Human Biochemistry: Metabolic Responses to Anorexia Nervosa - Analysis

This assignment delves into the metabolic adaptations that occur in individuals suffering from Anorexia Nervosa, an eating disorder characterized by an intense fear of weight gain and severe food restriction. The paper explores how the body responds to starvation by altering the metabolism of fats, proteins, and carbohydrates to meet its energy demands. It highlights key processes such as the body's reliance on fatty acids and ketone bodies, the conservation of glucose for the brain and red blood cells, and the role of gluconeogenesis. The analysis emphasizes the metabolic adaptations, including ketosis, reduced protein catabolism, and the mobilization of glycerol from adipose tissues. The paper concludes by discussing the impact of these metabolic shifts on energy production and the body's ability to maintain essential functions. It references key studies to support the discussion.

Running head: HUMAN BIOCHEMISTRY 1
Human Biochemistry
Name
Institution

HUMAN BIOCHEMISTRY 2
Anorexia Nervosa
Anorexia nervosa can be described as an extremely dangerous eating disorder that makes
individuals have an intense fear of gaining weight thus forcing them to starve or engage in
excessive physical activities (Zipfel et al., 2015). As a result, they may become dangerously thin
because they do not eat enough food to build their bodies appropriately. Due to anorexia nervosa,
the body may undergo some metabolic adaptations to satisfy its energy requirements by focusing
on the metabolism of fats, proteins, and carbohydrates. The body metabolizes proteins,
carbohydrates, and fats to produce energy for normal body functions. During starvation, the body
cannot anticipate the next meal. Therefore, the body undergoes metabolic adaptations to spare
proteins and conserve glucose at the same time. Under normal circumstances, the body breaks
down protein to maintain the level of glucose in the blood. Amino acids, therefore, become the
main source of glucose. The body keeps relying on fatty acids and ketone bodies as sources of
energy (Lee, Choi, Scafidi & Wolfgang, 2016). This overreliance allows the body to maintain the
level of blood glucose at around 65 mg/dL which is slightly lower than the normal range. Muscle
proteins are therefore conserved for an extended period of anorexia nervosa. This is accompanied
by a reduced amount of ammonia being released in the urine.
Free fatty acids are continually mobilized from the adipose tissues in the absence of insulin and
oxidation of fatty acids in the liver continues because the only site that regulates the oxidation is
adipose tissues. Acetyl-CoA accumulates and they are shunted through ketogenesis to produce
water-soluble forms of fat (Rudd, 2012). These water-soluble forms of fats are ketone bodies
which are mobilized to acetyl-CoA and use to produce energy. It is important to note that
anorexia nervosa leads to ketosis that is caused by an increase in the hepatic manufacture of
ketone bodies.

HUMAN BIOCHEMISTRY 3
Due to a reduction of protein catabolism as a result of anorexia nervosa, gluconeogenesis is
slowed down and the production of amino acids is also reduced. Adipose tissues, however,
release glycerol through the process of lipolysis to support the reduced rate of gluconeogenesis
(Andrade Jr, 2017). Metabolism takes place in the adipose tissues where hormone-sensitive
lipase is activated to regulate the oxidation of fatty acids (Rudd, 2012). The mobilized fatty acids
are then used to produce energy that is used by most tissues like the heart and muscles. The
energy produced by free fatty acids is, however, not used by the red blood cells.
It is also important to note that the degradation of muscle protein is decreased in anorexia
nervosa. This reduction in the degradation of muscle proteins is due to the muscles relying on
free fatty acids for energy. Glucose and ketone bodies are then saved for use by the brain (Rudd,
2012). Because the brain continuously uses ketone bodies, glucose is saved for use by red blood
cells since red blood cells cannot use energy generated by free fatty acids and sorely relies on
glucose as a source of energy. Since the demand for glucose by the brain is low, gluconeogenesis
reduces thus conserving muscle protein.

HUMAN BIOCHEMISTRY 4
References
Andrade Jr, M. C. (2017). Metabolism during fasting and starvation: understanding the basics to
glimpse new boundaries. J Nutr Diet, 1, e02.
Lee, J., Choi, J., Scafidi, S., & Wolfgang, M. J. (2016). Hepatic fatty acid oxidation restrains
systemic catabolism during starvation. Cell reports, 16(1), 201-212.
Rudd, D. (2012). Elsevier's integrated review biochemistry 2nd edition [Book
Review]. Australian Journal of Medical Science, 33(4), 182.
Zipfel, S., Giel, K. E., Bulik, C. M., Hay, P., & Schmidt, U. (2015). Anorexia nervosa: aetiology,
assessment, and treatment. The lancet psychiatry, 2(12), 1099-1111.