Metaboli
adapt
c ati
on
prduri
olong
ng ed
starvation
well fed state 1-4 hrs after food
:
post prandial state : 4-16hrs after food
fasting state : 16-48 hrs after food
short term starvation : 2-4 days after
prolonged
food
starvation >5 days after food
deprivation
:
What is
starvation ?
It is the metabolic stress
which imposes certain
metabolic compulsions on the
organism.
what happens during fasting
?
Glucose level
decreases
Glucagon level Insulin level
increases decreases
How Glucose l e v e l s are maintained during
prolonged starvation .?
Glycogenolysis
Gluconeogensis
lipolysis
G l u co s e uti lised b y
Renal
RB
Brai cortex
Glycogenolysi
s
Glycogenolysi
s During fastin
G LY C O G E N
Glycogen phospholylase Glycogen
g, a t fi r stb l o o debranching
enzyme
d g luc o selevel
ismaintained
by hepatic GLUCOSE
g lh yecgol gy e
T con ig sei ns s. t o
resare suffi
cient for
a b o u t1 8 h o u r s .
Gluconeogenesi
s
GG
GLUT Glucos
G 2 e
Glucose 6 phosphate
G Fructose 1,6 fructose 6
bisphosphatase
phosphate
Glucos fructose 1,6 fatty
Glycerol
e bisphosphate acids
Glucose 6 phosphatase G-3- DHA lipolysis
Glucose 6 P P Glycerol 3-
phosphate
phosphate
Phosphoenol
SER OAA
PEPC
K pyruvate
Pyruvate Alanin
Pyruvate
carboxylase
e
Acetyl Alpha
Malat OA CoA glutamat ketoglutarate
Glucose alanine Branched chain
e A e cycle
amino acids
Leucine
Malate Isoleucine
Gluconeogenesi
Energy
GLUCONEOGENESIS
It is theprocess by which gl
ucosemolecules are produ
ced from non
c a r b o h y d r a t ep r e c u r s o r s . T h e s e i
ncludelactate, glucogenic amin
o acids,glycerolpart of fat an
d p r o p i o n a t e C o A d e r i v e dKEY f rGLUCONEOGENIC
o ENZYMES
m o d d c h a i nfSITE
a t t: y a c i d s
:
Gluconeogenesis mainly occurs
Pyruvate carboxylase
in Liver, and to a lesser extent
in renal cortex . The pathway is Phosphenol pyruvate
carboxykinase
partly mitochondrial and partly
cytoplasmic.. Fructose 1,6
Glucose 6
bisphosphotase
SUBSTRATES OF
GLUCONEOGENESIS
The amino acids released from muscle form the major
substrate.
The amino nitrogen is transferred from other amino acids
to pyruvate to form alanine.
The amino acid group reaches the Liver as alanine, where
it is transmitted to give pyruvate for gluconeogenesis.
The glucose alanine cycle serves to transport The
amino nitrogen of other amino acids to Liver in
Harmless form
Lipolysis
LIPOLYSIS bra in cannot
TRIACETYLGLYCERIDE utilize f a t t y
[camp mediated acids
lipolysis]
Glycerol FattyAcids
Beta-Oxidation
Substrate for Acetyl CoA
gluconeogenesis
Ketogenesis Mitochondria
Ketone Bodies
Live
r
LIPOLYSIS
Starvation is accompanied by increased degradation of fatty acids ( from the fuel reserve
triacyl glycerol) to meet the energy needs of the body .
This causes an overproduction of acetyl coA which cannot be fully handled by citric acid cycle.
TCA cycle is impaired due to deficiency of oxaloacetate , since most of it is diverted for
glucose synthesis to meet the essential requirements for tissues of brain (often
unsuccessful).
The result is an accumulation of acetyl CoA and it's diversion for Overproduction of ketone
bodies.
Major organs during Adipose
tissue
starvation
Brain
skeletal
muscle
liver C a r bm e t a b o l i s
C a r b m C a r b m e t a b o l i m :
e t a b o l i s m : s m : Glucose
Reduced
Increased gluconeogenesis
preferred
Reduced
increased glycogenolysis fuel l i p i d
l i p i d m e t a b o l m e t a b o l i s m
l i p i d m e t a b i s m : First 2 weeks : :
o l i s m :
Both FA and KB are utilised
Glucose by Synthesis of
TCA cannot cope up with excess by the muscle as source
gluconeogenesis TRIACYLGLYCEROL
production of Acetyl CoA of energy
> 3 weeks :
Fatty acid oxidation increases p r o t e i nm e t a b o l i More degradation
Increase of
release of
s m : Ketone bodies for TRIACYLGLYCEROL
fatty acids
Acetyl CoA is converted into Gluconeogenesis in liver energy needs
muscle protein Amino ( Fuel for various tissues
fatty acid except brain tissue )
acid
ACIDOSIS
Lipolysis cannot continue indefinitely since excessive production of
ketone bodies leads to metabolic acidosis .
When the bicarbonate buffering capacity is exceeded, the pH falls
and hyperventilation occurs as compensatory mechanism .
Since glucose levels are comparatively low duringprolonged
Starvation, secretion of insulin is reduced, but more glucagon is
secreted.
A fall in T3 level leads to decrease in basal energy requirements by
25% .
DEATH FROM STARVATION :
Metabolic acidosis and dehydration,
unless corrected efficiency, will lead to
death .
A normal person has fuel reserves to live up
to
45 -60 days.
Th
a
y o
