Homeostasis: Blood Glucose Regulation and Consequences of Imbalance

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This essay provides a comprehensive overview of homeostasis, focusing on blood glucose regulation in the human body. It explains the importance of maintaining a steady state for optimal bodily function, detailing the roles of key hormones like insulin and glucagon in regulating glucose levels. The essay explores the mechanisms of glucose uptake and storage in various tissues, including the liver, muscles, and fat cells. It also discusses the body's response to fluctuations in blood glucose levels, including the impact of sleep and the counter-regulatory hormones such as epinephrine, cortisol, and growth hormone. Furthermore, the essay highlights the implications of disrupted glucose homeostasis, such as in type 2 diabetes, and explores the health consequences and management strategies including lifestyle modifications and medications. The essay emphasizes the critical role of glucose homeostasis for overall health and survival.
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Running head: HOMEOSTASIS
HOMEOSTASIS
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1HOMEOSTASIS
Introduction:
Homeostasis is considered as the state of the steady, physical condition maintained by the
body. Yang and Zubcevic (2017) as discussed by this dynamic state of equilibrium of the body
is considered as the optimal condition for the body to gain the normal functioning. A range of
existing literature suggested that in order to maintain homeostasis and normal functioning, a
human body using various parameters such as body temperature, blood glucose, the
concentrations of sodium, potassium and calcium ions and fluid balance. Each of these
parameters is directly regulated by a various homeostatic factor which collaborates maintain
healthy body functioning (Orr, Fetter and Davis 2017). While a range of homeostatic factors is
present to maintain healthy functioning, Glucose homeostasis is of essential importance to
human health because of the fact that glucose is a source of energy, especially for the human
brain (Roh and Kim 2016). Therefore, maintaining acceptable levels of glucose in the body is
essential for human survival since the inappropriate level of blood glucose can give rise to
clinical manifestations of diabetes. This essay aims to provide an explanation of the biological
concept of homeostasis by using blood glucose as an example. This essay will illustrate the
homeostasis of blood glucose and the consequence of inadequate management in the following
paragraphs.
Discussion:
Glucose homeostasis has emerged as the foundation of energy supply as well as
maintenance in the human body during the transition of foetal to a newborn. However, despite
various research conducted on the homeostasis of the human body, the understanding of the vital
role of glucose and threshold level for maintaining homeostasis remain incomplete. Imamura et
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2HOMEOSTASIS
al. (2016), highlighted that blood glucose levels are controlled within narrow limits where the
primary sensor of the glucose is beta cells. The detailed mechanism of the homeostasis through
blood glucose will be discussed in the following paragraphs.
The glucose homeostasis is maintained by the fine regulation of uptake of peripheral
glucose by hormones followed hepatic glucose formation as well as glucose consumption during
the ingestion of carbohydrates. Normal glucose homeostasis is primarily maintained by two
major hormones such as glucagon and insulin. In the blood, Glucose levels are typically
estimated in terms of milligrams per deciliter (mg/dl) where a normal range of glucose in the
blood must be within 70 to 110 mg/dl (Pillinger et al. 2017). In general, if glucose levels
fluctuate from this normal range, quantities of insulin along with glucagon produced by the
pancreatic cells will be tuned in order to bring glucose levels into threshold level. The insulin is
formed by the beta cells of the pancreas which facilitate the transportation of glucose into the
body. Likewise, glucagon is also produced by the pancreatic cells which increases blood glucose
levels by encouraging the breakdown of glycogen into glucose. Due to the consumption of food
containing carbohydrates, the blood glucose level generally exceeds the normal range of 70 to
110 mg/dl. The beta cells of pancreases respond to an increased level of blood glucose by
releasing insulin into the body and simultaneously inhibiting the secretion of glucagon by
decreasing the normal functioning of the neighbouring alpha cells (Ding et al. 2020).
Consequently, the high level of insulin, as well as low glucagon levels, influence effector tissues
such as liver cells, muscle cells, and fat cells. While glycogen generally stored in the liver, in
blood triglycerides are present as very-low-density lipoprotein or VLDL that enter into the
adipose tissues and it is stored as fat (Montgomery et al. 2016). Fat metabolism is highly
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3HOMEOSTASIS
dependent on glucose homeostasis. special glucose transporters such as GLUT4 is one such
transport that facilitates the uptake of glucose by fat cells where it is converted into the
triglycerides and stored in the fat cells with VLDL-derived triglycerides which were produced in
the liver (Holland et al. 2017). The number of GLUT4 gradually increased in the human body
when insulin acts on the fat cells and facilitate the uptake of glucose. Reno et al. (2017),
highlighted that a similar mechanism is also exhibited by muscles while up taking blood glucose
where muscle cells use insulin-sensitive GLUT4 glucose channel to facilitate glucose uptake and
convert the present glucose into muscle glycogen. While muscle glycogen is appeared to
function as an immediate restored source of available glucose (glucose 6-phosphate) for optimal
muscle functioning, the liver glycogen breaks down to glucose and transport it to other parts of
the body as an energy source for other organs (Araujo Nunes and Rafacho 2017).
