doctors can determine if someone has type 2 diabetes through a glycated hemoglobin A1C test. This blood test determines the percentage of blood sugar levels in the sample. If an individual is below 5.7 percent blood sugar level they are considered normal. If an individual is between 5.7 and 6.4 they are considered prediabetic.  If the person is considered diabetic they have blood sugar percentage above 6.5 for two test in the past 3 months (“Type 2 Diabetes”, 2019).

t2d_signal_diagram1.png

Symptoms

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People with type 2 diabetes may experience:

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  • Increased thirst

  • Frequent urination

  • Fatigue

  • Increased hunger

  • Slow-healing sores

  • Blurred vision

Figure 1. Healthy Insulin Pathway

 

Pathway 1: Insulin binds to the insulin receptor causing an activation of IRS (insulin receptor substrate) 1-4. From the activation of the IRS to bind either to p85a or p55a. The binding of either p85a or p55a  activates pI3 kinase (P13K) and activates the three isoforms of p110, a catalytic subunit. The p110 subunits activates phosphoinositide-dependent protein kinase 1 and 2  (PDK).  PDK 1 or 2 activates atypical protein kinase C activates GLUT 4 and allow for glucose to be uptake in the cell.


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Pathway 2:  Cbl and CAP binds to activate TC10, a g protein and allows for the activation of GLUT 4.

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Modified from Meyts, P. D. (2016, April 27). The Insulin Receptor and Its Signal Transduction Network. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK378978/

t2d_signal_diagram2.png

Figure 2. Insulin Resistance

 

Pathway 1:  Protein-tyrosine 1B dephosphorylates tyrosine n the insulin receptor. This causes the cell signaling pathway to stop and causes glucose not to be uptake in the cell.

 

Pathway 2: Interleukin 6 activates SOCS-3. SOCS-3 causes the IRS to become degraded. 

 

Modified from Stumvoll, M., Goldstein, B. J., & Van Haeften, T. W. (2005, April 08). Type 2 diabetes: Principles of pathogenesis and therapy. Retrieved from https://www.sciencedirect.com/science/article/pii/S014067360561032X

Therapy/Treatment

 

Metformin lowers glucose production. Absorbed through the gut. Serotonin receptor and high affinity receptor are used to absorbed metformin (Brøsen & Christensen 2015).  Side effects are nausea and diarrhea.

 

Meglitinides increases insulin production. Binds to the sulfonylurea receptors from pancreatic beta cells (Luna & Feinglos 2001).

 

Thiazolidinediones reduces pro-inflammatory cytokines that promote insulin resistance (Stumvoll, Goldsteinm, Van Haeften 2005).  It has been seen to increase adiponectin a protein that help increase insulin response and anti-inflammatory. It has seen to have side effects of weight gain, adipose cell differentiation and triglyceride storage. In addiontion, it has been seen to have fluid retention.

References:

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Brøsen, K., & Christensen, M. M. (2015, May 06). A Comprehensive Review of Drug–Drug Interactions with Metformin. Retrieved from https://link.springer.com/article/10.1007/s40262-015-0270-6

 

Diabetes Home. (2019, January 14). Retrieved from https://www.cdc.gov/diabetes/library/socialmedia/infographics.html

 

Differences Between Type 1 and Type 2. (n.d.). Retrieved from https://www.diabetes.co.uk/difference-between-type1-and-type2-diabetes.html

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Jaworowska, A., Blackham, T., Davies, I. G., & Stevenson, L. (2013, May 01). Nutritional challenges and health implications of takeaway and fast food. Retrieved from https://academic.oup.com/nutritionreviews/article/71/5/310/2460221

 

Luna, B., & Feinglos, M. N. (2001, May 01). Oral Agents in the Management of Type 2

Diabetes Mellitus. Retrieved from https://www.aafp.org/afp/2001/0501/p1747.html

 

Prentice, A. M., & Jebb, S. A. (2003, November 05). Fast foods, energy density and obesity: A possible mechanistic link. Retrieved from https://onlinelibrary.wiley.com/doi/full/10.1046/j.1467-789X.2003.00117.x

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Statistics About Diabetes. (2018, March 22). Retrieved from http://www.diabetes.org/diabetes-basics/statistics/

 

Type 2 Diabetes. (2019, January 09). Retrieved February 27, 2019, from https://www.mayoclinic.org/diseases-conditions/type-2-diabetes/symptoms-causes/syc-20351193

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Type 2 Diabetes. (2017, May 01). Retrieved February 27, 2019, from https://www.niddk.nih.gov/health-information/diabetes/overview/what-is-diabetes/type-2-diabetes

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Type 2 Diabetes. (n.d.). Retrieved from https://www.cdc.gov/diabetes/basics/type2.html

About Us

This website was developed by students in the Cell Membrane Physiology Course (PCB 4783C) at Florida Gulf Coast University in Spring 2018. The goal of this project was to allow students to delve more deeply into a subject of their own interest while applying the knowledge from this course to broaden their understanding. By sharing this information, these young scientists are also developing their scientific communication and adding to the public knowledge on human health and disease through understanding the underlying signaling mechanisms. 

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T: 239-590-7244

E: Lrhodes@fgcu.edu

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