Biochemistry 1 Assignment: Hormone and Enzyme Roles in Metabolism

This biochemistry assignment explores the roles of insulin, glucagon, and cytochrome c oxidase. The assignment begins by detailing the function of insulin and glucagon as pancreatic hormones, highlighting their opposing roles in regulating blood glucose levels. Insulin, secreted by beta cells, lowers blood glucose, while glucagon raises it. Cortisol's impact on insulin resistance and gluconeogenesis is also discussed. The second part of the assignment focuses on cytochrome c oxidase, the final enzyme in the respiratory electron transport chain, and its crucial role in ATP synthesis. The assignment explains how cytochrome c oxidase transfers electrons to oxygen and the implications of its deficiency, including various types of COX deficiency with varying symptoms and severity, affecting multiple tissues and potentially leading to severe metabolic disorders. The assignment is supported by cited references that provide more in-depth information on the subject matter.

Running Head: BIOCHEMISTRY
BIOCHEMISTRY
Name of the Student
Name of the University
Author Note

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1. Insulin and glucagon are the pancreatic hormones that are secreted by islet cells.
Both are secreted in reaction to concentrations of blood sugar. However, they work in the
opposite manner. The beta cells of the pancreas generally secrete insulin. Insulin secretion
stimulus is increased blood glucose (Güemes, Rahman & Hussain, 2016). Insulin affects
number of cells, including muscles, fat cells and red blood cells. The cells absorb glucose
from blood in reaction to insulin, having the net impact of reducing the concentrations of high
blood glucose to the standard range.
However, huge amount of glucagon is secreted when the blood glucose gets low. The
impact of glucagon is to release the insulin into the bloodstream that has been stored by the
liver in its cells, with the net impact of raising blood glucose. The glucagon also induces the
liver to create glucose from the construction blocks of the other nutrients contained in the
body (Güemes, Rahman & Hussain, 2016).
Cortisol is secreted from the adrenal gland as a steroid hormone. It makes fat and
muscle cells resistant to insulin action and increases liver glucose output. Cortisol mitigates
the intervention of insulin under ordinary conditions (Moon et al., 2014). Under stress or
when a synthetic cortisol is provided as a drug, the concentrations of cortisol increase and
individual becomes insulin resistant. At an early stage of fasting, cortisol stimulates
gluconeogenesis and activates anti-inflammatory and anti-stress pathways. In liver and
muscle glycogenolysis, cortisol also plays a significant but indirect role, breaking down
glycogen to glucose-1-phosphate and glucose. This is achieved by influencing glucagon
passively (Moon et al., 2014).
2. The purpose of cytochrome c oxidase is that it is the last enzyme in the membrane-
based cell chain of the respiratory electron transport chain (Yoshikawa & Shimada, 2015). It
gets an electron from each one of four cytochrome c molecules as well as transfers them to

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the single molecule of dioxygen, turning molecular oxygen into two water molecules
(Blomberg & Siegbahn, 2014). Cytochrome c is mainly regarded as a main participant in the
life-supporting function of ATP synthesis for its function in the mitochondria. However,
cytochrome c is released into the cytosol when a cell gets an apoptotic stimulus and causes
programmed cell death through apoptosis (Schüll et al., 2015). The deficiency of Cytochrome
C Oxidase causes a very rare hereditary metabolic disorder characterized by cytochrome C
oxidase (COX) or Complex IV enzyme deficiency, an important enzyme active in sub
cellular structures that helps control energy production (Blomberg & Siegbahn, 2014). There
are four kinds of COX deficiency distinguished by symptoms and onset age: benign type of
infant mitochondrial type, type of French-Canadian type, type of infant mitochondrial
myopathy, and of Leigh syndrome. COX deficiency may be restricted to skeletal muscle
tissues or may affect several tissues such as the core, kidney, liver, brain and/or connective
tissue that is also known as fibroblasts; in other instances, COX deficiency may be
widespread that is it can be systemic. The range and severity of signs and symptoms may
differ commonly among people impacted and may rely on the type of the current situation
(Schüll et al., 2015).

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References
Blomberg, M. R., & Siegbahn, P. E. (2014). Proton pumping in cytochrome c oxidase:
Energetic requirements and the role of two proton channels. Biochimica et Biophysica
Acta (BBA)-Bioenergetics, 1837(7), 1165-1177.
Güemes, M., Rahman, S. A., & Hussain, K. (2016). What is a normal blood
glucose?. Archives of disease in childhood, 101(6), 569-574.
Moon, H. J., Choi, K. H., Lee, S. I., Lee, O. J., Shin, J. W., & Kim, T. W. (2014). Changes in
blood glucose and cortisol levels after epidural or shoulder intra-articular
glucocorticoid injections in diabetic or nondiabetic patients. American journal of
physical medicine & rehabilitation, 93(5), 372-378.
Schüll, S., Günther, S. D., Brodesser, S., Seeger, J. M., Tosetti, B., Wiegmann, K., ... &
Brinkmann, K. (2015). Cytochrome c oxidase deficiency accelerates mitochondrial
apoptosis by activating ceramide synthase 6. Cell death & disease, 6(3), e1691.
Yoshikawa, S., & Shimada, A. (2015). Reaction mechanism of cytochrome c
oxidase. Chemical reviews, 115(4), 1936-1989.