A similar mechanism is observed in the body for maintaining homeostasis when optimal
glucose level falls under the normal range. The reduction of blood glucose is common amongst
the individuals who are suffering from hypoglycaemia. Since insulin is the only hormone in
mammals which lowers the blood glucose, a decline in plasma glucose reduces the secretion of
this hormone (Santiago, Clegg and Routh 2016). When glucose level dropped under the beta
cells respond to such a crisis by inhibiting the secretion of insulin and simultaneously increasing
glucagon secretion from the neighbouring alpha cells. Consequently, the reduction of insulin
level inhibits the blood glucose uptake by muscle cells, liver cells, and fat cells. In the liver, liver
cells are strongly stimulated to produce glucose by breaking glycogen through the process of
glycogenolysis. Likewise, apart from glycogenolysis, the body involve into gluconeogenesis for
producing glucose from other non-carbohydrate resources such as lactate and amino acid which
further transported to blood for balancing the level of blood glucose (Deem et al. 2017).
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4HOMEOSTASIS
Therefore, through these processes, the body is able to maintain normal homeostasis and normal
functioning. As discussed by Burke, van Loon and Hawley (2017) usually glycogen restored in
muscles remains in the muscles for immediate use as energy. The stored glycogen is only broken
down when individuals involve in physical activity and the stored glycogen converted to
glucose-6-phosphate followed by pyruvate which further entered into the Kreb’s cycle or citric
acid cycle. The pyruvate can be converted to the lactate to meet the demand of the body. This
lactate along with the bi-products of the TCA cycle that are reimbursed to the blood. The hepatic
cells absorb only the lactate, and by the procedure of energy-consuming as well as
gluconeogenesis converts it back to glucose.
Apart from the glucagon and insulin, epinephrine, cortisol and growth hormone are also
taking part in glucose metabolism. Nwokolo et al. (2019) suggested that epinephrine takes part
in the homeostasis is secreted from the chromaffin cells of the adrenal medulla when a low
plasma-glucose concentration detected in the body. The metabolic action of the epinephrine is
facilitated through β2-adrenergic receptors. The receptors increase the availability of
gluconeogenic precursors and plasma FFAs to increase hepatic and renal glycogenolysis.
Furthermore, glucose uptake also reduced in the skeleton muscle through epinephrine. The effect
of epinephrine on the production of glucose is temporary and similar to glucagon (Deem et al.
2017). However, it is considered as the potent hypoglycaemic factor because of the constant
effect on the uptake of glucose.
Similarly, cortisol and growth hormone are glucose counter-regulatory hormones which
increase the enzymes used in gluconeogenesis and reduces the transportation of glucose. Cortisol
plays a crucial role in the impairment of insulin (Deem et al. 2017). While glucagon and
epinephrine work immediately after a discrepancy in the level of the glucose, the effect of
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5HOMEOSTASIS
growth hormone after several hours of consumption of carbohydrate. They both work in a
synergistic manner in order to regulate plasma glucose concentration. Apart from these
hormones, gastrointestinal inhibitory hormone and GLP-1 incretine take part in the homeostasis
only after consumption of carbohydrates as a meal (Shi et al. 2017). After carbohydrate
consumption when blood glucose level increased, both facilitate an increase in the secretion of
insulin, indicating a higher increase in plasma insulin in response to oral consumption of glucose
compared to another form of glucose consumption. According to plasma glucose consumption,
GLP-1 influences the secretion of insulin, suppresses the secretion of postprandial glucagon,
influences body weight through gastric emptying and reducing the intake of food frequently.
Qaid and Abdelrahman (2016) suggested that in healthy subjects, utilization of glucose differs
throughout the span of 24 hours. Many researchers suggested that in the case of young
individuals, fasting during daylight wakefulness is highly associated with a sudden fall in
glucose levels in the blood. On the other hand, during night-time sleep, glucose levels of the
blood continued to be stable, it is only declining slightly despite prolonged fasting (Deem et al.
2017). In the basal state, during a prolonged fast for overnight, hepatic glucose production, as
well as renal glucose production, are directly accountable for providing the basal glucose to
peripheral tissue of the body. Around 75–80% of utilization of glucose during the prolonged
fasting takes place in insulin-independent cells such as the brain cells, gut cell as well as red
blood cells (Shi et al. 2017). However, insulin-dependent cells like muscle cells as well as
adipose cells have minimal requirements for glucose as energy sources in the fasting state. Sleep
is one of the prime factors for maintaining glucose homeostasis of the body. Many researchers
suggested that in case of sustained starvation state during night-time wakefulness, glucose levels
reduced gradually but the glucose level remain within the threshold level during daytime sleep.
