THE EFFECT OF MONOSODIUM GLUTAMATE ON BLOOD

GLUCOSE LEVELS IN MICE

By:
Name : Pratiwi Kusuma Kurniawati
Student ID : B1B017007
Group :9
Entourage : II

PRACTICAL REPORT OF ENDOCRINOLOGY

MINISTRY OF RESEARCH, TECHNOLOGY AND HIGHER EDUCATION

JENDERAL SOEDIRMAN UNIVERSITY
FACULTY OF BIOLOGY
PURWOKERTO
2019
 I. INTRODUCTION

1.1 Purpose

The purpose of the effect of monosodium glutamate on blood glucose levels in

mice practical activity is to evaluate the effect of monosodium glutamate on
pancreatic gland activity with an indicator of blood glucose levels.

1.2 Benefit

The benefits of the effect of monosodium glutamate on blood glucose levels in

practical activity are:
1. Students gets skills in measuring blood glucose in mice which is the same
principle as measuring blood glucose in humans by using GlucoDr.
2. Students can able to know and hone their skills in conducting intragastric
gavage technique using mouse oral gavage in test animals.
3. Students can find out is there any effect of giving too much Monosodium
Glutamate to blood sugar homeostasis in the body.
4. Students can find out is there any effect of giving too much Monosodium
Glutamate to the work mechanisms of the endocrine glands especially
pancreatic gland in secreting hormones to regulate blood sugar homeostasis
in the body.
 II. MATERIAL AND METHODS

2.1 Material

The tools that used in this laboratory activity are aquarium with the aeration,
aquarium, net, camera, specimen tray, millimeter block, scissor, basin, and analytical
scale.
The materials that used in this laboratory activity are juvenile nilem fish,
thyroxine hormone (T4) that is Euthyrax amount 20μg/L and 40 μg/L, anti-thyroxine
hormone (PTU) that is Prophyl-thiouracil amount 20μg/L and 40 μg/L, and pellet.

2.2 Methods

The methods used in this practical activity are :

1. All tools and materials are prepared.
2. Three fish are taken from the aquarium.
3. Fish are weighed before being treated.
4. The fish are treated according to the directions that written by the assistant on the
board.
5. Each of 3 fishes are cut off in the abdomen and pectoral fins, one fish placed in
an aquarium that has been given by hormone thyroxine (T4) amount 20μg/L or
40 μg/L, one fish placed in an aquarium that has been given by anti-thyroxine
(PTU) amount 20μg/L or 40 μg/L, and one fish placed in aquarium that is not
given anything (control).
6. Fish are fed with as many as 2 or 3 pellets every day.
7. Aquarium is cleaned every 3 days.
8. The general condition of fish were observed every day
9. Other parameters such as total fish body length, fin length, and fish body weight
were observed and measured every week.
10. Observation and measurement data are written in a table that has been made by
groups.
11. A tabulation table of data from all groups is written and attached to the report.
3.2 Discussion

