7"he ..

Cow - Ca rh
N
ul 'Fa ' Foo d'P3ramid
..,e:.,
,,.-
. -
s
_...,

B Y: -
IDR. MEGHA GAUR
BDS
I

1
 CONJT£NT
• Introduction S
- Carbohydrates

- Classification of
carbohydrates
- Functions of carbohydrates

- What is metabolism?

• Major metabolic pathways of carbohydrates

- Introduction about each pathway

- Step of reactions in every metabolic

pathway
- Clinical Aspects 2
• Polysaccharides and clinical aspects

• Role of hormones in carbohydrate metabolism

• Dental aspects of carbohydrate metabolism

• Recent issue related to carbohydrate metabolism

• Summary of carbohydrate metabolism

• Conclusion

• References
4
 '
, .
-
- I
-
.. ,, ''
I,
I
CARBOHYDRATE: \
\
►Most abundant organic molecule on earth.
►Carbohydrates are defined as aldehyde or keto
derivatives of polyhydric alcohols.

►For example: Glycerol on oxidation is converted to

D-glyceraldehyde, which is a carbohydrate derived from the
trihydric alcohol (glycerol).

►[orAllit carbohydrates have the general formula C H

0 20
O
0

I I
I I
\ I
\\ I

' _,, I

' ',
' ....
5
 CLASSIFICATION OF
CARBOHYDRTE
Monosaccharides Erythrose,
Ribose,Glucose

Disaccharides Sucrose, lactose

. CARBOHYDRATE V
Oligosaccharides Maltotriose

Polysaccharides Starch , cellulose,

dextrin ,
dextran
6
 fUNCTIONS OF
-
► Main source of energy in the body.
CARBOm(DRsATES ,
','
/
,, ,

Energy
,; '\
1
'

production from carbohydrates will be 4 k

► calories/g (16 kofJoules/g).
Storage form energy (starch and glycogen).
►Excess carbohydrate is converted to fat.
►Glycoproteins and glycolipids are
components of
cell membranes and receptors.
I
\
\

'
►
\

,, ,,
Structural basis of many organisms. For
; ,/
,,
I
I

example,
 METABOLIS
taking place M
housands of chemical reactions are
inside a cell in an
organized, well co-ordinated and
purposeful manner; all these
reactions are called as
METABOLISM.

TYPES OF
METABOLIC PATHWAY:
Catabolic Pathway
Anabolic Pathway
Amphibolic
Pathway

TAGES AND
PHASES OF
METABOLISM:
P ri mar y
Food molecules
Simpler molecules
c==>
Amphibolic pathway

Anabolic Catabolic

Proteins, carbohydrates, C02+H20

lipids, nucleic acids
etc.
9
MAJOR PATHWAYS
OF
CARBOHYDRATE
METABOLISM

10
[ 1) Glycolysis
]
[ 2) Citric Acid ]
Cycle
( 3) Gluconeogenesis )
[ 4) Glycogenesis )

( 5) Glycogenolysis )

[ 6) Hexose monophosphate shunt )

( 7) Uronic Acid Pathway ]
[ 8) Galactose Metabolism )
[ 9) Fructose Metabolism )
[ 10) Amino sugar ) 1
metabolism 4
 6LYCOLYSI
S £MBD£
-MEYERHOFPATHWAY (OR)
£ M PATHWAY
..
···································································

················ - ..
Definition:
pyruvate or lactate, with the production of ATP: .
. Glycolysis is defined as the sequence of .
.
··· ··············· ······· ······
reactions converting glucose (or glycogen)
. ·········· ··· ··· ··· ············· ······· ······ ·········· ······ ················
······ ········· ··
····to
··· 16
 ,, ,--------------------------------------------------------------------,,..... '
,
II ,, Salient features:
- - - - - - -
/ '
', 1) Takes place in all cells of the body. '\
2) Enzymes present in "cytosomal fraction" of the \\

3) cell. Lactate - end product - anaerobic condition.

