fructose metabolism

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FRUCTOSE METABOLISM

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Fructose Metabolism. ATP ADP. ATP ADP. 2) dihydrous aceton PO 4. + Glyceraldehyde-3-PO 4. Phospatase. F-1-PO 4. F-1,6 diPO 4. Isomerase. Phospatase. G-6-PO 4. Glucose. Fructose. 1) Glyceraldehyde. F-1-PO 4. It is converted into glucose in liver and intestine. CHO | - PowerPoint PPT Presentation

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Page 1: Fructose Metabolism

FRUCTOSE METABOLISM

Page 2: Fructose Metabolism

IT IS CONVERTED INTO GLUCOSE IN LIVER AND INTESTINE .

Fructose F-1-PO4 1) Glyceraldehyde

Phospatase

2) dihydrous aceton PO4

ATP ADP

F-1,6 diPO4

+Glyceraldehyde-3-PO4

F-1-PO4

Isomerase

G-6-PO4 Phospatase

Glucose

ATP

ADP

Page 3: Fructose Metabolism
Page 4: Fructose Metabolism

- ESSENTIAL FRUCTOSURIA :

INHERITED DUE TO DEFICIENCY OF FRUCTOKINASE ENZYME

( BENIGN ) .

- HEREDITARY FRUCTOSE INTOLERANCE :

DEFICIENCY OF ALDOLASE B ACCUMULATION OF FRUCTOSE-1-

PHOSPHATE WHICH DECREASE PHOSPHORYLASE ENZYME OF

GLYCOGENOLYSIS WHICH LEAD TO HYPOGLYCEMIA .

NAD NADH+H

dehydrogenaseAldose reductase

CHO|

H-C-OH|

R

CH2OH|

H-C-OH|

R

CH2OH|

C=O|

R

NADHph + H+

Glucose Sorbitol Fructose

Page 5: Fructose Metabolism

GALACTOSE METABOLISM

Page 6: Fructose Metabolism

CONVERSION OF GLUCOSE INTO GALACTOSE :

UDP - Galactose ( Activedonnes) :

1- Glycolipid synth.

2- Lactose formation .

3- Mucopolysaccharide.

4- glycosaminoglycone ( GAGs ).

Page 7: Fructose Metabolism
Page 8: Fructose Metabolism
Page 9: Fructose Metabolism

GALACTOSEMIA IT IS THE INCREASE IN BLOOD GLACTOSE CONC. DUE TO INABILITY TO METABOLIZE GALACTOSE.CAUSES: INHERITED ENZYMES DEFICIENCY A) GALACTOKINASE. B) GALACTOSE-1-P-URIDYL TRANSFERASE. C) EPIMERASE.EFFECTS: 1- CATARACT. 2- LIVER FAILURE. 3- MENTAL RETARDATION.

Blood Glucose

Plasma Glucose level:A. Fasting level 70-110 mg/dl.B. one hour after meal 120-150.C. two hours after carbohydrate meal (post prandial ) till 140.

Page 10: Fructose Metabolism

1. FROM C,H,O IN DIET.

2. GLUCOGENIC COMPOUND.

3. PROPIONATE.

4. LACTATE ( IN SKELETAL MUSCLE AND RBC ).

5. AMINO ACID TRANSFERRED FROM MUSCLE TO LIVER.

6. DIETARY CARBOHYDRATE E.G. STARCH.

7. FROM LIVER GLYCOGEN THROUGH GLYCOGENOLYSIS

(FOR 18 H FASTING).

8. AMINO ACID AND OTHER METABOLITES

( GLUCONEOGENESIS ).

LIVER AND KIDNEY CAN CONVERT THESE SUBSTRATES

INTO GLUCOSE.

Source of blood glucose:

Factors that add glucose to blood1. Carbohydrate diet.

2. Glycogenolysis.

3. Gluconeogensis.

Page 11: Fructose Metabolism

FRUCTOSE REMOVE GLUCOSE FROM

BLOOD

1. UPTAKE BY TISSUE

2. EXCRETION IN URINE

3. UTILIZATION

A. OXIDATION

B. LIPOGENESIS

C. GLUCOGENESISETABOLISMI. Regulation of Blood Glucoseblood glucose is maintained 70-110mg because:

hyperglycemia (increase blood glucose) can cause cerebral

dysfunction but its effect on extra cellular osmolarity.

