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Nutrition Bio > Cho > Flashcards

Cho Flashcards

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1
Q

Talk about digestion of cho

A

1- only a very small amount of ingested cho are monosaccharides, most of them are in complex forms like glucogen and starch and cellulose and disaccharides
2-digestion of starch and glycogen starts in the mouth by secretion of salivary amylase that partly digest them to dixterin and few moles of maltose
3-no digestion for cho in stomach due gastric acidity
4-in small intestine pancreatic amylase is secreted to completely digest them to maltose
5- brush border of intestinal mucosa secretes enzymes like maltase , lactase, isomaltase and sucrase that digest disaccharides
Maltase and isomaltase ~> 2 glucose
Lactase~> glucose and galactose
Sucrase~> glucose and fructose
6- uptake of glucose by na / glucose transporter an active transport system
7- there are non digestable carb like dietary cellulose that is made of glucose united linked by b1-4 glucosidic linkages and in human there is no b1-4 glucosidase that can digest such bond

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2
Q

Def of lactose intolerance

A

Deficiency in lactase enzyme in the brush border of enterocytes that digest lactose into galactose and glucose

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3
Q

Percentage of lactose intolerance patients

A

More than three quarters of the adults are lactose intolerant

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4
Q

Aetiology of lactose intolerance

A

1- may be congenital ( rare)
2- may be acquired ( common)

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5
Q

Effects of lactose intolerance

A

Lactose accumulation in intestine
1- increased osmotic pressure: the water will drawn from the tissues ( causing dyhdration)
To the large intestine causing diarrhea
2- increased fermentation of lactose by bacteria
Leading to production of Co2 gas that cause distension and abdominal cramps

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6
Q

Intestinal absorption of monosaccharides

A

Different sugars have different mechanisms of absorption as glucose and galactose are absorbed by SGLUT -1 ( sodium dependant monosaccharide cotransporter 1 ) and fructose is absorbed by GLUT -5 ( sodium independent monosaccharide transporter 5) and all these are are transported into portal circulation by GLUT -2

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7
Q

Transport of glucose to cells

A

Two transport mechanisms
Na dependant monosaccharide cotransporter (SGLUT)
Na independent monosaccharide transporter
(GLUT)

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8
Q

Na dependant monosaccharide cotransporter system

A

•This is an energy-requiring process

• that transports glucose from low glucose concentrations outside the cell to higher concentrations within the cell

•The carrier is a sodium-dependent

•SGLT -1 is found in the intestinal mucosa (enterocytes) of the small intestine , SGLT-2 is found in proximal tubule of the nephron and contribute to renal glucose reabsortion

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9
Q

Na independent monosaccharide transporter system

A

family of 14 glucose transporters in cell membranes. (GLUT-1 to GLUT-14 )There are 4 major glucose transporters ,each with a different affinity according to its physiologic role. Normal glucose concentration in peripheral blood is 4-6 mM

GLUT-1
Most tissues (brain, Basal uptake of glucose
red cells)
(-1mM)

GLUT-2
Liver. Uptake and release of
Pancreatic b cells glucose as glucose
(-15 mM). Sensor

Upt
GLUT-3
Most tissues. Basal uptake
(-1 mM)

GLUT-4
Skeletal muscle
Adipose tissue. Insulin stimulated glucose
(-5mM). uptake , stimulated by exercise

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10
Q

Fate of glucose in tissues

A

1- oxidation
•Glyolysis followed by krebs cycle and they are the major pathways
•Pentose phosphate pathway and uronic acid pathway and they are minor pathways

2- storage in form of glycogen and fats
3- conversion to important substances
• lactose to form milk
• fructose to semen
• ribose and dehydroxyribose to form RNA AND DNA

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11
Q

Def of glycolysis

A

Oxidation of glucose to give 2 pyruvate and 6 or 8 ATP ( in case of o2 presence) or 2 lactate and 2 ATP (in case of o2 absence)

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12
Q

Location of glycolysis

A

Cellular location : cytosol
Organ location : in all tissues but it has more physiological importance in
• CELLS WITH NO MITOCHONDRIA Eg RBC
•CELL WITH FEW MITOCHONDRIA Eg testes and leukocytes
• cell with that undergo frequent o2 lack eg sk m during excercise

