Carbohydrate Metabolism

I Ketut Suardana
Nursing Departement
Polytechnic of Health Denpasar
 Introduction
What is CH
classification.; Poly, Oligo, Disaccharida, monosac
The important CH for our body:
 Amylum/starch/pati : polysacharida
Hydrolized: di-saccarida  mono saccharide
 Hexosa and pentosa
Glucosa and ribosa.
 Metabolism : Anabolism and catabolism
 What is metabolism
 Metabolism is the sum of all of the
enzymes-catalyzed reactions that take
place in cells and can be viewed as having
two contrasting processes :
* catabolism : energy yielding reactions in which
complex mol are broken down to small molecule
* anabolism : energy requiring reactions in which
simple precursor molecule are converted into
complex mol.
 Energy yielding in catabolism
 Catabolism of C-H, lipids, aa to a simpler
end-product such as CO2, H2O and
amonia is accompanied by the synthesis
of ATP.
 ATP is utilized for various cellular
functions such as :
 synthesis of protein,RNA,DNA for growth, adaptation and repair,
 synthesis of fat and glycogen,
 performance of mechanical work,
 active ion transport,
 absorptions of nutrients against the gradient.
GLUCOSE ABSORPTION
 Pathway involved in the
pathogenesis of T2DM
Glucose

Glucose transporter
Glucose

Hexokinases Glucose-6-phosphatase
P
Glucose-6-phosphate

HEXOSAMINE BIOSYNTHESIS PENTOSE PHOSPHATE

PATHWAY PATHWAY

GLYCOLYSIS GLYCOGEN SYNTHESIS

Fig. Cellular fate of glucose showing the major metabolic pathways:

glucose transports and phosphorylation, glycolysis, glycogen synthesis,
pentose phosphate pathway, and hexosamine biosynthesis pathway
Bouche et al. Endocrine Reviews 25: 807-830, 2004
 GLUT-2
Glucokinase
Glucose G-6-P ATP
NIMGU
Beta cell pancreas

Glu-
NIMGU ins
cose (+)
NEFA
Glucose uptake GLUT-4
Glucose Glycerol Triglyceride
(+) (+)
ins (+) ins ins
Insulin-sensitive tissue
Insulin-independent tissue Adipose tissue

NIMGU Glycogen
ins cats
(+) (+)
Glucose G-6-P ins
GLUT-4 (+) CO2

Glycolysis

ins (+)
Skeletal muscle
 CH Metabolism.
1. Glycolysis. Oxid of Glucose/glycogen pyruvat &
lactate.
2. The oxidation of pyruvat to acetyl-CoA: prior to
TCA cycle.
3. TCA Cycle: the final common pathway
for oxidation of CH,fat and protein.
4. The HMP-shunt : alternative pathway for
glucose oxidation
5. Oxidative phosphorylation in respiration chain
of Mitochondria.
GLYCOLYSIS
 GLYCOLYSIS
 3 stages of glycolysis
1. Investment stage (2 ATP invested)
2. Splitting stage (compound of 6 Carbon
splitt into 2 substance of 3 Carbon atom)
3. Yielding stage (4 ATP produce)
Total ATP production on glycolysis are 2
ATP
Slide 3 of 22
Oxidation of pyruvat to acetyl-CoA.
 Before entering TCA-cycle, pyruvat must
be oxidatively decarboxylated to acetyl
CoA.
 Catalyze by pyruvat dehydrogenase
complex
 Need thiamin pyrophosphate as enzyme
 Role of Acetyl CoA
lipids polysaccharides proteins

fatty acids monosaccharides amino acids

Acetyl CoA
fatty acids ketone bodies

triglcerides and cholesterol

phospholipids citric acid cycle
bile salts steroids
CO2 + H2O + ATP
TCA CYCLE
 The Citric Acid Cycle
 Final stage for the metabolism of
carbohydrates, fats and amino acids.
 Oxidative cycle
- requires oxygen
- aerobic
 Also called the Krebs’ cycle
for Hans Krebs who first described it.
 The Citric Acid Cycle
acetyl CoA

citrate
oxaloacetate A 9 step
cis-aconitate
process that
malate
takes the
isocitrate
acetate from
acetyl-CoA
fumarate and converts
-ketoglutarate it to CO2
succinate succincyl
CoA
 Citric Acid Cycle Enzymes
acetyl CoA
Aconitase
Citrate synthase citrate
oxaloacetate
cis-aconitate
Malate
dehydrogenase Aconitase
malate isocitrate

