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Running head: A LOOK AT ADIPOSE BUILD-UP IN LITERATURE

A Look at Adipose Build-Up in Literature

Trevor J. Parrett
Hope College

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Since the 1960s, America has been lied to and misguided when it comes to dietary and
nutritional advice. For five decades, doctors and the multi-media have suggested that consumers
must exercise more and eat less in order to lose weight. Countless physicians coach patients that
they must create a calorie deficit between the food taken in and the energy expended throughout
the day. The fault in todays common knowledge arose in a time when researchers found a
correlation without causation between the lack of carbohydrates eaten and the rise in heart
disease (Taubes, 2011, p. 144-160). Gary Taubes popularized the fault in this belief in his book
Why We Get Fat And What To Do About It. He claims that obesity is fundamentally a disorder
of excess fat accumulation (Taubes, 2011, p. 9). To truly understand the causes and
consequences of obesity, the inner workings of the body and the chemical processes of adipose
build-up must be examined. Essentially, it is the abuse of carb-loaded foods that has driven
Americas bodies to react in alien ways. The human body can be thought of as a factory, one that
must adjust and compensate for the excess of a foreign food; for, sugar, coffee, and canned goods
are not foods of a natural diet (Taubes, 2011, p. 23).
Background Information
Fat is not created equally. Two forms of fat exist: white fat and brown fat. Brown fat is
given its name due to the presence of iron in the cells, which exists in the mitochondrion.
Because brown adipose tissue contains mitochondria, it is predisposed to be metabolically active.
This means that, unlike white adipose tissue, brown tissue burns fat, yielding heat and usable
energy. When deposits of brown fat in the body are low, a protein called early B cell factor-2
(Ebf2) is expressed. When the protein is expressed in high levels, white fat is transformed into
brown fat. The presence of brown fat is significant in that it has the ability to burn more calories
when animals are overfed, protecting them from obesity. White fat is the savings account of the

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two. While brown fat is fluid in that it is frequently synthesized and consumed, white fat holds
on to energy and is more difficult to rid (Collins, 2013). The regulation of the deposition of
excess fat in white tissue defines the rate of weight gain and where weight is allocated, though it
is unclear what regulates the quantities of these two forms. Ideally, future research will reveal
how the deposits of brown fat can be maximized, while those of white fat, depleted. To learn
more about brown fat acquisition is to take steps toward overcoming the obesity epidemic.
Genetics
Obesity has a large genetic component. Recall how people who are related have similar
body types. In all, there are 20 genes that influence why humans get fat and where that fat goes
(Taubes, 2011, p. 63). Not only does the body allocate fat differently per family, but it also
allocates fat uniquely to each gender. Females have a greater proportion of fat below the waist
than males. Genetics can also influence how prone someone is to an obesity related disease.
Lipodystrophy, for example, is a disease that affected some 200 American women in the mid1950s. Those prone to the disease gradually loose fat from their upper body and gain it on the
lower body (Taubes, 2011, p 70). The diseases to which humans are prone parallel the threats that
a safety manager must be prepared for in a factory. The same way the expertise of a safety
manager can influence how quickly a problem can escalate, fat gain can be accelerated or
implicated by genetics.
The Body as a Factory
Insulin, a hormone secreted by the pancreas, single-handedly controls most of the fat
acquisition in the human body. Insulin helps the body keep up with the raised blood sugar levels
by signaling cells throughout the body to increase the rate at which they are pumping in glucose

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from the bloodstream (Taubes, 2011 114). Like a factory, the body continuously receives new
shipments, synthesizes fragments of each shipment into what is needed, and exports the product
for the good of the company. The brain, as it typically does, represents the chief executive
officer, or president of the company. Like a CEO, it has branch managers. The brain recruits
hormones to send signals to different areas of the stomach cavity, or branch offices. Insulin
embodies the position of the floor manager, coordinating what goes where and when operation
occurs or needs to be shut down. Those who unload the incoming shipments to the company
mimic the function of lipoprotein lipase, or LPL. They
work to pull sugars out of the bloodstream into fat or
muscle cells that "express" LPL so that the sugars can
be stored (Taubes, 2011, p. 91). Adipose tissue stores
the sugars that are not being used (in the form of fat);
fat is released back into the bloodstream as sugar when
energy is needed. Adipose tissue stores fatty acids in
the form of triglycerides - 3 fatty acids and one glycerol (Taubes, 2011, p.116). Triglycerides are
far too large to exit the cell without intervention by hormone-sensitive lipase (HSL), a catalyst.
HSL is an overstock worker. It breaks down triglycerides into their component fatty acids so the
triglycerides can escape the adipose tissue and return into the circulation. However, when the
time comes, insulin suppresses the function of HSL and the process begins its cycle again
(Taubes, 2011, p.120).
Deposition of Fat into and Extraction of Fat from Adipose Tissue
Believe it or not, fat accumulation begins as soon as a person thinks about food. The mere
sizzling of a steak, picture of a plate of pasta, or smell of popcorn is enough to get the process in

