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Anorexia Nervosa Analysis 2022

Design a draft conference poster on the topic of metabolic adaptations in anorexia nervosa.

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Added on  2022-09-12

Anorexia Nervosa Analysis 2022

Design a draft conference poster on the topic of metabolic adaptations in anorexia nervosa.

   Added on 2022-09-12

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Running head: ANOREXIA NERVOSA 1
Anorexia Nervosa
Name
Institutional Affiliation
Anorexia Nervosa Analysis 2022_1
ANOREXIA NERVOSA 2
Introduction
Anorexia Nervosa is an eating disorder that is characterized by reduced body weight due
to inadequate energy intake and a great fear of weight gain. There is also an inaccurate
perception of owns weight. Individuals may control weight gain through excessive exercise,
restricted food intake or expulsion of food by vomiting or use of laxatives. Symptoms of the
disorder are indicative of starvation and include fatigue, dizziness, sleeping problems, low blood
pressure, electrolyte imbalance and osteoporosis. Irregular or absence of menstruation in girls
and women also occurs. (Fazeli and Klibanski, 2018. The disorder might pose a threat to life due
to complications that may arise. These include heart and kidney diseases. It is diagnosed if a
reduction of 15% of ideal body weight occurs.
Hormonal and metabolic adaptations arise due to the reduced nutrient intake. There is a
reduction in protein catabolism and the adipose tissue. For efficient energy utilization the basal
metabolic rate, growth and reproductive processes decline. . (Müller et al, 2015) Other
adaptations include development of growth hormone resistance, functional hypothalamic
amenorrhea and non-thyroidal illness syndrome. These provide short term reprieve. The levels of
some hormones change. There are low levels of estrogen, testosterone, leptin, T3
(Triiodothyronine), insulin and leptin. Cortisol, Norepinephrine, epinephrine, glucagon, ghrelin
and β-endorphin increase in concentration. Growth Hormone levels are elevated and maintain
euglycemia. This is partly through fat mobilization. . (Méquinion et al., 2013).
Anorexia Nervosa Analysis 2022_2
ANOREXIA NERVOSA 3
Figure 1.1 Hormonal changes as a result of Anorexia Nervosa
Glucose is continually maintained at a constant level within the body. Short time periods
without nutrient intake result in mobilization of glycogen. Glycogen stores in the body are
however, exhausted in hours and thus by the end of the day are over. Glycogen is stored within
the liver and muscles. The muscles don’t have glucose-6- phosphatase and thus utilize the
glycogen within its own cells without exporting to other organs. The liver thus supplies other
body parts with glucose during these periods. At such instances, blood glucose levels are low.
Insulin levels consequently decline with a surge in glucagon. Glucagon is produced from the
alpha cells in the pancreas. Its main target organ is the liver. Adipose tissue is also under
glucagon control. Epinephrine inhibits insulin secretion while promoting glucagon production.
Glycogen phosphorylase is phosphorylated and thus converted to the active phosphorylase a
form. This occurs through a cyclic Adenosine Monophosphate cascade(cAMP). Glycogen
synthase is inhibited. Diminished binding of glucose to phosphorylase a reduces its susceptibility
to phosphatase. The phosphatase and phosphorylase a remain bound together with synthase
remaining phosphorylated and thus inactive. Gluconeogenesis however, requires an input of
Anorexia Nervosa Analysis 2022_3
ANOREXIA NERVOSA 4
energy in form of ATP.Thus oxidative phosphorylation has to be functional. The transfer of
protons via the electron transport chain also occurs. Depletion of glycogen reserves in the liver
leads to gluconeogesis from alanine and lactate. Liver gluconeogenesis is stimulated with
glycolysis being reduced due to low amounts of Fructose 2-6-Bis-phosphate (F-2, 6-BP). The
Phosphofructo-kinase-1 (PFK-1) activity which is the key control enzyme of glycolysis is thus
inhibited. There is also an accumulation of citrate. This accumulation along with that of Acetyl –
CoA leads to inhibition of glycolysis. Gluconeogenesis is stimulated by activation of pyruvate
carboxylase and fructose-1, 6 bisphosphatase. Cortisol also stimulates gluconeogenesis by
stimulating activity of PEP Carboxylase.
The glucose from the liver is released into the blood. The decreased insulin levels
however limits entry into muscle and adipose tissue. The liver utizes fatty acids as an energy
Anorexia Nervosa Analysis 2022_4

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