Fumarase Isocitrate
dehydrogenase
fumarate
-ketoglutarate
Succinyl
dehydrogenase succinate succincyl -Ketoglutarate
CoA dehydrogenase
Succinyl CoA synthase complex
 Energy & the Citric Acid
acetyl CoA Cycle
citrate H O 2

oxaloacetate
cis-aconitate H 2O
NADH

malate isocitrate
CO2
H 2O +
NADH
fumarate
-ketoglutarate

FADH2 Coenzyme A
succinate succincyl
CoA
GTP + Coenzyme A CO2 + NADH
GDP
OXIDATION PHOSPHORYLATION
 It is occur in inner mitochondrial
membrane of mitochondria (respiration
chain)
 Couple of oxidation and phosphorylation
 1 mol of NADH oxidized  3 ATP
 1 mol of FADH2  2 mol ATP
 1 GTP produce 1 mol ATP
 Pentosa Phosphate Pathway
 The primary pathway for formation of
nucleotide, DNA and RNA.
 This pathway branched from glycolysis at
a level of G-6P.
 This is also describe of “shunt” rather than
pathway.
 Important Enzymes are G6PDH, PGK,
PGM, Enolase, Pyruvate Kinase(PK), LDH
Pentosa Phosphate Pathway (3)
 The major product is NADPH
 In nucleated cell, with active lipid biosynthesis,
NADPH used in redox reactions  biosynthesis
of fatty acid, cholesterol and steroid hormon and
bile salts.
 Liver used for hydroxilation reactions  for
detoxification and excretion of drugs.
 RBC shunt about 10% of glucose  use primary
for the reduction of gluthation an important
intermediate in antioxidant defence.
 Gluconeogenesis

 The synthesis of glucose from

noncarbohydrate precursors
 Occurs primary in the cytosol
 Liver & kidney cortex (glucose)
 Substrates for gluconeogenesis:
1. Lactate
2. Amino acids
3. Glycerol
4. Propionate
 Gluconeogenesis
 During fasting and starvation, when glycogen
liver is depleted, gluconeogenesis is essential
for blood glucose homeostasis
 The energy provide from the metab of fat
release from adipose tissue, and carbon
skeleton provided from 3 sources such as
lactate, amino acids, and glycerol release from
triglyceride during lipolysis in adipose tissue.
Substrates for Gluconeogenesis 1. Lactate
2. Amino acids
3. Glycerol
4. Propionyl-CoA

Figure 16.4: Outline of pathways for glucose synthesis

from the major gluconeogenic precursors
2. Amino acids:
Many amino acids can be converted to glucose; they are referred
to as glucogenic.
3. Glycerol:
In general, lipids are poor gluconeogenic precursors.
In animals, fatty acids cannot undergo net conversion to
carbohydrates.
4. Propionate: propionyl-CoA
Generated either from the breakdown of some amino acids or
from the oxidation of fatty acids with odd numbers of carbon
atoms.
 Glucose homeostasis
 Plasma glucose concentration reflects
the balance between :
1. Glucose intake (abs from the gut)
2. Tissue utilization (glycolisis,PPP, TCA
cycle, glycogen synthesis)
3. Endogenous production of glucose
(glycogenolysis, gluconeogenesis)
Control of glucose homeostasis
 Control by:
1. Anabolic hormone, insulin and insulin like
growth factor.
2. Several catabolic hormone (glucagon,
cathecolamine, cortisol, and GH = anti insulin
= counter-regulatory hormone
Glucose level acts as a signal that initiate the islet
hormonal response. Glucose stimulates the
secretion of insulin and suppresses glucagon
secretion.
 Hyperglycaemia
 Folin-Wu : 80-120 mg%
 O-toluidin : 60-100 mg%
 Glucose oxidase: 50-100 mg%

 More than normol value (depend to

method used  hyperglycaemia
 Hypoglycaemia
 Blood glucose level < 45 mg% (2,5 mmol/l) 
hypoglycaemia
 Hypoglycaemia caused by:
Over exercise, external insuline>>, insulinoma,
fasting, inhibition of endogenous glucose
production.
 Sign and symptom : palpitation, sweating,
trembling, and feeling hunger
 If it is continue  neuroglycopenia  confuse
and unconciousness fatal.
 Hypoglycaemia is medical emergency.