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Research paper on diabetes

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Review of Research Paper on Insulin

Review of Research Paper on Insulin Continue reading.

Let's go back to the 1920s, when diabetes was discovered and the study of glucose
began. There was a scientist named Minkowsky, and he wondered what caused diabetes. So, he
did something crazy: He took a urine sample from a normal patient and a sample from a
diabetic patient, and tasted them! He observed that the sample from the diabetic patient was
sweet, so he concluded that diabetes had something to do with high glucose levels (lots of
sugar in the blood).


In the same decade, two scientists named Benting and Best performed another
experiment to see which chemically made pancreas would do the best job in lowering glucose
levels. This led to the discovery of insulin.
Moving on to the 1940s, scientists were curious about what exactly insulin had to do
with glucose. Basically, insulin increases the amount of glucose that gets transported to the
plasma membrane of every cell in your body, so the breakdown of glucose will be faster.
Now, the question was quantity vs. quality: did insulin actually make the glucose
transporters work better, or did insulin simply increase the number of glucose transporters
within each cell? This is what this paper answers.


When looking at the methods in this paper, it is easy to get lost and confused amidst all
the scientific terms and complicated language. However, when broken down into simpler terms,
the methods used in the experiment in the paper become much clearer and create a basis for
understanding for the remainder of the paper.

Following is a short and understandable explanation of the methods used in the paper and also an explanation of the experiment that was performed to reach to conclusions in the paper.

* The first method mentioned in the paper is the collagenase method. This method refers to the collagen
that holds the fat cells that were extracted from the rats together.
* This method is simply the breaking down of the collagen between the cells in order to separate and isolate them.
* Another method used in the paper is refereed to when talking about homogenizing the cells.
* This method refers to mixing up and grinding of the fat cells to make into an evenly distributed soup like
substance that can then be used in the experiment.

# When the homogenized soup is prepared, it is them put into a centrifuge tube and centrifuged.

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# This is a machine that spins the substance quickly in order to make heavier particles sink to the bottom and lighter materials to stay at the top of the tube.
# This method is used to separate out the different membranes in the cells.
# Some membranes are studded with a cell structure called ribosomes that make the membrane heavier and so sink in the centrifuge.
# A sucrose gradient is used to determine the density of each layer of cell membranes.
# A sucrose gradient consists of a sugary substance that the homogenized cells are put into and centrifuged because sucrose has a known structure of densities from the bottom most dense) to the top (least dense).
# The membranes with the same density as the sucrose will stay at a certain level in the gradient, that with the same density as the membranes, with a known density.
# The different membranes are separated in the centrifuge tube and then the tube is divided into sections or fractions as they are called in the paper.
# Each of these fractions is then tested to determine the uptake of insulin into the membranes.
# This determines where the vesicles with the highest uptake of insulin are.

In order to properly understand their results, Suzuki and Kono had to graph their data. They chose to divide the sucrose gradient into 16 fractions. The higher the number, the higher the density of sucrose. They then graphed the amount of glucose transport activity in each fraction.
FOR BASAL CELLS (cells without insulin) THE GRAPH LOOKED SOMETHING LIKE THIS:

FOR THE CELLS THAT INCLUDED INSULIN, THE GRAPH LOOKED SOMETHING LIKE THIS:

Both kinds of cells have two peaks (high points) of glucose transport. We will call them Peaks A and B, as labeled on the graphs. It is important to note that the basal cells have a much higher Peak B and a very small Peak A. Likewise, the cells with insulin had a lower Peak B and a higher Peak A.
o This shows:
+ The amount of glucose transport stays relatively the same with or without insulin BUT
+ The location of glucose transport changes once insulin is added
* The scientists further quantified their data by realizing that the proteins 5’ AMPase and UDPGal:N-acetylglucosamine galactosyltransferase were involved.
o They already know that:
+ 5’ AMPase marks the plasma membrane (so we know that if it is present, so is the plasma membrane). The plasma membrane is on the outer periphery of the cell.
+ Also, UDPGal:N-acetylglucosamine galactosyltransferase marks the Golgi apparatus (so we know that if it is present, then so is the Golgi apparatus). The Golgi apparatus is deep in the cytoplasm, or inside, of the cell.
* Knowing these two things, they looked for the presence of these two proteins. They found that the presence of these two proteins within the sucrose gradient were about equal in the basal cells and the cells plus insulin.
* The graphs for the presence of the two proteins look something like this:

FOR BASAL CELLS:

FOR CELLS PLUS INSULIN:

THIS MEANS THAT:

* Peak A is related to the 5’ AMPase. Since this protein marks the plasma membrane, we can say that Peak A represents the glucose transport activity in the plasma membrane.
* Peak B is related to the UDPGal:N-acetylglucosamine galactosyltransferase. Since this protein marks the Golgi apparatus, we can say that Peak B represents the glucose transport activity in the Golgi apparatus.
* Because the transport activity sort of “evens out” the peaks in the cells that have insulin, we can assume that more glucose transport is going on in the plasma membrane, and not in the Golgi, once insulin is added.

Great! So Suzuki and Kono have just found out that one model for insulin’s effect on glucose transport is right: that insulin affects location of the transporter. But, they still need to show that the other model is not right: that insulin affects the rate of glucose transport by “signaling.” How do they do this? They make another graph!

So, the model that they are trying to say is wrong says that insulin causes the transporter to have a greater affinity for glucose and hold it tighter, allowing the glucose transport rate to go up. The way we measure this “glucose affinity” is by the number Km. The smaller this number is, the higher affinity the transporter has for glucose.

So, Sazuki and Kono made a graph of how fast the 16 fractions of the sucrose gradient took up glucose. (Basically, they graphed the velocity, or 1/v of glucose transport). They cahrted the differences in these velocities between Peaks A and B in order to find the right Km values for each. Basically, they found that the Km values for both Peaks A and B are about the same.

* the affinity the transporter has for glucose is the same in all parts of the cell
* insulin does not affect the affinity the transporter has for glucose

Taking these things into account, Suzuki and Kono now know that insulin does not “signal” the transporter to hold glucose tighter!

Years, little was known about glucose transport activity other than that it was associated with the plasma membrane. When insulin was discovered in the 1920s, it was not clear what it‘s affect on glucose would be. It was known that transporters were involved in glucose transport activity, however little was known about how these transporters were stimulated by insulin. After considerable research, scientists were left with two possible theories about insulin’s affect on glucose levels.

The possibilities were that either insulin increases the breakdown of glucose, or insulin increases glucose transport to the plasma membrane. They observed the translocation of glucose transporters and finally came to the conclusion that insulin increases glucose transport to the plasma membrane. Even more specifically, it was concluded that insulin increases the number of glucose transporters in the plasma membrane, rather than increasing the activity of glucose. This is accomplished when insulin signals the Glut4 vesicle with it’s transporter, and the vesicle in turn, fuses with the plasma membrane. These conclusions support the findings that the addition of insulin causes glucose levels to go down and explain exactly how it all works. The illustration below depicts how this process works:

This figure depicts an insulin receptor which binds an insulin molecule, signaling to the cell, causing translocation of the GLUT4 vesicle, fusion of the vesicle to the plasma membrane, and subsequent increase in glucose transport into the cell.

WHAT THE RESEARCH HAS LED TO:

The findings of this experiment proved that insulin caused the location of glucose transport to change, but it did not explain how insulin actually caused this to happen. In the years following the publishing of these findings, it was discovered how to clone five kinds of glucose transporters.

Of these five transporters, it was discovered that the action of glucose transporter 4 (GLUT4) was directly influenced by the presence of insulin. It has been concluded that insulin stimulates glucose intake by GLUT4 by sending out a signal which is received by transmitter proteins on the surface of the transporter. This causes GLUT4 to transport the glucose molecule to the plasma membrane through the same mechanism as exocytosis.