II. hypoglycemia cause impairment of cerebral function as

brain is very

dependent on blood glucose for energy

Page 12: Fructose Metabolism

Regulation of Blood GlucoseRegulation of glucose

1- hormonal 2- hepatic 3-renal

1) Hormonal regulation:

Page 13: Fructose Metabolism

*INSULIN:INSULIN IS HORMONE SECRETED BY Β-CELL OF LANGERHANS

OF PANCREAS. IT IS ONLY HORMONE WHICH REDUCE BLOOD

GLUCOSE LEVEL.

1. TRANSFER GLUCOSE INTO CELLS.

2. INCREASE GLYCOGEN STORAGE.

3. STIMULATE GLUCOSE OXIDATION.

4. DECREASE GLYCOGEN BREAKDOWN.

5. DECREASE GLYCONEOGENSIS.

6. INCREASE LIPOGENSIS.

Page 14: Fructose Metabolism

*GLUCAGON:HORMONE SECRETED BY Α CELL OF PANCREAS INCREASE

BLOOD GLUCOSE BY:

1. INCREASE GLYCOGEN BREAKDOWN BY INCREASE ADENYL

CYCLASE AND INCREASE

GLYCONEOGENSIS.

2. CATECHOL AMINES : FROM SUPRARENAL MEDULLA ↑ BLOOD

GLUCOSE BY :

A) ↑ GLYCOGENOLYSIS

B) ↑ GLUCOSE UP TAKE BY LIVER

3. GLUCOSTEROID AS CORTISOL : BY SUPRARENAL CORTEX .

↑ BLOOD G BY :

A) ↑ GLUCONEOGENESIS

B) ↓ OF GLUCOSE UP TAKE BY TISSUES

4. GROWTH HORMONE SECRETED FROM ANTERIOR PITUITARY

GLAND

A) ↓ OF G UP TAKE BY TISSUE

B) BLOCKS INSULIN ACTION IN ALL MEMBRANES.

Page 15: Fructose Metabolism

*IN FASTING STATE:1. IT ADD GLUCOSE TO BLOOD BY

GLYCOGENOLYSIS AND GLUCONEOGENESIS.

2. CONVERT FATTY ACID ( ACETYL COA) → KETON BODIES.*IN FED STATE :

1. CONVERT GLUCOSE INTO GLYCOGEN. 2. CONVERT GLUCOSE INTO FATTY ACID

2) Hepatic regulation

Blood glucose is filtered in glomular filtrate and reabsorbed again.

* If blood glucose exceeds certain limit (180 mg/dl), glucose will increase

and exceed the capacity of tubular enzyme to reabsorb. So it will appear

in urine (called glycouria). Renal Threshold

3) Renal regulation

Page 16: Fructose Metabolism

1. HYPERGLYCEMIA: IT IS RISE OF BLOOD GLUCOSE CAUSES: 1. DIABETES MELLITUS 2. RECEIVE I.V. FLUIDS CONTAINING GLUCOSE 3. SEVERE STRESS 4. IN CEREBRO-VASCULAR ACCIDENTS5. DISTURBANCE IN HYPERGLYCEMIC HORMONES

II) HypoglycemiaIf blood glucose decreased (less than 45 mg/dl), that would cause cerebral dysfunction if prolonged cause death (so "GLUCAGON" must be taken)Symptoms :Headache, Confusion, Hunger, Anxiety, Slurred speech, palpitationCauses :

1. Fasting2. due to organ disease :

- Pancreatic: insulinoma (Tumor)- liver disease: hepatic carcinoma

3. Glycogen storage disease4. Starvation5. Adrenocortical disease (↓ epi)

Page 17: Fructose Metabolism

STIMULATIVE:

1. DRUGS: OVERDOSE OF INSULIN

2. OVERDOSE OF ORAL HYPOGLYCEMIC

AGENTS

3. LIVER POISON AS CHLOROFORM,

ALCOHOL

4. POSTGASTRECTOMY (INCREASE

ABSORPTION OF GLUCOSE)