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13
Q

Phases of glycolysis

A

1- peraparatory phase
• named also priming phase
• it includes the first 5 enzymtic reactions
• 2 ATP are consumed in this phase
• it ends by convervion of glucose into 2 glyeroldyhyde 3 p

2- pay off phase
• named also energy producing phase
• it includes the second 5 enzymtic reactions
• it ends by conversion of mentioned to 2 pyruvate and 4 ATP and 2 NADH

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14
Q

Steps of glycolysis

A

حدوتة مصرية

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15
Q

Importance of phosphorylation of glucose

A

Phosphorylated sugars can’t penetrate the cell membrane as they have no transporter for them thus irreversible phosphorylation of glucokinase to glucose trap them into the cell as cytosolic glucose 6-p thus comitting them to further metabolism in the cell

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16
Q

Difference between glucokinase and hexokinase

A

Both consume ATP AND Mg for their functions

Glucokinase
Site : Liver and -cells of pancreas.

Substrate: only glucose

Activity : Its activity is inducible by the presence of high glucose level in the cell.

Affinity of glucose :Its Km for glucose is high and operates
only when blood glucose level is above 100 mg/dl

Functions:In ß cells of pancreas, glucokinase
functions as the glucose sensor for insulin secretion inactivation mutations can impair insulin secretion result in maturity onset diabetes of the young ( MODY)
In the liver, it facilitates glucose phosphorylation during the well-fed state.

Allosteric inhibition: Not inhibited by
glucose-6-phosphate

Effects of hormones: -Induced by insulin
-Inhibited by anti-insulin hormones

Effect of food : increased by feeding & inhibited by fasting

Hexokinase

Site : All tissue cells.

Substrate: glucose and other hexoses

Activity: It is a constitutive enzyme.

Affinity of glucose: It has low Km for glucose i.e., high affinity for glucose. This permits efficient phosphorylation & subsequent metabolism of glucose even
when tissue concentrations of glucose are low.

Functions: It ensures glucose energy supply for tissues
even in fasting states.

Allosteric inhibition :Allosterically inhibited by glucose 6-phosphate

Eff of hormone: Not affected by hormones

Effect of food: Not affected

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17
Q

TAlk about PFK 1-2

A

1- PFK -1 is the rate limiting and controlling enzyme in glycolysis
2- PFK -1 is inhibited by ATP and citrate and activated by AMP
3-Insulin stimulates and glucagon inhibits PFK-1 in hepatocytes by an indirect mechanism
involving PFK-2 and fructose 2,6-bisphosphate. F2,6-BP activates PFK-l

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18
Q

Talk about Aldolases

A

There are two types of them
Aldolase A : presents in all tissues and split fructose 1,6 bip

Aldolase B : in liver and kidney and split fructose 1-p

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19
Q

Talk abot glyceraldehyde 3 p dehydrogenase

A

1- add Pi to its substrate results in production of high phosphate containing compund ( 1-3 biphosoglycerate)
2- reduce NAD TO NADH

3- arsenate inhibits the conversion of glyceraldehyde 3 p to 1-3 biphosphoglycerate by mimiking the p in reaction , the arsenate will let glycolysis go on but no ATP production

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20
Q

Talk about Lactate dehydrogenase

A

• only used in anerobic glycolysis
• it re oxidise the NADH TO NAD replenishing the oxidised co enzyme of glyceraldehyde 3p dehydrogenase
• without mitochondria and o2 the glycolysis will stop when all the available NAD is reduced to NADH , by reducing pyruvate to lactate and oxidation of NADH lactate dehydrogenase prevents this problem
• in aerobic tissues , lactate does not normally form in significant amount except for in where the o2 is poor ( skeletal muscle during excercise ) most ATP IS generated by anerobic glycolysis and lactate production increases ( lactic acid )

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21
Q

Fate of pyruvate

A

• in anerobic conditions, pyruvate is reduced to lactate
• lactate formation is obligatory end product of glycolysis in RBCS , parts of retina , skeletal muscles during exercise

~ in aerobic conditions, pyruvate is transported to mitochondria and acts as substrate to two enzymes pyruvate dehydrogenase and pyruvate carboxylase producing actyel CoA and oxaloacetate for krebs cycle
( actyel CoA ~> TCA ~> co2 and +ATP
~> fatty acid synthesis. )

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22
Q

Significance of lactate formation

A

Under anaerobic conditions NADH is re-oxidized to NAD replenishing oxidized coenzyme for glyceraldehyde 3 p dehydrogenase

Wash out excess pyruvate which cannot pass membranes.