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motion. As soon as someone thinks about eating, he begins secreting insulin. The insulin signals
the fat cells to shut down the release of fatty acids (by inhibiting HSL) and take up more fatty
acids (via LPL) from the circulation. So begins the feeling of hunger. Upon the first bite, still
more insulin is secreted. The carbs from the food that is consumed are digested and enter the
circulation as fructose, causing blood sugar levels to rise. In order to be able to store the energy
that is coming in, humans secrete more insulin. In this step, the insulin works to tell the adipose
tissue to absorb the incoming nutrients. Fat from the diet is stored as triglycerides in the fat cells,
as are some of the carbohydrates that are converted into fat from the liver. The fat cells get fatter,
as does the person. The fat is trapped in the adipose tissue until insulin levels drop and HSL can
begin to work again (Taubes, 2011, 124).
Communication between the Stomach and Brain on Food Exposure
The CEO has many modes of communication with its office branches. By way of
hormones, there is constant communication between the stomach and the brain. The
hypothalamus, which regulates food intake, energy expenditure, and the deposition of energy in
fat tissues to maintain homeostasis, circulates many of these hormones (Guyenet, 2012, p.164). If
people consistently reduce fat intake, fat mass declines and so does leptin, and this signals the
hypothalamus to stimulate hunger and make the body use calories more efficiently in an attempt
to regain body fat. However, overeating causes an increase in fat mass and leptin suppresses
appetite and increases calorie use until body fat stores have declined back to baseline (Guyenet,
2012, p.164). This ultimately results in a negative feedback loop between hunger and fat storage.
Because neither can be satisfied, the result is an obese individual.

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Dopamine Receptors and the Reward Pathway
Dopamine receptors in the brain play a large role in the reward pathway of food
consumption. The reward deficiency hypothesis states that increased food intake is an attempt to
generate more reward in compensation for reduced mesolimbic dopamine signaling (Berthound
& Shin, 2011). As Berthound and Shin describe, Differences in mesolimbic dopamine signaling
are most strongly implicated in altered food anticipatory and consumatory behaviors and
obesity. In English, this means that people received a high after they ate food due to the reward
pathway. The reward received on the first bite of a meal is directly correlated with the time since
the individuals last meal. If someone has not eaten in a while, the food storages tell the brain to
increase the reward once food is obtained (Guyenet, 2012, p.169). In obese individuals, D2
receptors were negatively correlated with BMI (Wang et. al., 2001). Obese individuals crave
carbs more because they have more insulin, which is more effective at stashing away the fat and
leaving less available for usable energy (Taubes, 2011, p.142). Because the reward response is
exaggerated in those who are overweight, the human reward center works to reinforce eating
sugars to an unhealthy degree. Some people get addicted to food in the same sense that people
become addicted to drugs. At this point, the factory is not operating at optimal production,
storing more than it is able to rid. Low D2 receptors, in the nucleus recumbents of the brain, have
also been reported in individuals addicted to various types of drugs (Berthound & Shin, 2011).
With more bland diets, the reward pathways "back off" and reduce reward (Guyenet, 2012,
p.170). Research conducted by Pennsylvania State also showed that exercising can increase
dopamine release, increasing the number of active dopamine receptors (Wang et. al., 2001). This
shows that the effects of obesity are not only reversible, but that the epidemic is nearly
preventable if people take care of their mind and body.

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Surgery and Effects
Studies, like those conducted by Berthound and Shin, have proven that the most effective
way to counter the effects of obesity is through bariatric surgery. Their focus is on the Roux-en-Y
surgery, one in which the esophagus is connected to the intestine. Post-surgery, patients have
shown a decreased preference for carbohydrates. Furthermore, the majority of patients lack
affinity for food altogether. As the article explains, The lower gut hormones glucagon-like
peptide-1 and peptide YY, which are substantially elevated after the surgery, are instrumental in
returning glucose to homeostatic levels (Berthound & Shin, 2011). The authors continue on to
predict that these hormones work with the brain and affect the reward pathway, though it is not
thoroughly explained. Ultimately, it leads to the reestablishment of normal levels of insulin and
leptin, two hormones proven to be active in fat regulation.
Concluding Words
The obesity epidemic is one that will continue to be a prevalent problem in society if not
taken seriously. While some continue to argue that it is purely a problem of calories-in/caloriesout, the science proves that it is much more complex. Not only does the problem exceed the
boundaries of the gastrointestinal tract, but it originates the second that the body detects a food
stimuli. Though science is unable to pinpoint a single cause as to why the obesity epidemic rose,
it is essential that all processes of the body are considered. And although further research is
needed, biologists and chemists have come a long way. Those in the field have identified the
hormones that allow organs to communicate, discovered surgeries that cure obesity and keep fat
off, revealed how different foods affect fat deposits, and explored how people could be prone do
obesity since day one. Good science is equivalent with fact. That which is proven and can be

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reproduces, becomes widely accepted. If nothing else, the obesity epidemic is curable. There is
hope in science and success in inevitability.
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References
Berthound, H., & Shin, C. A. (2011). Food Reward Functions as Affected by Obesity and
Bariatric Surgery. International Journal of Obesity, S40. Retrieved March 4, 2015.
Collins, F. (2013, March 26). Brown Fat, White Fat, Good Fat, Bad Fat. In National Institutes of
Health.
Guyenet, S. J. (2012, March 9). Seduced by Food: Obesity and the Human Brain. In S. Engdahl
(Ed.), Opposing Viewpoints: Obesity (pp. 162-172). Farmington Hills, MI: Greenhaven
Press.
Taubes, G. (2011). Why we get fat and what to do about it. New York: Alfred A. Knopf.
Wang, G., Volkow, N. D., Logan, J., Pappas, N. R., Wong, C. T., Zhu, W., & Netusll, N. (2001,
February 3). Brain Dopamine and Obesity. The Lancet, 357, 354-357