4) Pymvate(finally oxidized to CO2 & H20 ) -
end product of aerobic condition.
5) Tissues lacking mitochondria - major pathway
- ATP synthesis.
6) Very essential for brain - dependent on
glucose for energy.
7) Central metabolic pathway
I
\
8) Reversal of glycolysis - results in gluconeogenesis. I
I
\

,,
I
\\ I

',, ,
, , - ,, 17

,
 , ;- - ''
,
, '
;

I,
, \
I \
I
I ' \
\
,;

Reactions of Glycolysis

1) Energy Investment phase (or)

priming phase

2) Splitting phase

3) Energy generation phase

I
I
I
I
I
; ; ; '
, , , , 1 8
'------------------------------------------------------------------
• Glucose is phosphotylated to glucose-6-phosphate by hexokinase (or) glucokinase .

• Glucose-6-phosphate undergoes isomerization to give fructose -6- phosphate in the presense

of
phospho-hexose isomerase and Mg2+

• Fructose-6-phosphate is phoshorylated to fructose 1,6-hisphosphate by phosphofructokinase.

• Fructose 1,6-bisphosphate glyceraldehyde 3-phosphate + dihydroxyacetone

phos phate.(a ldola se
enzyme)
• 2 molecules of glyce raldehyde 3-phosphate are obtained from 1 molecule of
glucose

• Glyceraldehyde 3- 1,3-hisphosphoglycerate(g/ycera/dehyde3-phosphate hydrogenase)

phosphate
• 1,3-bisphosphoglycerate 3-phosphoglycerate (phosphoglycerate
kinase)

• 3-phosphoglycerate 2-phosphoglycerate (phosphoglycerate mutase)

• 2-phosphoglycerate phosphoenol pyruvate (enolase + Mg 2+ & Mn2+)

• Ph osphoenol pymvate pyruvate [enol] (pyruvate kinase) pyruvate L-Lactate

[keto]
(lactate dehydrogenase)
 Energy production of glycolysis:
.
l
■■ •• • • • ■ • • • • • • • ■ • • • • • • • ■ • • • • • • • • • • • • • • • ■ • • • • • • • • • • • • ■ • • • • • • ••

ATP production = ATP produced - ATP utilized

• • • • • • • • • • • • • • • • • • • • • • • • ■ • • • • • • • • • • • • • • • ■ • • • • • • • • • • • • • • • ■ • • • • • • • • • •■ • • • •

i
·- •• ■• • • • • • • • • ■ • • ■ • • • • • • • • • • • • • • • ■ • • ■ • • • • • • • • • • • • • • • • • • • • • • • • • ■ • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • ■ • • • • • • • • • ■ • • • • • • • • • • • • ■ • • • • • ■ • • • • • • • •

ATP J:!rOd uced ATP utilized Net energy

In absence of oxygen 4ATP 2ATP 2ATP

(anaerobic glycolysis) (Substrate level From glucose to glucose
phosphorylation) - 6-p.
From fructose -6-p to
2ATPfrom 1,3 fructose 1,6 p.
DPG.

2ATPfrom phosphoenol
pyruvate
In presence of oxygen 4ATP 2ATP 8 ATP /
(aerobic glycolysis) (substrate level -From glucose to glucose - 6 ATP (Pyruvate
phosphorylation) 6-p. dehydrogenase
2NADH,ETC,
2ATPfrom 1,3 BPG. From fructose -6-p to Oxidative
2ATPfrom phosphoenol fructose 1,6 p. phosphorylation )
pyruvate.

+ 4ATPor6ATP
(from oxidation of 2
NA DH +H i n
mitochondria).
22
 CLINICAL ASPECT

1) Lactic acidosis
Normal value - 4 to 15 mg/dl.
- Mild forms - strenous exercise,
shock, respiratory diseases, cancers
- Severe forms - Impairment/collapse of
circulatory system - myocardial
infarction, pulmonary embolism,
uncontrolled hemmorrhage and severe
shock.
19
2) Cancer and glycolysis :

- Cancer cells - increased uptake of glucose

and glycolysis.