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23
Q

Energy produced under anaerobic condition

A

2 ATP

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24
Q

Energy produced under aerobic conditions

A

6 or 8 ATP

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25
Q

Electron shuttle

A

Cytoplasmic NADH is re-oxidized to NAD and delivers its electrons to one of 2 electron
shuttles in mitochondria,In the malate, shuttle, electrons are passed to mitochondrial
NADH and then to the ETC ,In the glycerol phosphate shuttle, electrons
are passed to mitochondrial FADH2.
Cytoplasmic NADH oxidized using the malate shuttle produces approximately 3 ATP by oxidative phosphorylation.
Cytoplasmic NADH oxidized by the glycerol phosphate shuttle produces approximately 2 ATP by oxidative phosphorylation.

26
Q

Biological importance of glycolysis

A

1-Important source of energy (8 or 6 ATPs or 2 ATPs under aerobic or anaerobic).
2. It is the main route for glucose metabolism.
3. It is an important metabolic pathway for fructose and galactose.
4. It connects between carbohydrate, lipid and protein metabolism.
5. Its reversibility is important for gluconeogenesis.
6. Production of important metabolic intermediates e.g: Dihydroxy acetone phosphate (DAHP)
which gives glycerol 3-phosphate that is used for synthesis of TAG and
phospholipids or as a shuttle ,3 phosphoglycerate can give serine.

27
Q

Regulation of glycoletic pathway

A

The rate of glycolysis is controlled the rate of the three irreversible enzymes
(key enzymes) namely:
1. Hexokinase.
2. Phosphofructokinase-1.
3. Pyruvate kinase.

Short term regulation:
1. Hexokinase is allosterically inhibited by glucose-6-P (negative feedback).
2. Phosphofructokinase-1 is the rate limiting enzyme of glycolysis and is:
Allosterically activated by AMP (low energy signal) & fructose 2,6 bisphosphate

Allosterically inhibited by ATP and citrate ( high energy signals).
3. Pyruvate kinase is:
Allosterically activated by fructose 1,6 bisphosphate( feed forward activation)
Allosterically inhibited by ATP.
Regulated by phosphorylation and dephosphorylation (covalent modification). The
active form is dephosphorylated.

Long term regulation (effect of hormones):
1. Insulin: It is secreted after meal in response to high blood glucose level. It stimulates
synthesis of all key enzymes of glycolysis except hexokinase which is a constitutive enzyme.
Also, it stimulates pyruvate kinase by dephosphorylation.
2. Glucagon: It is secreted in response to low blood glucose level. It inhibits the synthesis of
all key enzymes of glycolysis except hexokinase. Also it inhibits pyruvate kinase by
phosphorylation of the enzyme protein.

28
Q

Basic enzyme of glucose phosphorylation

A

Hexokinase

29
Q

What are the irreversible glycolitc enzymes

A

1- glucokinase
2- hexokinase
3- PFK 1-2
4- pyruvate kinase

30
Q

RBCS and glycolysis clinical correlation

A

RBCS has biphosphoglycerate mutse that produces 2,3 BPG from 1,3 BPG in glycolysis which binds to HBA decreasing the affinity of it to o2 and making shift to the right in o2 dissociation curve

31
Q

What is warburg effect

A

is defined as an increase in the rate of glucose uptake and
preferential production of lactate, even in the presence of oxygen. It has
been an adaptation mechanism to support the biosynthetic requirements of
uncontrolled proliferation. As the increased glucose consumption is used as a
carbon source for anabolic processes needed to support cell proliferation, eg:de novo generation of nucleotides, lipids, and proteins and other multiple substances

32
Q

Pyruvate kinase deficiency

A

It is the second most common genetic deficiency that causes a hemolytic anemia ,Characteristics include:
Chronic hemolysis
Increased 2,3-BPG that decrease o2 affinity
Abscence of heinz bodies

Mechanism of hemolysis: The red blood cell has no mitochondria and is totally dependent
on anaerobic glycolysis for ATP. In pyruvate kinase deficiency, the decrease in ATP
causes the erythrocyte to lose its characteristic biconcave shape and signals its destruction
in the spleen. In addition, decreased ion pumping by Na+/K+-ATPase results in loss of ion
balance and causes osmotic fragility

33
Q

What is empagliflozin

A

is a SCLT2 inhibitor that is used as an oral hypoglycemic to treat type II diabetes. It prevents urinary glucose reabsorption.

