Protein Energy Malnutrition Path o Physiology Adaptation and Management

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Protein Energy Malnutrition (PEM) Pathophysiology Adaptation and

Management
Presentation · October 2018
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Protein Energy Malnutrition (PEM)
Pathophysiology Adaptation and
Management
Ashraf Soliman MD PhD FRCP
Rania Elalaily MSc Ped
Nada Soliman MBChB
Carbohydrate and Fat
Metabolism
Diagrams
•Monireh Dashty Rahmatabady

02/10/2018 Soliman AT PEM-Update
Summary of biochemical reactions in
carbohydrate metabolism.

Anthropometry
Diagnostic Classifications
Examinations
Diagnostic Criteria for PEM

Adaptation Metabolism
During Food Deprivation

Metabolic adaptation to a brief period of fasting
• There is refusal of the myocardium and skeletal muscle to use glucose.

Instead, they switch over exclusively to free fatty acid and ketone metabolism.
• The glycogen reserves in humans never get completely depleted. There is at all
times a hepatic reserve, waiting to mobilise and rescue the organism from some
sort of horrible situation.
• The Cori cycle plays a more important role. 36g of the daily glucose is converted
into lactate, which shuttles back to the liver.
• The liver uses free fatty acids to power the process of gluconeogenesis.
Thus, any lactate converted back to glucose is really free fatty acid energy
converted to glucose.
• All these Cori-cycling anaerobic glycolysis tissues are running on free fatty acid
energy, and glucose and lactate merely act as vessels which contain that energy.

Hormones
responsible
for the
metabolic
adaptation to
brief fasting

Cori Cycle

•
• Its all through increasing the rate of lipolysis.
• And the rate of lipolysis in fatty tissues is governed
by the intracellular content of cAMP, which
responds to both insulin and noradrenaline.
Hormonal
control of
adaptation

The major hormonal player in this adaptation
is insulin : Lipolysis
• With the absence of regular glucose peaks (given the lack of eating) insulin levels drop.
• Insulin is the primary inhibitor of lipolysis, because the tyrosine kinase activity of its
intracellular domain activates a phosphodiesterase, which keeps intracellular cAMP
levels low.
• As insulin levels drop, the background sympathetic activity becomes unopposed, and the
hormone sensitive lipase begins to dismantle their triglyceride stores, releasing delicious
fatty acids into the bloodstream.
•
There are three lipases in the pathway, because there are three fatty acid molecules
attached to the glycerol. Only the first lipase is hormone-sensitive.)
• Noradrenaline increases the rate of lipolysis (by affecting the bored and lonely beta-3
receptor), and insulin decreases the rate of lipolysis.
• The catecholamine excess associated with critical illness definitely causes lipolysis, even
in absence of exogenous catecholamines.

Proteolysis
Proteolysis in fasting is not studied as well

as lipolysis, but it is clear that an insulin Which brings up an interesting question.
deficit also activates proteolytic pathways Nobody ever just lies there and starves
(because the administration of small quietly for their first few days in the ICU.
amounts of intravenous dextrose seems to What happens to these patients?
inhibit proteolysis)
They still starve.

But, if 150g (600kcal) or so of simple
carbohydrate is delivered every day (which In short, feeding your patient
is 3 litres of 5% dextrose, the proteolytic even a tiny amount of
pathway is switched off. Lipolysis continues, carbohydrate will prevent
but the exogenous glucose results in
enough insulin release to abort the ketosis and protein catabolism.
ketogenesis.

Adaptation to
prolonged
fasting

Summary
WITH PROLONGED STARVATION, THE

PROTEOLYSIS RATE OF PROTEIN CATABOLISM
CANNOT CONTINUE REDUCES.
A FASTING PERSON
AT A RATE OF 75 THIS CAN BE SEEN FROM REQUIRES MUCH LESS
GRAMS PER DAY. EXPERIMENTS, AS A DECREASED RATE FLUID THIS WAY, WHICH
THIS WOULD BE OF URINARY NITROGEN (UREA) MUST HAVE BEEN AN
INSANE, AND ALL EXCRETION. BECAUSE THE RATE OF EVOLUTIONARY
OF THE PROTEIN UREA PRODUCTION IS SO LOW, THE ADVANTAGE.
WOULD BE OBLIGATORY RATE OF URINE
DEPLETED VERY PRODUCTION IS ALSO LOWER.
QUICKLY.

• The adaptation to prolonged starvation
is primarily a change in the pattern of
ketone use.
• The brain gives up its addiction to
glucose, and survives on a diet of
ketones.
Protein • At this stage, nothing else uses glucose-
catabolism every tissue in the body either burns
fatty acids, burns ketones, or uses the
Cori cycle.
• Because there is a decreased need for
glucose, there is a decreased need for
gluconeogenesis, and thus a decreased
need for protein catabolism.

Figure 1. Conceptual framework on the relationship between malnutrition, infections and poverty.
Rytter MJH, Kolte L, Briend A, Friis H, Christensen VB (2014) The Immune System in Children with Malnutrition—A Systematic Review. PLOS ONE
9(8): e105017. https://doi.org/10.1371/journal.pone.0105017
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0105017

Thank You
Soliman AT PEM-Update 02/10/2018
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See discussions, stats, and author profiles for this publication at: https://www.researchgate.

Protein Energy Malnutrition (PEM) Pathophysiology Adaptation and

Presentation · October 2018

Ashraf T Soliman Rania Elalaily

SEE PROFILE SEE PROFILE

IDA Project View project

The user has requested enhancement of the downloaded file.

•Monireh Dashty Rahmatabady

02/10/2018 Soliman AT PEM-Update

02/10/2018 Soliman AT PEM-Update

02/10/2018 Soliman AT PEM-Update

• There is refusal of the myocardium and skeletal muscle to use glucose.

02/10/2018 Soliman AT PEM-Update

02/10/2018 Soliman AT PEM-Update

02/10/2018 Soliman AT PEM-Update

02/10/2018 Soliman AT PEM-Update

02/10/2018 Soliman AT PEM-Update

Proteolysis in fasting is not studied as well

They still starve.

02/10/2018 Soliman AT PEM-Update

02/10/2018 Soliman AT PEM-Update

WITH PROLONGED STARVATION, THE

02/10/2018 Soliman AT PEM-Update

02/10/2018 Soliman AT PEM-Update

02/10/2018 Soliman AT PEM-Update

Soliman AT PEM-Update 02/10/2018

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