- Blood vessels unable to supply adequate oxygen -

HYPOXIC condition - Anaerobic glycolysis I
hypoxic glycolysis - Involvement of Hypoxic
inducible transcription factor (HIF).

- Treatment: Use drugs that inhibit vascularization

of tumours
20
Pasteur effect : Inhibition of glycolysis by
oxygen (Phosphofructokinase) .

Crabtree effect : The phenomenon of

inhibition of oxygen consumption by the
addition of glucose to tissues having high
aerobic glycolysis.

21
 RAPARPORT - LEUBERING CYCLE

• Supplementary pathway/ Shunt pathway to glycolysis .

• Erythrocytes

• Synthesis of 2,3-bisphosphoglycerate (2,3-BPG).

• Without the synthesis of ATP.

• Help to dissipate or waste the energy not needed by

RBCs.

• Supply more oxygen to the tissues.

CITRIC ACID CYCLE
KREBS CYCLE
TRICARBOXALIC ACID/TCA
r·
-...........................·.... l
j to C O 2 a nd
!
.
l
HThis
0. Cycle utilizes about two-third of
.-...........................·....
• 2
total
j o xygen consumed by the
\body.
'- ........ .... ... ..... ... . ...
, ,
..
•
1

j
.... ... ...... • ......•.•" 23
 Location
ofi TCA

• Hans • Mitochondrial • 65-70% of

Adolf matrix the ATP is
Krebs synthesized
• 1937 • In close
proximity to •Name: T C A
• Studies of the electronic used because
oxygen transport at the ouset
consumptiom chain. of the cycle
. .
1 n p igeon tricarboxylic
breast muscle. acids
participate.

24
 Reactions of citric acid cycle
1) Formation of citrate : Condensation of acetyl CoA and
oxaloacetate catalysed by citrate synthase.

2) & 3) Citrate is isomerized to isocitrate aconitase (two

steps).

4) & 5) Formation of Q-ketoglutarate : enzyme isocitrate

dehydrogenase.

6) Conversion of Q-ketoglutarate to succinyl CoA :

through oxidative decarboxylation, catalysed by ¢­
ketoglutarate dehydrogenase complex. 25
?)Formation of succinate : enzyme succinate
thiokinase
GTP + ADP ATP+ GDP (nucleoside
diphosphate kinase)

8) Conversion of succinate to fumarase :

enzyme succinate dehydrogenase

9) Formation of malate : enzyme fumarase

1O) Conversion of malate to oxaloacetate :

enzyme malate dehydrogenase.

26
 ,, ,
--------------------------------------------------------------------,,,, '
, ,
'
'
( /•
, TCA cycle is strictly aerobic in contrast to glycolysis. \
\

• Total of 12 ATP are produced from one acetyl CoA :-

During the process of oxidation of acetyl CoA via citric

acid cycle 3 NADH & 1 FADH2.

Oxidation of 3 NADH by electron transport chain

coupled with oxidative phosphorylation results in 9
ATP, FADH2 2 ATP.

One substrate level phosphorylation.

I
\\ ,,
I

,
\
' , , ,, , ,,
, ,,, I

28
 ASPECTS
- -;;;;:;;:;;-;.:::;;;-
Mitochondrial
-TCACYCLE
- - - encephalopathy
occurs due to
fumarase
deficiency .

It is a
mitochondrial
myopathy affecting
both the skeletal
muscles and brain .
29
 &LUCONE.06ENESIS
,.

The synthesis of glucose from non-

carbohydrate compounds is known as
gluconeogenesis.

Major substrate/precursors : lactate, pyruvate, glycogenic

amino acids, propionate & glycerol.

,.

'

-Takes place in liver (1kg glucose) ; kidney matrix( 113rd)

. 30
l01portance of Gluconeogenesis

Brain,CNS,
Under anaerobic
erythrocytes,testes condition, glucose
and kidney medulla is the only source
dependent on to supply skeletal
glucose for cont.
muscles.
supply of e nergy.

