Charlietheunicorn411
Obesity Becoming the “Norm”?
An epidemic is quickly spreading across the United States - obesity.-no citation? It stems
from direct observation.-That is very funny. Get rid of this sentence and cite it or get rid of the
first sentence too. Obesity is the state of having a large amount weight that is disproportionate to
one’s height, in other words, the extreme case of being overweight.-I don’t think the second half
of this sentence is necessary. You still didn’t define it. It is weight relative to height as judged by
what? BMI (Body Mass Index) is used to determine whether one is overweight or obese.-You
just “defined it” and now you say this? A BMI of over 25 is overweight and a BMI over 30 is
obese. -general to specific. I think the general is…what is BMI? (not what does it stand for, what
is it?) Fifty-four percent of adults are considered overweight and twenty-two percent of the
overweight are also obese-why don’t you just say the percentage that is obese and why isn’t this
the first sentence? Also, is this in the US or in the world??; Twenty-five percent of children are
also considered obese (Hill & Peters, 1998).-no semicolon, put both together and get rid of the
overweight part The main contributor to obesity of these people is often inherited genes from
ancestors.-this, to me, is a ridiculous statement. The main contributor is eating too much. Early
humans lived in an environment where food was scarce and difficult to obtain. Because of these
hard conditions,-do you need to say this? humans developed genes that retained energy from
consumed food. Unfortunately, in the twenty-first century, with the wide availability of food,
these genes are starting to cause obesity in many people because they are inclined to retain
energy from food-is that what the paper said? Or did it say that we don’t have the ability to get
rid of excess very easily because we have never been in the presence of excess until now??? (Hill
& Peters, 1998). If researchers can determine the relationship between genes and weight gain, it
may lead to a discovery of a cure for obesity-I don’t like this vague and “heading nowhere”
sentence. Be specific and transition into the rest of your manuscript. Work on the intro and get it
back. (Comuzzie & Allison, 1998).
Scientists found a surprising correlation between genes and weight regulation system by
studying how hunger, a part of the system, worked. They discovered a protein that caused people
to feel full (a molecule that carries out the work of the cell), Leptin. The scientists began to
research deeply into the molecule in order to understand how it was able to end desire for food.
Through many observations, scientists were able to see how Leptin worked. They saw that
Leptin was able to satiate hunger by blocking a protein called Neuropeptide Y (NPY) that caused
it. Scientists also learned that the amount of Leptin was controlled by how much food (energy),
such as fats, is in the body. When the body is low on energy, less Leptin is produced to disable
Neuropeptide Y, to make the body feel hungry. When the body has a sufficient amount of
energy, more Leptin is produced to disable more NPY, to make the body full. This is done so
that the body feels hungry when it needs food and feels full when it doesn’t(Loftus, et al., 2000;
Erickson, et al., 1996; Comuzzie & Allison, 1998). As the first step to seeing the relationship
between genes and weight regulation, scientists started to examine the amount of Leptin and
NPY in people. They saw that obese mice compared to people of normal weight had smaller
amounts of Leptin; however, the two groups of people had the same amount of NPY. Therefore,
while the normal weighted had the amounts of Leptin and NPY at a balanced state, the obese had
more NPY than the Leptin could make up for. The low amounts of leptin caused obesity in the
obese people because they were only disable a portion of the larger amounts of NPY in the obese
people. This lead to constant hunger in the obese people, even when they did not need food, and
further caused them to gain weight through overeating. Scientists, with this information
concluded that one way genes caused obesity was by having coded information that determined
the amount of production of these molecules.
Based on their knowledge of the two protein molecules, scientists if a cure for obesity
could be based on reduction of the amount of NPY for Leptin to target, would cause less hunger.
To test this question, scientists gathered two groups of obese mice. The control group was ob/ob
mice, mice with a gene that with information to produce a minute amount of Leptin. The group
were Leptin-deficient, but made a normal amount of NPY. Therefore, most of their NPY was left
untargeted by Leptin which caused an overwhelming expression of NPY that promoted feeding.
As a result, these mice ate voraciously from great hunger. Furthermore, this group had a slow
metabolic rate. (The experiment never explained why) The experimental group was ob/ob mice
that were genetically engineered to produce small NPY, and their Leptin deficiency remained the
same. Interestingly enough, the second group of mice only had minor symptoms of obesity. They
did not have as much cravings for food as the control group did and also had a higher metabolic
rate than that of the first group (paper never explained the metabolic rate here either). Scientists
also learned that Leptin was more complex than they had thought it was. Since, the reduction of
NPY did not completely cure obesity in the experimental group mice, scientists saw that Leptin
also affected other unknown obesity-linked factors. This is because if NPY was the sole target of
Leptin, reducing the amount of NPY would have made up for the small amount of Leptin. These
variables are still yet to be found.Although NPY removal alleviated the symptoms of obesity, it
has not been experimented on humans. (reason not known, but it is probably because we would
have to genetically alter humans in order to do so, since NPY is continuously made and therefore
would have to be continuously removed). However, the idea may resurface in the future.
