High fructose corn syrup.edited
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Effect of High Fructose Corn Syrup
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Effect of High Fructose Corn Syrup
High fructose corn syrup (HFCS) has increasingly become a primary form of sugar in
most human diets due to its benefit over sucrose in taste, cost, and preparation method. HFCS
is derived from corn starch, composed of glucose polymers such as amylose and amylopectin.
To create it, the starch must first be converted into glucose, which is then partially
transformed into fructose by enzymes. The resulting syrup has different fructose content such
as the HFCS-55, which has 55 percent fructose and 45 percent glucose, primarily used in
foods and beverages such as soft drinks, baked goods, and processed foods. The fructose in
HFCS establishes health concerns when utilized in excessive amounts. HFCS excessive
consumption is a significant health problem; its intake is associated with changes in
systematic and tissue-specific metabolic status, which affects individuals' bodies, causing
fatty liver disease, diabetes, obesity, and insulin resistance-related.
High intake of fructose increases the risk of fatty liver disease. Excess fructose
consumption can increase liver fat to a greater extent than an equal amount of glucose.
Fructose is a monosaccharide that is metabolized differently than glucose; it is primarily
metabolized in the liver. Generally, it is crucial to understand the detrimental impact of
fructose in HFCS in order to consume healthy and safe amounts (
DiStefano & Shaibi, 2021)
.
Almost every cell in the body can use glucose as an energy source. However, only the cells in
the liver can effectively process which can potentially effect liver, arteries, and heart,
especially when used in excessive amount. Decreasing the consumption of fructose will
reduce the risk of fatty liver diseases and promote the general public health.
HFCS affects the metabolic processes in the body. Generally, it is evident that glucose
is broken down by every cell in the body while fructose is largely broken down in the liver.
When fructose is ingested, the liver absorbs it and transforms it into fatty acids, glucose, and
glycogen. Several enzymes control this process, including fructokinase, which catalyzes the
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initial step in fructose metabolism. In addition, fructose metabolism is connected to the
process by which HFCS causes metabolic disease (
Bhat
et al., 2021)
. Hence, fructose quickly
absorbs into the liver and skips the phosphofructokinase regulation stage in glycolysis, which
results in hepatic insulin resistance. Also, an increase in diacylglycerol decreases the insulin
receptor's tyrosine phosphorylation, increases glucose production, and impairs glucose
tolerance. Hence, fructose boosts the liver's production of triglycerides, a form of fat kept in
adipose tissue, and can help cardiovascular disease grow.
HFCS has been implicated as a contributing factor to obesity. When consumed in
large amounts, fructose can produce fatty acids, which can contribute to the development of
insulin resistance, dyslipidemia, and obesity. Also, nigrostriatal and mesolimbic dopamine
(DA) pathways are important regulators of eating habits and obesity. Diet composition, such
as increased fat, independent of caloric intake and body weight, insulin resistance linked to
obesity, and increased body weight and adiposity. No matter how many calories are
consumed or how much weight a person has, an increased ratio of fat macromolecules in the
diet can cause changes in the DA system. Large HFCS intakes may increase body weight and
body fat. This is so because HFCS is metabolized from other sugars like sucrose (table
sugar). HFCS is broken down into glucose and fructose, with the liver processing the fructose
component. This process can result in the development of insulin resistance, which can
contribute to obesity and other health issues. Additionally, HFCS consumption at high levels
may cause an increase in appetite and overeating. According to one study, people who
consume much fructose, a key ingredient in HFCS, have lower levels of the hormones that
control hunger and fullness, making them more likely to feel hungry. To maintain a healthy
weight, limiting the consumption of added sugars, including HFCS, is recommended, and
focusing on a balanced diet that includes whole foods, fruits, vegetables, lean proteins, and
whole grains.
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HFCS causes more fat and stimulates feelings of hunger than ordinary sugar. HFCS
has a detrimental effect on appetite regulation as individuals feel hunger leading to more
consumption of more food, which can contribute to metabolic diseases. According to
research, HFCS consumption can cause a decrease in satiety and an increase in hunger
compared to other sweeteners. Fructose does not trigger the production of hormones like
leptin and ghrelin that control appetite. Adipose tissue produces the hormone leptin, which
instructs the brain to reduce food intake and raise energy expenditure (
Kisioglu & Nergiz-
Unal, 2020)
. The Ghrelin hormone is created in the stomach, instructing the brain to eat
more. If leptin were absent, we might keep eating even after the body has enough calories,
resulting in weight gain. Generally, consuming fructose does not trigger the release of leptin
or ghrelin, which can increase hunger and decrease satiety.