Effectively
Occurs to meet the clears,certain
basal req of the metabolites
body for glucose produced in the
in fasting for even tissues that
more than a day. accumulates
in blood

31
 Reaction of Gluconeogenesis
Gluconeogenesis: Ru n nin g Glycolysis in Rev er se

succlnate

'
malate
-
fl.., ••

rata

NAo malate
C0
..:oi
2 ,-.
r
ADP
f : :.p N A D H nalate dehydrogenase

phos oxaloacetate 36
 Cori Cycle
Glycog ,------------ ,
LIVE Glycoge I/ ,, I
I
I

R n
en ! The cycle
I
! I

: in volveing the :
Fattyacids Glucose- - - -----.:.ai synthesis of
---4-- Glucose glucose in liver
._;, from the skeletal
CJJGluconeo­ muscle lactate and
genesis the reuse of
glucose thus
synthesized by the
muscle for energy
purpose is known
as Cori cycle. I
, I

L----------------------33--
'
 Glucose-Alanine Cycle
Blood

Glucose

Live Muscl
r e
.---..
--
Urea it '-
Glucose &-phosphate Glycogen
Gfl/cogen k ° '
._..... ,.. , Gll,ICOSG 6-
i
t •
Pyruvate
Jr • ., Lactate Lactate IC )lo
•I
Pyruvate ..1'
I I l,. -
I Lactate : 1..'. NH
I 'ff:

i
II Blood pi1osphate ) .
2
I
I I
I Alanin
I Pyruvate • e
Alanine

So urc e: Mu rra y RK, Be n d e r DA, B o t h a m KM, Ke n ne lly PJ, Rodwell VW, Weil PA: Harper
's
Illu stra te d Bio ch e m ist ry, 28 th Ed iti on : h tt p ://www . a cce s s m e d ici n e . co m
C o p yright © Th e McGra w- Hill Co m pa n ie s , I n c. All rig ht s re s e rve d. 34
Clinical Aspects

influence
mobilized
 6LYC06.EN
M« rABOLISM
·······-··-·····

·································································
· \
,··-············
/. Gl ycogen is a storage form of glucose in animals. :
:.
. Stored mostly in liver (6-8%) and muscle (1-2%) .
.
.
Due to muscle mass the quantity of glycogen in muscle=
. 250g and liver =75g
.
.
Stored as granules in the
.
. cytosol.
: F unctions : Liver glycogen - maintain the blood glucose I
-.._ level Muscle glycogen - serves as fuel reserve ..•
·······································································································--·-·---···-·-····· - · .·. /
..
-··-··· 36
 6L'YC06£NESIS

□ Synthesis of glycogen from glucose.

□Takes place in cytosol.
□ Requires UTP and ATP besides glucose.
□ Steps in synthesis :
1) Synthesis of UDP- glucose
2) Requirement of primer to initiate glycogenesis
3) Glycogen synthesis by glycogen synthase
4) Formation of branches in glycogen
37
 I
G l u c o s e

I
Hexa inase (in m••scle)
Glucolcinase in l i v e r )
G l u c o s e 6 - p h o s p h a t e
',
P h o s p h a c amutose
.
G l u c o s e 1.p h o s p h - a t e

U DPg- l u c os e
'. p_yrophosphat ase
U DP - gl
u
. c os e
' Glyco e ;..,.
n-i_t:hase
cx:(1.-+4) g l u c o s y l u n i t s

1 Branching e n z y m e

Glycogen.
[cx:(1 -+ 4 ) and cx:(1-+6) g l u c o s y l
un.it.s]

Diag:a:am: S t e p s ofglycogenesi.s 42
 6L'YC06£NOLYSIS

D Degradation of stored glycogen in liver and muscle

constitutes glycogenolysis.

D Irreversible pathway takes place in cytosol.

D Hormonal effect on glycogen metabolism :

1) Elevated glucagon - increases glycogen degradation
2) Elevated insulin - increases glycogen synthesis

D Degraded by breaking majorly a-1,4- and a-1,6-glycosidic

bonds.