(Erickson, et al., 1996).
After the experimentation with NPY as a way to find a cure, scientists started to search
for alternatives. Scientists recently discovered two potential cures for obesity called C75 and
Cerulenin. They are able to counteract weight gain because of their ability to block NPY. In a
controlled experiment, mice were injected with these molecules and lost large amounts of
weight. This was because like Leptin, they cancelled out the NPY to make the mice to be devoid
of hunger. However, these molecules are very different from Leptin in other aspects. Under
normal conditions, starving mice have less physical activity and slower body function; however,
C75 and Cerulenin go against this decrease in energy use. Starving mice that were injected with
C74 and Cerulenin did not have any sign of energy conservation. They did not seem fatigue at
all. Scientists were astonished by these results. The reason behind these results was that although
these two molecules act as a substitute for Leptin, it does not affect the production of Leptin in
anyway. Leptin production carried on normally and therefore, both Leptin and these molecules
disabled all NPY. Therefore, mice did not feel the need to eat. The brain begins to believe it has
an adequate amount of energy because of the lack NPY expression when actually the body is
energy-deficient. Unfortunately, hopes for using these inhibitors for therapeutic use were dashed.
Mice needed continual injections of C75 and Cerulenin to stay lean because effects of these
molecules were dependent upon how long the drug was taken and thus, they were only
temporary (Loftus, et al., 2000).
A final attempt to cure obesity was attempted by experimenting with the breaking down
of fat. Scientists began to believe that the cure for obesity lies in lipolysis, the process of
breaking down fat. When they heard that animals had brown fat cells, fat that is broken down to
create heat, scientists thought that thermogenesis, the creation of heat, may be the cure. They
believed that the study of lipolysis would help them in their search because energy consumption
is primarily governed by molecules that break down brown adipose tissue (BAT) and white
adipose tissue (WAT), also simply known as brown and white fat, respectively. The difference
between these two fats is that brown fat is necessary for thermogenesis and white fat is necessary
for energy used in all processes except thermogenesis, such as physical and mental activity. In
order for BATs to function and maintain its properties, Beta-Adrenergic Receptors (βARs),
molecules that are necessary to break down fat, are needed. Experiments show a rapid decrease
in body temperature of mice that did not have Beta-Adrenergic Receptors because the mice were
unable to break down fat in order to remain at regular body temperature. Furthermore, mice that
lacked βARs did not have sufficient amounts of Uncoupling Protein – 1 (UCP-1). UCP-1’s are
also needed to break down BATs (Bachman, et al., 2002). Although humans have neither brown
fat nor UCP-1’s, the scientists also started to research because a protein similar to UCP-1’s was
found to be created in ordinary fat and muscle cells of humans. This find showed promise to
future treatments and therapy (Gura, 1998). βARs may in the future be utilized via injection or
other methods in the future to cause an increase in UCP-1, which would result in a higher rate of
lipolysis and energy conversion to heat which would ultimately lead to weight loss. This cure is
still being researched (Bachman, et al., 2002).
Although scientists have not come up with the official cure for obesity, there is still hope.
C75 and Cerulenin may be used as a way to lose some weight in order to carry out physical
activities to lose more weight. Research on Brown fat is being worked on. In 2009, scientists
have found brown fat in under the collar bone section of humans which have raised hope for a
cure through these fats. These experiments endlessly lead into the next through results that create
questions that demand an answer to. Scientists are still striving to find the official “cure” for the
large problem of obesity. (Loftus, et al., 2000; Erickson, et al., 1996; Bachman, et al., 2002;
Farmer, 2009).
References
Bachman, E.S., Dhillon, H., Zhang, C., Cinti, S., Bianco, A.C., Kobilka, B.K., & Lowell, B.B.
(2000) βAR Signaling Required for Diet-Induced Thermogenesis and Obesity Resistance,
Science, 297, 843-845.
Comuzzie, A.G., & Allison, D.B. (1998). The Search for Human Obesity Genes, Science, 280,
1374-1377.
Erickson, J.C., Hollopeter, G., & Palmiter, R.D. (1996). Attenuation of the Obesity Syndrome of
ob/ob Mice by the Loss of Neuropeptide Y, Science, 274, 1704-1707.
Farner, S.R.. (2009). Be Cool, Lose Weight, Science, 458, 839-840.
Gura, T. (1998). Uncoupling Proteins Provide New Clue to Obesity’s Causes, Science, 280,
1369-1370.
Hill, J.O., & Peters, J.C. (1998). Environmental Contributions to the Obesity Epidemic, Science,
280, 1371-1374.
Lazar, M.A. (2005). How Obesity Causes Diabetes: Not A Tall Tale, Science, 307, 373-374.
Loftus, T.M., Jaworsky, D.E., Frehywot, G.L., Townsend, C.A., Ronnett, G.V., Lane, M.D., &
Kuhajda, F.P. (2000). Reduced Food Intake and Body Weight In Mice Treated with Fatty Acid
Synthase Inhibitors, Science, 288, 2379-2381.