Based on the results obtained, the mean body weight of mice with a constant
increase in control treatment namely 25.13, 25.94, and 28.8. The treatment of 1 mg
dose is constant at week 1 and rises at week 2 i.e. 27.1, 27.16, and 29.48. The 3 mg
dose treatment also increased, namely 25.56, 33.68, and 34.75. The 6 mg dose
treatment also experienced a decrease in body weight in the second week, namely
from 30.39 and 30.89 to 29.59 in the 2nd week. While for the 9 mg dose, there was
an increase of 25.52, 29.60, and 31.02. According to the study of Muharani (2016),
the body weight of mice increased constantly for 2 weeks after being given MSG.
Fluctuating mice body weight in the lab can be caused by environmental stress so
that from week to week becomes not constant to rise. Acoording to He et al. (2008),
Long-term consumption of MSG can damage neurons in the arcuate nucleus and
interfere with the transmission of signals by leptin, which causes leptin resistance
and also obesity. MSG may have an effect on adipsin resulting in changes in body
composition. Adipsin is synthesized and secreted by adipocytes. Decreased
expression of adipsin is thought to be related to obesity in animal try. Mice given
MSG had 50% lower serum adipsin and had twice the body fat percentage greater
than the muscle mass of the control group.
Based on the results obtained, the mean blood glucose level of mice with a
occur decreasing in control treatment namely 139, 201.67, and 128. The treatment of
1 mg dose is constant increasing i.e. 127, 127.33, and 169. The 3 mg dose treatment
also increased, i.e. 115, 141.67, and 175.33. The 6 mg dose treatment also
experienced a increase in blood glucose level in the first week and decrease in
second week, namely from 119.67 and 175.33 to 146 in the 2 nd week. While for the 9
mg dose, there was an increase of 132.33, 157.67, and 161.3333. According to
Ismawati (2003), administration of MSG can increase blood glucose levels in mice.
Fluctuating blood sugar levels in the lab can be caused because when blood will be
taken the mouse is stressed so that the blood sugar level measured by GlucoDr
becomes unstable from week to week. Based on research conducted by Ismawati
(2003), administration of MSG can increase blood glucose levels in mice, the higher
the dose of MSG given, the higher the blood glucose level. This is reinforced by
research conducted by Muharani (2016),that the weight of mice before the treatment
of constant MSG administration was lower than after being given MSG. According
to Boonnate et al. (2015), MSG consumption might increase postpandrial glucose
levels and then stimulate insulin release. Indeed, MSG has been shown to have an
effect on insulin release. In human studies, serum insulin levels tended to be higher
in MSG-treated participants compared to controls and the level of serum insulin
correlated well with that of glutamate. Recall the involvement of the hypothalamus in
the regulation and action of insulin a hormone that metabolizes glucose. Since the
brain cells are damaged by MSG, they may be dormant to blood glucose level and or
the feedback regulatory mechanism may not function to regulate insulin secretion.
In the human body, glutamic acid is almost always in the form of glutamic
acid, due to conditions in the body that support the loss of hydrogen atoms from
glutamic acid. Glutamate is also produced by the human body and will bind to other
amino acids to form protein structures. Glutamate is known to be the main excitatory
neurotransmitter found in the CNS in mammals and is involved in various aspects of
normal brain function including cognitive, learning and memory functions
(Michaelis, 1998). In the consumption of Monosodium Glutamate, the free glutamic
acid produced in part will be bound in the intestine and the rest will be released into
the blood. Furthermore, free glutamic acid will spread throughout the body,
including going through the blood-brain barrier (blood-brain barrier) and bound to
the receptor. In the consumption of Monosodium Glutamate, the free glutamic acid
produced in part will be bound in the intestine and the rest will be released into the
blood. Furthermore, free glutamic acid will spread throughout the body, including
going through the blood-brain barrier and bound to its receptors (Suarez et al., 2002).
The mechanisms of excitotoxicity can occur from various factors. Overstimulation of
the glutamate receptor will be able to initiate various cascades that have the potential
to induce cell damage and death. Activation of NMDA receptors by glutamate causes
large amounts of calcium (Ca2+) influx, accompanied by sodium ions through the
AMPA receptor. Activation of mGlu receptors (specifically mGluR1) also causes
increased release of calcium ions coming out of the endoplasmic reticulum
(Erdmann, 2006).
Excessive administration of Monosodium Glutamate can cause behavioral
changes such as fear and anxiety that can increase aggressiveness. This behavior
change can be triggered by the replacement of important elements in the body such
as iron and zinc due to the presence of Monosodium Glutamate. Monosodium
Glutamate also enhances the mechanism of action of the adrenocorticotropic
hormone produced by the pituitary gland. The adrenocorticotropic hormone (ACTH)
activates the adrenal cortex to increase anxiety. Monosodium Glutamate causes
overlapping imbalances in neurotransmitters such as aggressiveness, anxiety, mental
disorders. Some research works show anxiety disorders change serotonin, which is
linked to changes in mood and anxiety. Studies have shown those changes in
serotonin in the cortex, hippocampus, striatum, hypothalamus, the olfactory lobe,
cerebellum and brain stem in rats exposed to MSG (Tawel, 2016).
In addition, Monosodium Glutamate affects the action of androgens, causing
a decrease that indirectly affects the shaft connecting the pituitary gland. This has a
negative effect on social behavior and sex-producing hormones. Lack of sex
hormones such as testosterone can cause behavioral changes because of its
importance in the regulation of aggression in mammals. Based on research, indicated
that exposure to MSG negatively affects the concentration of neurotransmitters
(Tawel, 2016).
Pancreas is part of the digestive system that makes and releases digestive
enzymes into the intestine, and also endocrine organs that make and release
hormones into the blood to control energy metabolism and storage throughout the
body (Longnecker, 2014). In a normal physiologic function of pancreas, the right
amount of insulin is produced to transport glucose into the cells. In pathological
pancreas, little or no insulin is produced, or the body cells do not respond to the
insulin that is produced leading to accumulation of glucose in the blood or elevation
of its levels (hyperglycaemia) resulting in diabetes mellitus. Despite these lines of
evidence, there is paucity of information on detailed markers of pancreatic function
with respect to MSG toxicity (Abdulsalam et al., 2018).
Glucagon is a protein hormone released by alpha cells from the islets of
Langerhans in response to low blood glucose levels and an increase in plasma amino
acids. The function of this hormone is primarily catabolic (decomposition) and is
generally opposed to insulin function. Glucagon works as an antagonist of insulin by
inhibiting the transfer of glucose into cells. Glucagon stimulates liver
gluconeogenesis and the breakdown of glycogen stores for use as an energy source
other than glucose. Glucagon stimulates the breakdown of fat and the release of free
fatty acids into the blood for use as an energy source (Elizabeth, 2001).
Insulin is released by beta cells of the islets of Langerhans. The main
stimulus that causes insulin release is an increase in blood glucose. Fasting blood
glucose levels under normal circumstances is 80-90 mg / 100 ml of blood. So insulin
secretion increases when fasting blood glucose levels exceed 100 mg / 100 ml of
blood, and return to basal levels within 2-3 hours. Insulin is the main hormone in the
digestive obsorbsive stage that appears immediately after eating. Insulin works by
binding to the insulin receptors found in most cells in the body. After binding to the
receptor, insulin works through a second intermediary to increase glucose transport
into cells. Once inside the cell, glucose can be immediately used as an energy
producer or stored in the cell preformance as glycogen. When glucose is brought into
the cell, the blood glucose level decreases (Ida, 2013).
MSG might be exerting some level of insignificant cytotoxicity effect on the
β-cells of islets of Langerhans of pancreas. In which oral administration of MSG was
observed to increased insulin levels MSG might have caused insulin resistance or
decrease insulin sensitivity of the target cells or tissues, thus, leading to decreased
glucose utilization, the increased level of which continued to trigger more release of
the insulin from the pancreatic β-islet cells. Since the hypothalamus is involved in
the regulation and action of insulin, a hormone that metabolizes glucose, damaged to
the brain cells following MSG-exposure may render them to become dormant to the
blood glucose level and or the feedback regulatory mechanism may not function to
regulate insulin secretion or action (Abdulsalam et al., 2018).
 IV. CONCLUSION AND SUGGESTION