D Steps in glycogenolysis:
3) Action of glycogen phosphorylase
4) Action of debranching enzyme
5) Formation of glucose-6-phosphate and glucose
 Glycogen

Glycogen p h o s p h o r y l a s e
a(l -..4J -.. a ( l -.. 4 ) -g lu
ca n t r a n s f e r a s e
/ A m y l o - a ( l -..6)-
glucosidase
G l u c o s e 1 . -r -p- - h o s p h a t e
Glucose 6-phosphate - - In m u s c l e
lr Phos p, ho g l u c o m ut a s
J Glucose 6 e- p h o s p h a t a s e
[Gl ci o s e I .. Ln l i v e r
Diagran1: Steps 40
 6LYC06EN STORA6E.
DISEASES
TYPE ENZYME DEFECT CLINICAL FEATURES

Type I (Von Gierke's Glucose-6 - Hypoglycemia, enlarged liver and kidneys,

disease) gastro-intestinal symptoms, Nose bleed, short
phosphatas stature, gout
e
Type II (Pompe's Acid maltase
deficiency. Di minished musc le tone , heart failure,
disease) deficiency enlarged tongue

Type Ill (Cori's Debranching enzyme Hypoglycemia, enlarged liver, cirrhosis, muscle
disease,Forbe disease) deficiency weakness, cardiac involvement

Type IV (Andersen's Branching enzyme Enlarged liver & spleen, cirrhosis,

disease) deficiency diminished muscle tone , possible nervous
system involvement

Type V (Mcardle's Muscle phosphorylase Muscle weakness, fatigue and muscle cramps
disease) deficiency
41
 TYPE ENZYME DEFECT CLINICAL FEATURES

Type VI (Her's Liver phosphorylase Mild hypoglycemia, enlarged liver, short

disease) deficiency stature in childhood

Type VII (Tarui's Phosphofructokinase Muscle pain, weakness and decreased

disease) deficiency endurance

Type VIII Liver phosphorylase Mild hypoglycemia, enlarged liver, short

kinase stature in childhood, possible muscle weakness
and cramps

TypeO Liver glycogen Hypoglycemia, possible liver enlargement

synthetase

42
 ..
.r
d • f • •• •

-
... .
•

Von Gie rke's disease)

Pompe's disease

43
 A

Cori's disease, Forbe

disease

Picture& 7A and 78 - Glycogen &t oraQe chease

type Ill

44
HEXOSEMONOPHOSPHATE
SHUNT
HMP Shunt/ Pentose Phosphate
Pathway/ Phosphogluconate
Pathway

45
Reactions of the HMP Shunt Pathway
PHASE 1 G l u c o s e 6 -p h o s p h a r e
(oxsdabve)
2 N A O P •

I R i : b u l o s e 5 -p h o s p h
a te

R,bose Xyf lose

5 - p h osp h . - t (C ) S - p h o s p h a1e (Cs,)

S e d o h u J o s e
7 - ph osp h .at e ( C 7 )

Fructos.e Erytho.se xvtulo

6-phosphate ( 4 -p h o s p h a t e - (C,- '5- p t , o s p h a t e ( C s )
A)

PHASE2 Fructo-se
J
-
( n o n o xida ) 6 - p h o s p h a i : e (C e , )

51
 Significance of HMP Shunt
• Pentose or its derivatives are useful for
the synthesis of nucleic acids and
nucleotides.
• NADPH is required :
-For reductive biosynthesis of fatty acids and
steroids.
- For the synthesis of certain amino acids.
I
- Anti-oxidant reaction I
'I
'I
- Hydroxylation reaction- detoxification '
!
!I
of drugs. '''
'
'
- Phagocytosis 'II
'I
''
 Clinical Aspects
• Glucose-6-Phosphate dehydrogenase
deficiency :
- Inherited sex-linked trait
- Red blood cells
- Impaired synthesis of NADPH
- hemolysis , developing hemolytic
anemia Resistance towards malaria
[Africans]
49
 Clinical Aspects
• Wernicke-Korsakoff syndrome:
- Genetic disorder
- Alteration in transketolase activity
- Symptoms : mental disorder, loss of memory,
partial paralysis

• Pernicious anemia : transketolase activity

i ncreases.
•

50
URONIC ACID PATmiAY
(OR)
GLUCORONIC ACIS PATHWAY

51
 Alternative oxidative pathway for glucose.

synthesis of glucorinc acid,pentoses and vitamin

(ascorbic acid).