5. GALACTOSEMIA

6. HEREDITARY LACTOSE INTOLERANCE

Page 18: Fructose Metabolism

DIABETES MELLITUSIt is a state of chronic hyperglycemia (Glucose urea). Relative or absolute

deficiency of insulin hormone Biochemical disturbance of diabetes mellitus1) Carbohydrate:↓Glucose uptake by tissue ↓oxidation ↑gluconeogenesis and↑glycogenolysis ↓intracellular glucose →hunger (polyphagia)* Increase blood glucose by: a) Increase plasma osmolarity → dehydration. b) Dehydration of brain cells (coma). c) Dehydration of body cells "thirst" (polydepsia). d) Glucose urea: frequent urination loss of vitamin B1 loss of K+, Na+

Protein metabolism: *Increase protein breakdown.

* Increase gluconeogensis (amino acid convert to glucose)1.phosphatase release2. excess breakdown of tissue protein (muscle

wasting)3. decrease antibody.4. poor wound healing.

Page 19: Fructose Metabolism

3) LIPID METABOLISM:

EXCESS LIPOLYSIS MOBILIZATION OF FREE FATTY ACID

AND GLYCEROL TO TISSUE AND LIVER LEAD TO:

1. LOSE WEIGHT.

2. HYPERLIPIDEMIA (ATHROSCLEROSIS)

3. FATTY LIVER

4. EXCESS KETON BODIES (KETONEMIA, KETOSIS), WHICH

LEED TO KETOTIC

COMA, HYPERKALEMIA

4) MICROANGIOPATHY:

DEGENERATION AFFECTED BLOOD VESSELS OF KIDNEY

AND RETINA OF EYE. (RENAL FAILURE, BLINDNESS.

Page 20: Fructose Metabolism

Non - insulin dependent NIDDM

Insulin - dependentIDDM

Type 2 (adult-onset Diabetes)

Type 1 (juvenile Diabetes) names

After 35 old During childhood Age of onset

obesity thin Nutriamial stute

80-90% of digorosed 10-20% of diabetes Presalenes

Very strong moderate genetic

Insulin resistance in insulin level

β cell destroyed no insulin Defect in β cells

Rare Common Ketosis

Hyperosmolar coma Keto acidosis Acute complications

responsive No response Oral hypoglycogenic drugs

Usually not reqaired Always necessary Treatment with insulin

Page 21: Fructose Metabolism

DIAGNOSIS OF DIABETES MELLITUS1. glucose tolerance test

2. fasting blood glucose not more than 110 mg/dl

3. two hrs post (prandial) must be within the normal fasting level.

4. Glycosylated hemoglobin (HbA1C) it is a glycated protein which results

from simple non enzymatic reaction between globin part of HB and

glucose, its level in the red cells is directly proportional to the blood

glucose level at the time of formation of such cell, this level remains as

it for the whole life span of red blood cells 120 days

* It is useful for monitoring the degree of control of diabetes mellitus

during last 8-12 weeks before the test.

Normal 4 - 7.2%

5. plasma fructose amine

Albumin under go glycosylation

6. Microalbuminurea early detection of D.M. in urine by special kits.

Page 22: Fructose Metabolism

Renal threshold

hours

1 2 3 4

200

100

500Glucose in blood

180

normal

diabetic

Glucose tolerance curve

Page 23: Fructose Metabolism

Type of ComaThe Cause &

Effect of Coma on:Hypoglycemic Coma Diabetic Coma

Insulin overdose Sever untreated D.M The Cause

The Effect on:

Normal Acetone smell Mouth

Normal Hyperventilation Respiration

Rapid, strong Rapid, week Pulse

sweat Dry Skin

Absent Present Urine glucose

Absent Present Urine acetone

Page 24: Fructose Metabolism

Hypoglycemic coma Diabetic coma

Insulin overdose Severe untreated D.M Causes

Normal Acetone smell Mouth

Normal Hyperventilation Respiration

Rapid, strong Rapid, week Pulse

Sweet Dry Skin

Absent PresentUrine

glucose

Absent presentUrine

acetone