4.1 Conclusion
Based on the result and discussion, it can be concluded that the administration
of monosodium glutamate affects the activity of the pancreatic glands which is
characterized by an increase in blood glucose levels in mice. The higher the
monosodium level is given, the higher the blood glucose level of the mice.

4.2 Suggestion
It will be better if students measured the weight and blood glucose level of
tested mice carefully.
 REFERENCES

Abdulsalam, H., Adamu, S., Sambo, S. J., Chiroma1, M. A., Gadzama, J. J.,
Mohzo1, D. L. & Atata, J. A., 2018. Monosodium glutamate-induced changes
on plasma markers of pancreatic function in adult male Wistar rats. Sokoto
Journal of Veterinary Sciences, 16(2), pp. 21-27.

Boonnate, P., Waraaswapati, S., Hipkaeo, W., Pethlert, A. S., Selmi, C.,
Prasongwattana, V. & Cha'on, U., 2015. Monosodium Glutamate Dietary
Consumption Decreases Pancreatic β-Cell Mass in Adult Wistar Rats. Plos
One, 10(6), pp. 1-14.

Erdmann N. B., Whitney N. P. & Zheng J., 2006. Potentiation of excitotoxicity in

HIV-1 associated dementia and the significance of glutaminase. Clinical
neuroscience research, 6(5), pp. 315-28.

He, K., Du, S., Xun, P., Sharma, S., Wang, H. & Zhai, F. 2011. Consumption of
monosodium glutamatein relation to incidence of overweight in Chinese adults:
China Health & Nutrition Survey (CHNS). American Journal of Clinical
Nutrition, 93, pp. 1328-1336.

Ismawati, I., 2003. Pengaruh Monosodium Glutamate terhadap Kadar Glukosa Darah
Tikus Putih (Rattus norvegicus) [skripsi]. Surabaya: Universitas Airlangga.

Michaelis E. K., 1998. Molecular biology of glutamate receptors in the central

nervous system and their role in excitotoxicity, oxidative stress and aging.
Prog. Neurobiol, 54(1), pp. 369-415.

Muharani, E., 2016. Pengaruh Pemberian MSG (Monosodium glutamate) pada Tikus
Sprague-Dawley Betina Usia Reproduktif Selama 2 minggu terhadap Kadar
Enzim Penanda Kerusakan Sel Hati (AST/ALT). skripsi. Jakarta: Universitas
Islam Negeri.

Suarez I., Bodega G. & Fernandez B., 2002. Glutamine synthase in brain: effect of
ammonia. Neurochem Int, 41(2-3), pp. 132-42.

Taweel, G. M. A., 2016. Effect of monosodium glutamate and aspartame on

behavioral and biochemical parameters of male albino mice. African Journal of
Biotechnology. 15(15), pp. 601-612.