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Starvation induced
metabolic
alterations
BY NAMRATA CHHABRA OCTOBER 24, 2015

A 23 year- old female was brought for

consultation by her mother who was

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Acid base balance
Alcohol metabolism
Biochemistry of cancer
Biochemistry of Digestion

fatigue, dizziness and loss of weight.

The patient was 6 feet 2 inches tall and
weighed 100 pounds. Further
questioning revealed that the young
woman had been virtually fasting for 4
months hoping to obtain a skinny
figure as a prelude to a career in
modeling.

Biochemistry of HIV Infection

Physical examination revealed

Biological Oxidation and ETC

dehydration and a fruity odor in her

Chemistry of Biomolecules
Diabetes mellitus
Endocrinology
Enzymology
Heme Metabolism
Hemoglobinopathies
Metabolism of Amino acids

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troubled by her daughters continuous

breath.
Laboratory results revealed Blood
glucose 50 mg%.
Which substance would most likely be
detected in abnormally high
concentration upon patients urine test?
A) Protein

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Starvation induced metabolic alterations Biochemistry for Medics ...

Metabolism of Carbohydrates

B) Hemoglobin

Metabolism of Lipids

C) Acetoacetate

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D) Lactate
E) Pyruvate
The correct answer is- Acetoacetate.
The patient shows many signs
ofAnorexia Nervosa (AN), which is an
eating disorder.
The etiology of AN is unknown but
appears to involve a combination of
psychological, biologic, and cultural risk
factors. The condition is characterized by
aversion to food that leads to a state of
fasting and emaciation. Patients often
have a distorted image of their own body
weight or shape and are unconcerned by
the serious health consequences of their
low weight. As weight loss progresses,
the fear of gaining weight grows; dieting
becomes stricter; and psychological,
behavioral, and medical aberrations
increase.
Metabolic alterations
Blood glucose homeostasis
Liver glycogen is exhausted in the first
day of fasting. After several months of
near starvation, the blood glucose in
these patients is maintained by
gluconeogenesis, primarily from amino
acids mobilized from tissue proteins
(figure-1). The impaired conversion of
amino acids in to glucose is responsible
for producing hypoglycemia in these
patients.

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Starvation induced metabolic alterations Biochemistry for Medics ...

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Figure-1- All the intermediates of TCA cycle,

beyond - Ketoglutarate are glucogenic,
since they ultimately produce oxaloacetate
which is channeled towards pathway of
gluconeogenesis. Acetyl co A is not
glucogenic, as firstly the conversion of
pyruvate to Acetyl Co A is irreversible and
secondly, in TCA cycle, it loses both of its
carbons in the form of CO2, hence it has
nothing to contribute to Glucose production.
Implications of hypoglycemia
Gluconeogenesis depletes the supply of
oxaloacetate, which is essential for the
entry of acetyl CoA into the citric acid
cycle (figure-1). Consequently, the liver
produces large quantities of ketone
bodies, which are released into the blood
(figure-2). After several weeks of
starvation, ketone bodies become the
major fuel of the brain. A persons
survival time is mainly determined by the
size of the triacylglycerol depot.

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Starvation induced metabolic alterations Biochemistry for Medics ...

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Figure-2- During starvation, hypoglycemia,

causes release of glucagon that promotes
lipolysis in the adipose tissue. The fatty
acids released are transported to liver. They
are oxidized to provide energy to the liver
cells. The end product, Acetyl Co A cannot
be completely utilized in TCA cycle, as it is in
a state of suppression due to mobilization
of oxaloacetate towards the pathway of
gluconeogenesis. Acetyl Co A is diverted to
the pathway of ketogenesis. The ketone
bodies are transported through blood to the
peripheral cells where they are used as fuel
molecules to provide energy. The ketone
bodies are produced in the liver but they are
utilized in the peripheral cells. The enzyme
(thiophorase) for their utilization is present
in all the peripheral cells except liver,
whereas the enzymes for ketogenesis (HMG
Co A synthase and HMG Co A lyase) are
present only in the liver mitochondria).
As a result of ketosis, the blood pH
becomes acidic, since the ketone bodies
are themselves acidic (ionic at pH 7.4),
and are excreted in the form of neutral
salts, hence they deplete the alkali
reserves of the body, causing acidosis.
Excess ketone bodies are excreted in

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Starvation induced metabolic alterations Biochemistry for Medics ...

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urine causing ketonuria. Acetoacetate, is

the primary ketone body, the other two
ketone bodies, beta hydroxy butyrate
and acetone are derived from
acetoacetate. Beta hydroxy butyrate is
the major ketone body found in urine,
acetone is excreted through breath.
Acetone like smell is observed in patients
of ketoacidosis, and it is a diagnostic sign
of diabetic ketoacidosis.
In the given options, acetoacetate is the
correct option considering the clinical
state of hypoglycemia induced
ketoacidosis.
As regards other options
A) Protein
B) Hemoglobin
D) Lactate
E)-Pyruvate
Protein cannot be there in urine in this
condition, as the kidney functions are
normal. Similarly hemoglobin also cannot
be found, since there is no apparent
cause of hemoglobinuria. Lactic acidosis
is not there hence lactate cannot be
excreted in urine. Pyruvate is not found in
urine, it is mostly utilized in many
pathways.
Hence Acetoacetate (C) is the most
appropriate option.

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