Kazuo Suzuki and Tetsuro Kono's: "Evidence That Insulin Causes Translocation of Glucose Transport Activity to the Plasma Membrane From an Intracellular Storage Site"

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5 Expert Ideas for Diabetes Research Paper Writing type 2 Diabetes research paper or type 1 diabetes research paper

it is not easy to deal with because of the complexity of the disease; therefore, the students have to absorb an extensive amount of knowledge in order to come up with an impressive paper. It has been observed that students come up with common ideas for writing the paper and this is why, they don’t get a good response from their teachers.

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First idea

There are many classification of diabetes which can be easily discussed in the paper along with the causes for each of them. This is how; you will bring awareness with the causes of the disease for the reader.

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Overview of Diabetes Type I

What is diabetes type I

Health implications of diabetes type I

What is physical activity?

Why do we need physical activity in our lives?

Physical Activity and Diabetes (Epidemiology)

For our seminar topic "physical activity and disease" we chose diabetes as the focus of our

Since diabetes is such a complex disease with many different forms, we decided to focus on

diabetes type I. This is known as insulin-dependent diabetes mellitus (IDDM). This type of

diabetes includes people who are dependant on injections of insulin on a daily basis in

order to satisfy the bodies insulin needs, they cannot survive without these injections.

OVERVIEW OF DIABETES TYPE I

What is diabetes type I?

In order to understand the disease we firstly need to know about insulin. Insulin is a

hormone. The role of insulin is to convert the food we eat into various useful substances,

discarding everything that is wasteful.

It is the job of insulin to see that the useful substances are put to best use for our

well-being. The useful substances are used for building cells, are made ready for immediate

expenditure as energy and also stored for later energy expenditure.

The cause of diabetes is an absolute or lack of the hormone insulin. As a result of this

lack of insulin the processes that involve converting the foods we eat into various useful

substances does not occur.

Insulin comes from the beta cells which are located in the pancreas. In the case of

diabetes type I almost all of the beta cells have been destroyed. Therefore daily

injections of insulin become essential to life.

Health implications of diabetes type I

One of the products that is of vital importance in our bodies is glucose, a simple

carbohydrate sugar which is needed by virtually every part of our body as fuel to function.

Insulin controls the amount of glucose distributed to vital organs and also the muscles. In

diabetics due to the lack of insulin and therefore the control of glucose given to

different body parts they face death if they don't inject themselves with insulin daily.

Since strict monitoring of diabetes is needed for the control of the disease, little room

is left for carelessness. As a result diabetic patients are susceptible to many other

diseases and serious conditions if a proper course of treatment is not followed.

Other diseases a diabetic is open to: Cardiovascular disease, stroke, Peripheral artery

disease, gangrene, kidney disease, blindness, hypertension, nerve damage, impotence etc.

Basically there is an increased incident of infection in diabetic sufferers. Therefore

special care needs to be taken to decrease the chances of getting these other serious

What is physical activity?

(Bouchard 1988) States that physical activity is any bodily movement produced by skeletal

muscles resulting in energy expenditure. Therefore this includes sports and leisure

activities of all forms.

Why do we need physical activity in our lives?

Physical activity and exercise helps tune the "human machine", our bodies.

Imagine a car constantly driven only to stop for fuel. It would be a client for all sorts

of damage, rusting, oil leaking, dehydration and the chances are most likely it would die

in the middle of the road not long after. This is what the body would be like if we didn't

exercise at all. We would be and as a result of todays lifestyle many of us are, the

perfect target to all kinds of diseases and infections.

For those of us who are carrier of some disease or illness we are still encouraged to

exercise by our physicians if we have the strength to. This is to help make our organs,

muscles, bones and arteries more efficient and better equipped to fight against the disease

or illness. This is our way of counter attacking. And if we are still healthy then we

reduce the chances of getting an illness or a disease.

PHYSICAL ACTIVITY AND DIABETES (EPIDEMIOLOGY)

Recently insulin injections have become available to dependant patients. However in the

pre-insulin era physical exercise was one of the few therapies available to physicians in

For an IDDM carrier to benefit from exercise they need to be well aware of their body and

the consequences of exercising.

If an IDDM carrier has no real control over their situation and just exercise without

considering their diet, time of insulin intake, type of exercise, duration of the exercise

and the intensity, then the results can be very hazardous to the patient.