34
Q

Notes on GLUT 1-4

A

GLUT-1 and GLUT-3 mediate basal glucose uptake in most tissues. Their high affinities for glucose ensure glucose entry even
during relative hypoglycemia. At normal glucose concentration, GLUT -1 and GLUT-3 are at Vmax.

GLUT-2, a low-affinity transporter, is in hepatocytes. After a meal, portal blood from
the intestine is rich in glucose. GLUT-2 captures the excess glucose primarily for storage. When the glucose concentration drops below the Km for the transporter, much of
the glucose leaves the liver and enters the peripheral circulation. In the ß cells
of the pancreas. GLUT-2, along with glucokinase, serves as the glucose sensor for insulin release.

GLUT-4 is in adipose tissue and muscle and responds to the glucose concentration in peripheral blood. The rate of glucose transport in these tissues is increased by insulin,
which stimulates the exocytosis of GLUT-4 transporters to the membrane

35
Q

Source of cyanide

A

Burning foam stuffing in furniture and mattresses)
thiosulfate can be used to destroy cyanide

36
Q

Co and cyanide who is more potent

A

Cyanide

Co binds to complex IV but less tightly than cyanide

37
Q

Mitochondrial pathway for glucose oxidation

A

In presence of o2 , pyruvate is transported to mitchondria by pyruvate co transporter with H proton to proceed as follow :-
• oxidative decarboxylation to give acetyl CoA
• carboxylation to give oxaloacetate

38
Q

oxidative decarboxylation done by

A

PDH Enzyme complex

39
Q

location of oxidative decarboxylation
Structure of PDH complex

A

1- mitochondrial matrix
2- multi enzyme that cntains 3 enzymes
• pyruvate decarboxylase
• dihydrolipyol transacetase
• dihydolipyol dehydrogenase

and 5 co enzymes ( derivatives of viamin b complex )
• thiamin pyrophosphate ( TPP)
• lipoamide
• Co enzyme A ( CoASH)
• flavin adenine dinucleotide ( FAD )
• nicotanamide adenine dinucleotide ( NAD)

40
Q

Prods of oxidative decarboxylation of pyruvate

A

Acetyl CoA and one mole of NADH+H that gives 3 ATP due to ETC and Co2

41
Q

Importance of PDH complex job

A

Converting pyruvate to acetyl CoA (irreversible step towards the complete oxidation of glucose)

42
Q

Significance of PDH complex

A

1- fat can’t be converted to cho because the irreversible function of PDH
2- PDH defect can lead to lactic acidosis and it can be due to arsenic that forms complex with lipoamide
3- thiomine deficiency affects PDH and hence the complete oxidation of glucose and may lead to lactic acidosis as well
4- PDH is also inhibited by arsenate

43
Q

Regulation of PDH COMPLEX

A

1- Allosteric effect

Activator : pyruvate
Inhibitor : acetyl CoA and NADH ( product inhibition)

2- covalent modification

Phosphorylation ~> inactive
DePhosphorylation ~> active

Phosphorylation is done by Mg ATP DEPENDANT PDH KINASE that is activated by acetyl CoA and NADH and ATP and inhibited by NAD and ADP and pyruvate

DEPHOSPHORYLATION is done by PDH phosphatase that activated by Mg and Ca and insulin

44
Q

Carboxylation of glucose
• def
• done by
• co enzymes

A

Co2 fixation
Pyruvate carboxylase
Biotin as co enzyme with ATP and Co2

45
Q

Krebs cycle
•def
• location

A

• the final common oxidative pathway that oxadizes acetyl CoA to give energy Co2 and H2o

• the enzymes are located in mitochondrial matrix except succinate dehydrogenase in inner mitochondrial membrane as it acta as complex 2 in ETC

