BIOCHEMISTRY 5: Mechanisms of Action of Key Metabolic Hormones

This biochemistry assignment provides an overview of the mechanisms of action for several key hormones. It details the processes by which insulin, growth hormone, adrenaline, cortisol, thyroxin, and glucagon exert their effects on the body. The assignment explains how insulin regulates carbohydrate and fat metabolism by binding to insulin receptors and stimulating various metabolic processes. It discusses how growth hormone influences glucose production and uptake, and how adrenaline increases plasma glucose levels. The assignment further explores how cortisol increases glucose levels through protein and lipid breakdown, and how thyroxin facilitates glucose production and induces hepatic insulin resistance. Finally, it explains how glucagon stimulates the liver to release glucose into the bloodstream. References are provided for each hormone's mechanism of action.

Running head: BIOCHEMISTRY 1
BIOCHEMISTRY
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BIOCHEMISTRY 2
Mechanism of action of Insulin
Insulin hormone is a type of peptide hormones which is synthesised by the beta cells of the
pancreas. Insulin is used in the regulation of the carbohydrate and fats metabolism in the
body, and also it facilitates the glucose absorption from the bloodstreams to the skeletal
muscles.
Insulin has the constructive-metabolic role of stimulating fatty acids, glycogen, and protein
synthesis. Insulin controls the process of gluconeogenesis in the liver. Insulin clings to the
Insulin receptor (IR) which is a heterotetrameric protein comprising of two extracellular
alpha units and two intracellular beta units. The adhering of the insulin hormone to the alpha
subunits of the insulin receptor encourages the tyrosine kinase activity internal to the beta
subunit of the receptor. The conjugated receptor has the power to auto phosphorylate and
phosphorylate and many intracellular substances such as the insulin receptor substrates
protein.
Mechanism of action of Growth hormone.
Growth hormones antagonizes the insulin’s action on the peripheral tissues such as the liver,
skeletal muscles and the adipose tissue therefore increasing the production of the glucose
from the liver and skeletal tissues and also aids in the decrease of the glucose uptake from
the adipose tissues. Growth hormone-induced lipolysis in the visceral adipose tissue and
subsequent increased circulating FFA also interferes with insulin signalling pathways which
results to the increase of the plasma glucose levels.
Mechanism of action of Adrenaline.
The increase of the plasma glucose level is due to the increased hepatic glucose output and
also the reduction of the glucose disposal rate. This results from the Adrenaline-induced

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suppression of the endogenous insulin secretion. The increased rise of the plasma glucose
level ids due to the alternation in response of the liver to epinephrine Adrenaline.
The action of epinephrine is enhanced by simultaneous elevations of glucagon and cortisol.
The former increases the magnitude, but not the duration, of the rise in hepatic glucose output
induced by epinephrine (Knights, 2013).
Mechanism of action of Cortisol
Cortisol increases the plasma glucose levels through a metabolic pathway which results in the
production of glucose from given non-carbohydrates carbon substances. The increase of the
plasmid glucose levels results from the breakdown of the proteins, from the breakdown of
lipids such as the triglycerides but not the fatty acids. The increase also results from the other
metabolisms which includes the pyruvate and lactate. The increase of the blood glucose by
Cortisol Is aimed to assist with the metabolism of the protein, carbohydrates and fats and also
to supress the immune system.
Cortisol is a naturally occurring glucocorticoid, and in most cases, it comes from cholesterol.
The secretion of Cortisol is tightly regulated by the CNS which are very sensitive. Cortisol
also activates anti-inflammatory and anti-stress (Greenstein, 2015).
Mechanism of action of Thyroxin.
Hormone thyroxin facilitates the production of endogenous glucose and at the same time
induces the hepatic insulin resistance. The thyroxin hormones increases the production of
glucose through the sympathetic projection to the liver, independently of the circulating
glucoregulatory hormones. This shows a unique central pathway for the control of the hepatic

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glucose metabolism by the thyroxin hormone, which results to the increase of the plasmid
glucose levels.
The Thyroid hormone is produced in the thyroid glands which contains follicles through
which thyroid hormone is synthesise by iodisation of the tyrosine residues in the
glycoprotein. The Thyroid hormone usually regulates the uptake of iodide which is mediated
by the iodide/sodium symporter that is followed by some steps which are necessary for
metabolic regulation in mammals; it is also required for amphibian metamorphosis. (Howell,
2012).
Mechanism of action of Glucagon
The impact of glucagon is to make the liver to discharge the glucose which had initially
stored in its cells into the bloodstreams. This results into the net increase of the blood
glucose. Glucagon is also known to induce the liver and other cells to produce glucose out of
the building blocks which are obtained from other nutrients found in the body such as the
proteins.
Glucagon is a protein hormone synthesised in the Alpha-cells of the Langerhans of the
pancreases. The main function of glucagon is to counteract the actions of insulin. It also
stimulates the breaking down of the glycogen into glucose. (Assan, 2016).

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References
Assan, R. (2016). Glucagon II. Berlin: Springer Science & Business Media.
Greenstein, A. (2015). Concise Clinical Pharmacology. Texas: Pharmaceutical Press.
Howell, W. H. (2012). Physiology and biophysics. London: Saunders.
Knights, K. M. (2013). Pharmacology for Health Professionals. London: Elsevier Australia.
Pessin, J. E. (2014). Mechanisms of Insulin Action. Texas: Springer Science & Business
Media.
Ridderstråle, M. (2017). Molecular mechanism of growth hormone action: involvement of
Janus kinase 2, insulin receptor substrate-1 and -2 and phosphatidylinositol 3-kinase
in the acute insulin-like effects of growth hormone in primary rat adipocytes.
Chicago: Lund University.