Normal carbohydrate metabolism ,phosphate

esters are involved - but in uronic acid
pathway free sugars and sugar acids are
involved.

Steps of reactions :
1) Formation of UDP-glucoronate
2) Conversion of UDP- glucoronate to L-
gulonate
3) Synthesis of ascorbic acid in some animals
 D- G l u c u r o n i c a c i d
Glu c u r o n a t
e reduct:ase

L-Gulonate Pentose phosphate

A ld o n o la ct o n a s e Pathway

L- Gulono lactone

2- keto-gulonolactone

L - Ascorbic acid
53
 Clinical Aspects

• Effects of drugs : increases the pathway to achieve

more synthesis of glucaronate from glucose .
- barbital,chloro-butanol etc.

• Essential pentosuria : deficiency of ylitol­

dehydrogenase
- Rare genetic disorder .
- Asymptomatic .
- Excrete large amount of L-
xylulose in urine
- No ill-effects 54
METABOLISM OF
6AI.ACTOSE

6.af a c t o k J n a s . e
ADP
UDP-Glucose
U r i d y l l r J n fr.r., e

f iJu c Ii'! 1 P
o
P fl o g l o c-;o mu t a
o ,;p- s e

fiL Y C OL YS.I
S 55
 Disaccharide lactose present in milk - principle source of of galactose.

Lactase of intestinal mucosa! ce lls hydrolyses lactose to galactose and

glucose.

Within cell galactose is produced by lysosomal degradation of glycoproteins

and glycolipids.

CLINICAL ASPECTS :

-Classical galactosemia : deficiency of galactose-1-

phosphate uridyltransferase. Increase in galactose level.

- Galactokinase deficiency : Responsible for galactosemia

and galactosuria.

- Clinical symptoms : loss of weight in infants, hepatosplenomegaly, jaundice,

mental retardation , cataract etc.

- Treatment: removal of galactose and lactose from diet.

 METABOLISM OF
FRUCTOSE
Sorbitol/Polyol Pathway:
Conversion of glucose to fructose via sorbitol.

Glucose to Sorbitol reduction by enzyme aldolase (NADPH).

Sorbitol is then oxidized to fructose by sorbitol dehydrogenase

and
NAO+.

Fructose is preferred carbohydrate for energy needs of sperm

cells due to the presence of sorbitol pathway.

Pathway is absent in liver.

 METABOLISM OF AMINO
SU&ARS
,I , ..
.... ►When the hydroxy1group of the sugar is replaced by the
I
I

amino
group, the resultant compound is an amino sugar.
►etc.Eg. G l ucosamine,galactosamine,mannosamine,sialic acid
► E ss e nti a l c o m po ne nt s of glycoproteins,
glycosaminoglycans, glycolipids.
►Found in some antibiotics.
►20 % of glucose utilized for the synthesis of amino I
I
sugars - , III
,
connective tissues. ...
- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
- - - - - - .
-- --
 ELECTRON TR$ANSPORT CHAIN
REACTIONS
• Electron transport chain is a series of
protein complexes located in the inner
membrane of mitochondria .
I I Figure J- 1 3 : Electron Tr a n s p o r t C h a i n

)
COMPLEX I IV SYNTHASE

@ C O MP L EX
© ©
II

NADH
POLYSACCHARJOl!tS
&
CIJNICAL
ASPECTS

60
Proteoglycans & Glycosaminoglycans
Seven glycosaminoglycans :

1 ) Hyaluronic acid
2) Chondriotin sulfate
3 ) Keratan sulfate I
4 ) Keratan sulfate II
5) Heparin
6 ) Heparan sulfate
7 ) Dermatan sulfate
61
 Functions of glycoaminoglycans
• Structural components of extracellular matrix.

• Act as sieves in extracellular matrix.

• Facilitate cell migration.

• Corneal transparency.

