fructose metabolism
Post on 02-Jan-2016
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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
- 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
GALACTOSE METABOLISM
CONVERSION OF GLUCOSE INTO GALACTOSE :
UDP - Galactose ( Activedonnes) :
1- Glycolipid synth.
2- Lactose formation .
3- Mucopolysaccharide.
4- glycosaminoglycone ( GAGs ).
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.
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.
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
Regulation of Blood GlucoseRegulation of glucose
1- hormonal 2- hepatic 3-renal
1) Hormonal regulation:
*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.
*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.
*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
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)
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
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.
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.
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
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.
Renal threshold
hours
1 2 3 4
200
100
500Glucose in blood
180
normal
diabetic
Glucose tolerance curve
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
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
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