HFCS also contributes to diabetes, inflammation, and high triglycerides. A preclinical
study suggests that consuming fructose alters the digestive tract's cells in a way that makes it
more able to absorb nutrients. Large HFCS intakes may result in an increase in body weight
and body fat because HFCS is metabolized otherwise from other sugars like sucrose (table
sugar). HFCS is broken down into glucose and fructose, with the liver processing the fructose
component. This process can result in the development of insulin resistance, which can
contribute to obesity and other health issues. Additionally, HFCS promotes the growth of
insulin resistance, a crucial aspect of type 2 diabetes. Elevated blood sugar levels result from
insulin resistance, established when the body's cells stop responding to insulin. As such, this
can ultimately result in type 2 diabetes, a chronic disease marked by elevated blood sugar
levels and insulin resistance (
Khan
et al., 2021
)
. Furthermore, reactive carbonyls found in
HFCS may harm cells and tissues, aggravating disorders like diabetes. One of the primary
distinctions between the metabolism of glucose and fructose is that fructose does not cause
the pancreas to secrete insulin. Insulin is a hormone that signals cells to absorb glucose from
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the bloodstream, assisting in regulating blood sugar levels. As soon as glucose is taken,
insulin is released due to the rise in blood sugar levels. Fructose, on the other hand, does not
affect the release of insulin, which over time, can result in high blood sugar levels and insulin
resistance.
The United States of America Food and Drug Administration (FDA) regulates the use
of chemicals in food and consumer products, including HFCS. However, there is a growing
concern regarding the safety of excessive consumption of HFCS found in processed food
with high calories and low nutrients. As such, regulatory agencies such as the FDA should
continue to monitor the safety of these chemicals and update their regulations to effectively
protect public health and reduce the exposure of chemicals to human lives. As HFCS is
increasingly used as a sweetener in most food products and beverages, its excessive usage
should be regulated to minimize the profound effect on the human body. Regarding their
metabolism and health implications, there is debate and confusion surrounding fructose,
sucrose, and HFCS. Generally, a connection exists between fructose, HFCS, or sucrose and
heightened health risks such as heart disease, metabolic syndrome, or fatty infiltration of the
liver or muscle.
HFCS have had significant financial and medical impact on the healthcare systems
and has negatively impacted the society. Chronic fructose consumption has been linked to
several health issues, including insulin resistance, obesity, liver problems, and diabetes. The
liver's fructose kinase catalyzes the initial step in fructose metabolism, a reaction that is not
controlled by feedback. As a result, eating high fructose foods can reduce ATP levels, raise
uric acid levels, and increase nucleotide turnover. As such, there is need to regulate the
consumption of HFCS to minimize or even eliminate its impact on the public health.
However, future research is crucial in preventing or inhibiting fructose metabolism in the
6
liver, along with dietary management, for preventing and managing chronic metabolic liver
disorders brought on by fructose.
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References
Bhat, S. F., Pinney, S. E., Kennedy, K. M., McCourt, C. R., Mundy, M. A., Surette, M. G., ...
& Simmons, R. A. (2021). Exposure to high fructose corn syrup during adolescence in
the mouse alters hepatic metabolism and the microbiome in a sex‐specific
manner.
The Journal of Physiology
,
599
(5), 1487-1511.
https://doi.org/10.1113/JP280034
Chakraborti, A., Graham, C., Chehade, S., Vashi, B., Umfress, A., Kurup, P., ... & Bibb, J.
(2021). High fructose corn syrup-moderate fat diet potentiates anxio-depressive
behavior and alters ventral striatal neuronal signaling.
Frontiers in neuroscience
,
15
,
669410.
https://doi.org/10.3389/fnins.2021.669410
DiStefano, J. K., & Shaibi, G. Q. (2021). The relationship between excessive dietary fructose
consumption and pediatric fatty liver disease.
Pediatric obesity
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(6), e12759.
https://doi.org/10.1111/ijpo.12759
Khan, M. S., Ikram, M., Park, T. J., & Kim, M. O. (2021). Pathology, risk factors, and
oxidative damage related to type 2 diabetes-mediated Alzheimer’s disease and the
rescuing effects of the potent antioxidant anthocyanin.
Oxidative medicine and
cellular longevity
,
2021
.
https://doi.org/10.1155/2021/4051207
Kisioglu, B., & Nergiz-Unal, R. (2020). The potential effect of maternal dietary sucrose or
fructose syrup on CD36, leptin, and ghrelin-mediated fetal programming of
obesity.
Nutritional neuroscience
,
23
(3), 210-220.
https://doi.org/10.1080/1028415X.2018.1491151