46
Q

Steps of krebs cycle

A

8 steps
1 r ~> a keto glutarate dehydrogenase
~> fumrase

Aconitase there is no r
And no p زيادة

47
Q

Regulation ofcitrate synthase

A

<2>
1- is activated by ADP and NAD Acetyl Coa and oxaloacetate
2- inhibited by ATP NaDH and citrate and succinyl CoA

48
Q

Aconitase inhibitor

A

1- inhibited by fluroacetate resulting in preventing isocitrate and accumulation of citrate

49
Q

Talk about isocitrate dehydrogenase

A

<4>
The major control enzyme
Is activated by ADP and NAD
Is inhibited by ATP and NADH
there are 3 types , one of them is NAD specific present in mitochondria and the 2 are NADP specific present in mitochondria and cytosol

50
Q

Talk about a ketoglutarate dehydrogenase complex

A

<3>
1- activated by ADP and NAD
2- inhibited by ATP AND NADH and succinyl CoA and arsenate
3- like PDH complex , it is multi enzyme that needs thiomin, lipoc acid, NAD , FAD and CoASH

51
Q

Talk about succinate thiokinase ( succinyl CoA synthatase

A

1- CATALYSE substrate level phosphorylation converting GDP TO GTP

52
Q

Talk about succinate dehydrogenase

A

• is inhibited by malonate and oxaloacetate
• located in inner mitochondrial membrane as it acts as complex 2 for ETC

53
Q

What is the main regulatory mechanism of krebs cycle

A

The respiratory control ( prescence of O2) :-

The activity of TCA depends on the activity of ETC which is dependent upon the availability
of oxygen and ADP and the rate of ATP utilization. O2 decreas affects TCA through regeneration of oxidized dehydrogenase co factors as NAD AND FAD

54
Q

What is the irreversible reactions in krebs cycle

A

1- citrate synthase
2- a ketoglutarate dehydrogenase complex

55
Q

Energy produced in citric acid cycle

A

1- ATP ~> succinate thiokinase
2- NADH which gives 3ATP ~> isocitrate dehydrogenase

3- NADH which gives 3 ATP ~> a ketoglutarate dehydrogenase complex

4- NADH which gives 3 ATP ~> malate dehydrogenase

5- FADH2 which gives 2 ATP ~> succinate dehydrogenase

12 ATP

56
Q

How 38 ATP COMES FROM GLUCOSE OXIDATION

A

Pyruvate ~> acetyl CoA ( NADH ~> 3ATP )
Acetyl CoA ~> Krebs cycle ( 12 ATP )

Glycolysis gives 2 pyruvate
2 * 15 = 30

Glycolysis ~> 8 or 6 ATP ( according shuttle)

So it is 38 or 36

57
Q

Roles of vitamins in TCA CYCLE

A

niacin ( vitamin b3) in form of NAD

Riboflavin ( vitamin b2) in form of FAD

Thiomin pyrophosphate and pantothenic acid that is co factor for PDH and a ketoglutarate dehydrogenase

58
Q

Importance of Krebs cycle

A

1- it the final oxidative pathway for acetyl CoA coming from lipids protein and cho
2- it connects protein lipid and cho metabolism
3- it is the main energy source ( except for cell with no mitochondria or anerobic tissue)
4- it is a source of succinyl CoA that is used in Hb synthesis and detoxification and ketone bodies
5- it is an amphibolic pathway : TCA metabolites have more than one function and occur at the crossroads of catabolic and anabolic pathways , therefore TCA plays an important role in : gluconeogensis and lipogensis and transamination

Gluconeogensis : all members are glucogenic , they are converted to oxaloacetate, the latter can generate PEP by PEP carbokinase

Transamination
Oxaloacetate ~> asprtate
a ketoglutarate ~> glutamate
Pyruvate ~> alanine

Lipogensis : actyel CoA is asource for fatty acid synthesis

59
Q

What is special about krebs cycle

A

There is no hormonal control of the cycle

Not affected by fasting or fed state

Control is exerted by energy status of the cell through Allosteric activation or deactivation

60
Q

Other names of Krebs cycle

A

• TCA
• citrac acid
• acetyl CoA cycle

61
Q

Oter Name of glycolysis

A

EMP = embeden myerhof pathway
Parnas cycle

Nutrition Bio (8 decks)

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