• Anticoagulant (Heparin).

• Components of synaptic & other vesicles.

62
 Mucopolysaccharidoses

MPS I (Hurler Alpha-L-Iduronidase Mental reta rdation, micrognathia, coarse facial

syndrome) features, macroglossia, retinal degeneration,
corneal clouding , cardiom yopathy,
hepatosplenomegaly

MPS II (Hunter lduronate sulfatase Mental retardation (similar, but milder,

syndrome) symptoms to MPS I). This type
exceptionally has X-linked recessive
inheritance
MPS IIIA Heparan sulfate N
(Sanfilippo A) sulfatase

MPS IIIB Alpha- Developmental delay, severe hyperactivity,

(Sanfilippo B) Acetylglucosami nidase spasticity, motor dysfunction, death by the
second decade

MPS IIIC Acety1transferase

(Sanfilippo C)
63
MPS IVA Galactose-6-sulfatase
(Morquio A)
Severe skeletal dysplasia, short stature,
MPS IVB (Morquio Beta galactosidase motor dysfunction
B)

MPS VI N acetylgalactosarnine 4 Severe skeletal dysplasia, short stature,

(Maroteaux Lamy sulfatase motor dysfunc tio n, kyphosis, heart defects
syndrome)

MPS VII (Sly) Beta gluco Hepatomegaly, skeletal dysplasia, short

ronidase stature, corneal cloudin g, developmental
delay

MPS IX (Natowicz Hyaluronidase deficiency Nodular soft-tissue masses around joints,

syndrome) episodes of painful swelling of the masses,
short-term pain, mild facial changes, short
stature, normal joint movement, normal
intelligence 68
Hunter's syndrome

• Short and broad mandible

•Localized radiolucent
lesions of the jaw
•Flattened
temporomandibular
joints
• Macroglossia
•Conical peg-shaped teeth
with generalized wide
spacing
•Highly arched palated with
flattened alveolar ridges
• Hyperplastic gingiva
ROL£ OF HOR$MON£S
IN CARBOHYDRATE
METABOLISM

66
 Regulation of Blood glucose
• Postabsorptive state: Blood glucose is 4.5-
5.5mmol/L.

• After carbohydrate meal: 6.5-7.2mmol/L

• During fasting : 3.3-3.9mmol/L

67
 Metabolic & hormonal
mechanisms
regulate blood glucose
Maintenance of stable levels of glucose in blood is by
level
Liver.
Extrahepatic tissues.
!Hormones
 Regulation of blood gl.ucose levels
Insulin

se uptak
gen sy

Muscle
t Blood
!$
glucose

Pancreas

Adipose tiss
ue 69
 Role of glucagon
! Blood
Blood glucose j
glucose

!$
Pancreas

aver

'
· Triglycf:!rlde degreidatio ' -r"
-.a . :: l , = . , '
.- _..,.
e

- - - - . . E a t t y ac(ds · ·... Amino acjd,s

_

Adipose tissue
70
 Role of thyroid hormone
It stimulates glycogenolysis & gluconeogenesis.
Hypothyroid Hyperthyroid
►
is
Fasting blood
lowered. ►blood
Fasting
glucose
glucose is elevated
► Patients have
decreased ability to
utilise glucose.
►utilise
Patients
glucose at normal or
► Patients are less
sensitive to insulin
increased rate

than normal or
hyperthyroid patients.
71
 Glucocorticoids
Glucocorticoids are antagonistic to insulin.

Inhibit the utilisation of glucose in extrahepatic

tissues.

Increased gluconeogenesis .

72
 Epinephrin
e
Secreted by adrenal medulla.

It stimulates glycogenolysis in liver & muscle.

It diminishes the release of insulin from pancreas.

73
 Other Hormones
□ Anterior pituitary hormones
Growth hormone:
Elevates blood glucose level & antagonizes action of
insulin.
Growth hormone is stimulated by hypoglycemia
(decreases glucose uptake in tissues)
Chronic administration of growth hormone leads
to diabetes due to B cell exhaustion.
74
 SEX HORMONES

Estrogens cause increased liberation of

insulin.