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6HOMEOSTASIS
Therefore, mechanisms observed during the sleep cycle of the human are highly regulated for
preventing inappropriate hypoglycaemia amongst individuals and adequately maintain the
glucose homeostasis. During experimental investigations, the majority of the investigations
involves continuous intravenous glucose infusion suggested that a drastic decrease in the glucose
tolerance suggested during the first half of the night-time sleep cycle for reaching a minimum
level which altered during the middle half of the night-time sleep cycle followed by an increase
in glucose structure (Nwokolo et al. 2019). Therefore, sleep associated with a decrease in
tolerance of glucose observed due to low utilization of peripheral as well as cerebral glucose
utilization where cerebral utilization of the glucose is approximately 20% of the total glucose
utilization by the body.
Type II diabetes is one such disease that disrupts normal glucose homeostasis. In
Australia, approximately 1 million individuals are experiencing type two diabetes and the
prevalence of type two diabetes is slightly higher amongst men compared to women. According
to a recent survey of Australia, diabetes type two is considered as one of the major reasons for
high morality since diabetes type two contributed to approximately 11% of deaths in 2017
(Harding et al. 2016). Due to lack of physical activity, obesity and excessive consumption of fat
associated food individuals experience type two diabetes which is described by high blood sugar,
lack of adequate insulin as well as insulin resistance. In the case of insulin resistance, the liver
failed to release the glucose appropriately into the blood (Plummer et al. 2016). Consequently,
the body failed to produce adequate hormone for breaking glucose and pancreases is required to
work harder for producing adequate insulin. Over the years, constant pressure on pancreatic cells
leads to pancreatic cell damage followed by a lack of production of pancreatic cells. Therefore,
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7HOMEOSTASIS
constant increase in blood glucose directly disrupts the glucose homeostasis of the body.
Uncontrolled type 2 diabetes can lead to several symptoms as well as complications. Other
mechanisms include an increase in the metabolism of lipids within fat cells, high level of
glucagon blood, increased retention of water and salt by the kidney, lack of incretin and lack of
appropriate regulation of the glucose metabolism by CNS (Plummer et al. 2016). Therefore, in
order to manage the health condition and maintain proper glucose homeostasis, the most
effective interventions would be modifications of lifestyle such as consumption of low fat and
carbohydrate food, aerobic exercise and medications.
Conclusion:
On a concluding note, it can be said homeostasis is a dynamic state of equilibrium that
facilitates the normal functioning of the body. Normal human body uses various parameters such
as body temperature, blood glucose, and concentrations of sodium, potassium and calcium ions
and fluid balance. Glucose homeostasis has emerged as the foundation of energy supply and
critical to the maintenance of normal body functioning. Insulin and glucagon both contributed to
the normal homeostasis. The beta cells of pancreases respond to an increased level of blood
glucose by releasing insulin into the body and simultaneously inhibiting the secretion of
glucagon by decreasing the normal functioning of the neighbouring alpha cells. Consequently,
the degradation of the glucose observed in the body. The reverse mechanism observed through
glucagon when glucose level reduced under the threshold level. Cortisol, epinephrine and growth
hormones also control the homeostasis through different mechanisms. Type two diabetes is one
such disease that disrupts glucose homeostasis. The maintenance of lifestyle can manage the
situation.
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8HOMEOSTASIS
References:
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glucose homeostasis, insulin resistance and diabetes. Current drug targets, 18(6), pp.619-628.
Burke, L.M., van Loon, L.J. and Hawley, J.A., 2017. Postexercise muscle glycogen resynthesis
in humans. Journal of Applied Physiology, 122(5), pp.1055-1067.
Deem, J.D., Muta, K., Scarlett, J.M., Morton, G.J. and Schwartz, M.W., 2017. How should we
think about the role of the brain in glucose homeostasis and diabetes?. Diabetes, 66(7), pp.1758-
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Ding, X., Iyer, R., Novotny, C., Metzger, D., Zhou, H.H., Smith, G.I., Yoshino, M., Yoshino, J.,
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Harding, J.L., Shaw, J.E., Peeters, A., Davidson, S. and Magliano, D.J., 2016. Age-specific
trends from 2000–2011 in all-cause and cause-specific mortality in type 1 and type 2 diabetes: a
cohort study of more than one million people. Diabetes Care, 39(6), pp.1018-1026.
Holland, W.L., Xia, J.Y., Johnson, J.A., Sun, K., Pearson, M.J., Sharma, A.X., Quittner-Strom,
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Imamura, F., Micha, R., Wu, J.H., de Oliveira Otto, M.C., Otite, F.O., Abioye, A.I. and
Mozaffarian, D., 2016. Effects of saturated fat, polyunsaturated fat, monounsaturated fat, and
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Jaiswal, N., Gavin, M.G., Quinn III, W.J., Luongo, T.S., Gelfer, R.G., Baur, J.A. and Titchenell,
P.M., 2019. The role of skeletal muscle Akt in the regulation of muscle mass and glucose
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Reno, C.M., Puente, E.C., Sheng, Z., Daphna-Iken, D., Bree, A.J., Routh, V.H., Kahn, B.B. and
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