In the first journal article that I used for this part of the research (Sutton 1981) had

conducted an investigation on "drugs used in metabolic disorders". The article is designed

to provide some background information on previous beliefs and research conducted early

this century. As well as his own investigations conducted during the beginning of the

1980's. He has compared the results and came to the same conclusion as the investigations

done early in this century.

Sutton's findings show that decrease in blood glucose following an insulin injection was

magnified when the insulin was followed by physical activity/exercise (see figure 1). This

shows that if a person gets involved in physical activity or exercise after insulin the

volume of glucose drops dramatically. This leads to symptoms of hypoglycemia. The reason

this occurs is that glucose uptake by muscles increase during exercise, in spite of no

change or even a diminishing plasma insulin concentration. As a result of this type of

information we know now that if a patient is not controlled through a good diet and program

then they could put themselves in danger. A person who might be poorly maintained and

ketotic will become even more ketotic and hypoglycimic.

Good nutrition is of great importance to any individual especially one that exercises. In

the case of diabetes even more consideration must go into the selection of food before and

after exercise. Doctors suggest large intakes of carbohydrates before exercise for diabetes

carriers to meet the glucose needs of the muscles.

The second article that I used was that of Konen, et al. He and his colleagues conducted

testing and research on "changes in diabetic urinary and transferrin excretion after

moderate exercise". This article was a report of the way the research was conducted and

The researched found that urinary proteins, particularly albumin, increase in urinary

excretion after moderate exercise. Albumin which is associated with micro- and

macrovascular diseases in diabetic patience was found to increase significantly in IDDM

patients, while remaining normal in non-diabetics. (See table 1 and 2 for results)

These results cannot be conclusive to say that this shows that exercise causes other micro-

and macrovascular diseases in diabetics. Since albumin is not associated with any disease

in non-diabetics then the same may be the case for diabetics as well. However further

research is required to find out why such a significant increase occurs in diabetic

patients and what it really means.

It obvious that there are many very complicated issues associated with diabetes which

cannot be explained at this stage. Therefore much more research is required and it's only a

matter of time for these complications to resolved.

Although there are no firm evidence to suggest that exercise will improve or worsen

diabetes still it is recommended by physicians.

Aristotle and the Indian physician, Sushruta, suggested the use of exercise in the

treatment of diabetic patients as early as 600 B.C. And during late last century and early

this century many physician claimed that the need for insulin decreased in exercising

The benefits of exercise in non-diabetic individuals is well known. For example reduce the

risk of heart disease. This makes exercise very important to diabetic carriers since they

are at a greater risk of getting heart disease than non-diabetics.

Unquestionably, it's important for diabetics to optimise cardiovascular and pulmonary

parameters as it is for non-diabetic individual. Improved fitness can improve one's sense

of well-being and ability to cope with physical and psychological stresses that can be

aggravated in diabetes.

In well controlled exercise programs the benefits are many, as shown on table 3.

In conclusion we can see that although there are many factors that need to considered when

a diabetic person exercises, still there are many benefits when an IDDM carrier controls

and maintains a good exercise program. The risks of other disease such as heart disease and

obesity are reduced.

1. Sutton, J.R, (1981), Drugs used in metabolic disorders, Medicine and Science in Sports

and Exercise, Vol 13, pages 266-271.

2. Konen, J.C, (1993), Changes in diabetic urinary transferrin excretion after moderate

exercise, Medicine and Science in Sports and Exercise, pages 1110-1114.

3. Bouchard, C, (1990), Exercise, Fitness and Health, Human Kinetics Publishers.

4. Burke, E.J, (1980), Exercise, Science and Fitness, Mouvement Publishers.

5. Sanborn, M.A, (1980), Issues in Physical Education, Lea and Febiger.

6. Marble, A, (1985), Joslin's Diabetes Mellitus, Twelfth Edition, Lea and Febiger.

7. Kilo, C, (1987), Diabetes - The facts that let you regain control of your life, John

Wiley and Sons, Inc.

8. Seefeldt, V, (1986), Physical Activity and Well-being, American Alliance for Health,

Physical Education, Recreation and Dance.

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