Testosterone decrease blood sugar

level.

75
 Hyperglycemia Hypoglycemia

►T hirst, dry ►Sweating

mouth
►Polyuria ►heart
T
rembling,pounding
►Ti redness,
►Anxiety, hunger
►
fatigue
Blurring of ►Confusion,
vision. drowsiness

► Nausea, ►Speech difficulty

headache, ►Incoordination.
► Hyperphagia ►Inability to 76
Mood change
 Clinical aspects
Glycosuria: occurs when venous blood
glucose concentration exceeds
9.5-10.0mmol/L

Fructose-1,6-Biphosphatase deficiency causes

lactic acidosis & hypoglycemia..
77
 Diabetes Mellitus
A multi-organ catabolic response caused by insulin
insufficiency

Muscle
- Protein catabolism for gluconeogenesis

Adipose tissue
- Lipolysis for fatty acid release

Liver

Ketogenesis from fatty acid oxidation

Gluconeogenesis from amino acids and

glycerol
Kidney 82
Renal ammoniagenesis.
TE

79
 Role of carbohydrates in dental caries
• Fermentable carbohydrates causes loss of
caries resistance.
• Caries process is an interplay between oral
bacteria, local carbohydrates & tooth surface

Bacteria+ Sugars+ Teeth -- Organic acids

j
Caries
80
 Role of carbohydrates in periodontal
disease
Abnormal Excessive carbohydrate
glucose metabolism intake
j j
Diabetes Obesity
Mellitus

Periodontal disease Periodontal disease

81
 R£C£NJT CLINICAL
ISSUES R£LAT£DTO
CARBOHYDRATES
METABOLISM

82
 Cystic Fibrosis
• CMD in Cystic Fibrosis is characterized by its
high rates and latent course.
• The patients with CMD have retarded physical
development, more pronounced morphofunctional
disorders in the bronchopulmonary system, lower lung
functional parameters, and more aggressive sputum
microbial composition. (Samoilenko VA et al.)

83
 CMD in Gout
• OGTT causes a 34% increase in the detection rate of
T2D in patients with gout.

• Carbohydrate metabolic disturbances are revealed in

the majority of patients with gout and associated with
obesity, hypertriglyceridemia, high serum UA levels,
chronic disease forms, the high incidence of CHD and
arterial hypertension.(Eliseev MS et al.)
84
SUMMARY OF
CARBOHYDRATE
METABOLISM
C A R B O H Y D R AT E S
FAT S

Fatty
Amino
acids Glucose acids

i Gyl cog e n e sls i

G lu co ae - fatty
6- acid
--... ►
spiral

------
-
.., /
111
P yruv1c a .- . L1pogenes . 1
1 // 1
c d/
-A -c-e ·-
o¥A /

citric+ lectron transport chain

acid
cycle •
AT P
H2 0
85
 PER DAY INTAKE OF
CARBOHYDRATE
• Carbohydrate Calculator
http://www.calculator.net/carbohydrate­
calculator.html?
ctype=metric&cage=25&csex
=f&cheightf eet=5&cheightinch= 1O&cpound=

160&cheightmeter=163&ckg=74&cactivity=1.
375&x=85&y=l0#

86
 CONCLUSION
• Carbohydrate are the measure source of energy
for the living cells. Glucose is the central
molecule in carbohydrate metabolism,
actively participating in a number of
metabolic pathway.
• One component of etiology of dental caries is
carbohydrate which act as substrate for
bacteria. Every effort should be made to
reduce sugar intake for healthy tooth.
Q1
 REFERENCE
1) BiochemistryS- U.Satyanarayana-3 rd Ed.
2) Textbook of Biochemistry- D.M.Vasudevan -
14 th Ed.
3) Textbook of Medical Biochemistry -
M.N.Chattergy - 17th Ed.
4) Text book of Physiology -Ganong -
24 th Ed.
5) Text book of Oral Pathology -
Shafers- 7 t h Ed.
6) Principles & practice of Medicine-Davidson - 88
st
I

89