Insulin Deficiency Research Paper

Diabetes occur when there is a combination of inadequate secretion of insulin by the pancreatic beta cells and the peripheral insulin resistance. Insulin resistance leads to a reduced glucose transport into the muscle cells, increases both hepatic glucose production and breaking down of fats because it has been attributed to the elevated level of free fatty acids and proinflamatory cytokines in the plasma.1

This is 36 year old WM. Patient has a history of insulin dependent DM, currently taking humulin 70/30 43 units in am and 40 units in PM. Patient is here requesting some paper work filled out for his driver's license also. Patient reports he is taking insulin as prescribed. Denies chest pain, SOB, N/V/ d, or fever, denies any pain 0/10. Patient denies any depressive moods.

It is characterized by varying degrees of insulin resistance and insulin deficiency. It is thought that the earliest defect in the pathogenesis, is impaired insulin action or insulin resistance. Resistance to the action of insulin will result in impaired insulin mediated glucose uptake in the periphery (by muscle and fat), incomplete suppression of hepatic glucose output and impaired triglyceride uptake by fat. To overcome insulin resistance, beta islet cell will increase the amount of insulin secreted. Higher circulating insulin levels will overcome the obstruction to the action of insulin. This state of hyperglycemia persist for many years. Abnormal fuel metabolism (hyperglycemia and dyslipidemia) occurs when there is a mismatch between insulin requirement, as dictated by insulin resistance, and insulin supply as dictated by beta cells function. For diabetes mellitus to develop, two deficits are necessary: insulin resistance, and insulin deficiency relative to the

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Insulin is considered to be a heat sensitive product which needs to be maintained at certain optimum temperatures for it to work effectively. The transportation from the laboratory to the consumer has to be taken into consideration as all temperature variation can cause the efficiency of the treatment to decrease. (Lens, 2010)

Insulin referred to as hormone is secreted using the pancreas which control glucose levels in the blood. Without insulin, cells cannot use the energy from glucose to perform the numerous functions within the body. The main metabolic fuel for cell utilization used in energy production are glucose and fatty acids. In addition, equilibrium between food intake and energy expenditure may depend on energy homeostasis and metabolism. However, glucose is the most important fuel with a normal level ranging from 4-3-6.5mmol/l needed for cell function and is controlled by multifaceted system between the pancreas, liver, adipose tissue, muscle and brain.

This decrease of sensitivity to insulin is thought to be caused by impaired endothelial function. Researchers found that a reduced signal of PGC-1, key regulator of biogenesis in skeletal muscle, causes impaired insulin sensitivity and reduced expression of certain genes. This study was also done of mice to get a better understanding of how the key regulator can effect protein synthesis. (Bowen, 2015)

Insulin also stimulates glucose transport and the synthesis of triglycerides. Insulin helps prevent lipolysis which is the catabolic breakdown of triglycerides. Insulin also increases the uptake of fatty acids coming from circulating lipoproteins by stimulating lipoprotein lipase activity in fat tissue. Insulin resistance in obesity is shown by decreased insulin-stimulated glucose transport and metabolism in adipocytes by impaired suppression of hepatic glucose output. (Kahn, B., 2000) These defects may result from decreased insulin signaling and downregulation of GLUT4 which is the major glucose transporter that responds to insulin. In obesity, there is increased expression of several protein tyrosine phosphatases (PTPs), that dephosphorylate

or action of insulin. During periods of low blood glucose, glucagon stimulates the breakdown of liver glycogen and inhibits glucose breakdown by glycolysis in the liver and stimulates glucose synthesis by gluconeogenesis. This increases blood glucose. When glucose enters the bloodstream from the intestine after a carbohydrate-rich meal, the resulting increase in blood glucose causes increased insulin secretion and decreased glucagon secretion. Insulin stimulates glucose uptake by muscle tissue where glucose is converted to glucose-6-phosphate. Insulin also activates glycogen synthase so that much of the glucose-6-phosphate is converted to glycogen. It also stimulates the storage of excess fuels as fat (Lehninger, 1993).

Insulin is a hormone that is used in the body to regulation of blood glucose levels. Lack of insulin or the body’s lack of ability to respond to insulin can lead to the development of diabetes. The insulin hormone helps to determine how the body uses and stores glucose and fat. It lets the liver know when to take blood glucose to ensure accurate levels of glucose. If the body has enough energy the liver is signaled to turn the glucose into glycogen.

It is characterized in a different way, and it is due to resistance to insulin or decreased sensitivity towards insulin, in addition to decreased secretion of insulin. The defect in response to insulin involves the receptor of insulin in the membranes of the cell.

Sincerely, I commend the hard work of people involved in the insulin discovery. It has really helped to manage the lives of patients with diabetes. I like the way Garrett’s dad motivated him to not see himself as a sick person but as a strong and healthy young man. This alone I believe gave him hope and encouraged him. As a parents, it is very important that we keep our children safe and protected at all times. They went through a lot to make sure they did not have any complications as far as maintaining blood glucose was concerned. They also stated the need to have an inter-professional team to deal with chronic and complex case such as diabetes. I recall the issue of Garrett’s dad calling in for a syringe order from the physician, this could

Normally insulin is released from pancreatic β cells into circulation in response to increases in plasma glucose levels and binds to its receptors and activates signaling cascades to promote glucose uptake and utilization into tissues such as liver, muscle and fat (Akintola and van Heemst, 2015). In the central nervous system (CNS) insulin play a minor role in the regulation of glucose uptake, but known to have and play multiple behavioral and metabolic effects, influencing eating behavior, peripheral metabolism, cognition and regulating synaptic plasticity in brain regions like the hippocampus (Morton et al., 2006; Akintola and van Heemst, 2015). In obesity, type 2 diabetes (T2D), and neuropathological processes where the shared characteristic

I grew up in Royal Oak Michigan and for most of my life I have struggled with being overweight and having attention deficit disorder. This has led to a lot of problems for me to this day. it started back in elementary school when I was about 8 years old, I was on a children’s soccer team had a lot of friends. The coach of this soccer team was my friends Camden B’s dad, I did not really like him at all and he knew I was overweight and he pushed me further I could possibly do because I was a lot bigger than the other kids but he did not really care about it at all, Then this lead to me losing my friend, and quitting the team having to make new friends was a problem for me because of me overweight problems not a lot of people talked to me.

Continuing on with myths, a person with diabetes can transmit this disease to another person. This is also not true because diabetes is not contagious. The closest way to transmit diabetes is the parent’s genes to their child. Lastly, people with diabetes can never have any sweets. This statement is false; a person with diabetes can eat sweets in moderation. But they must exercise and eat healthy meals.