1. Serum Triglyceride Test20
Serum Triglyceride Test
Fifth Stage Student By
Dr. Sakar Karem Abdulla
M.Sc. Clinical Biochemistry

2. Triglyceride
TG are the major fat in the human diet and comprise 85-90% of body lipids.
TG are serve as energy reserve for the body and store in adipose tissue as lipid droplets.
TG in human plasma can be exogenous (derived from food) or can be endogenous (synthesized in the body).
TG contain a glycerol backbone to which three fatty acid are esterified.

3. Triglyceride structure

4. Digestion of Triglyceride
Action of bile salts: which emulsified dietary fat and increase surface area for attacked by pancreatic digestive enzyme.
Action of pancreatic lipase: major enzyme that digest dietary TG to free fatty acid and 2-monoacylglycerol.
Secretion of bile salt and pancreatic enzyme are stimulated by cholecystokinin.

5. Absorption and transport of dietary TG
The FA and 2-monoacylglycerol produced by digestion are packaged into micelles which is tiny microdroplet emulsified by BS and absorb to epithelial cell of the intestine.
Within intestinal epithelial cell FA and 2- monoacylglycerol are condensed to form TG.
Intestinal cell package TG with Cholesterol, protein, phospholipid and fat soluble vitamin in chylomicron.

6. Digestion and absorption of triglyceride

7. Fate of dietary TG in chylomicron

8. Synthesis of TG TGs are produced in liver and adipose tissue.
In liver glycerol-3-phosphate is produced from glycerol by glycerol kinase or from DHAP derived from glycolysis.
In adipose tissue glycerol-3-phosphate is produced only from DHAP derived from glycolysis.

9. Synthesis of TG

10. Fate of VLDL-Triglyceride

11. Storage of TG in adipose tissue

12. Release of FA from adipose tissue TGs

13. Hypertriglyceridemia
Hypertriglyceridemia: means high plasma concentration of triglyceride that include two types:
Primary Hypertriglyceridemia
Secondary Hypertriglyceridemia

14. Primary Hypertriglyceridaemia
Chylomicron syndrome
Familial lipoprotein lipase deficiency
Apolipoprotein C2 deficiency
Familial dysbeta-lipoproteinaemia
Familial hypertriglyceridaemia
Familial combined hyperlipidaemia

15. Secondary Hypertriglyceridaemia
Alcohol
Obesity
Diabetes mellitus
Chronic kidney disease
Hypothyroidism
Certain drugs e.g. estrogen, B-blocker

16. Reagents composition
R1 Buffer: magnesium chloride, chloro-4- Phenol, preservative
R2 Enzyms: lipase, peroxidase, glycerol 3 phosphate oxydase, glycerol kinase, 4 – Amino-antipyrine, ATP
R3 Standard: Triglyceride 200mg/dl
Reagent preparation: add the content of vial R2 into vial R1, mix gently until complete dissolution.

17. Principle of S.TG test
Triglycerides→ glycerol + free fatty acids(by Lipase)
glycerol+ ATP→ glycerol 3 phosphate + ADP (by glycerokinase)
glycerol 3 phosphate + O2 → dihydroxyacetone- phosphate+H2O2(by glycerol 3 phosphate oxydase)
H2O2+4-chlorophenol+PAP → quinoneimine + H2O (by peroxidase)
The absorbance of coloured complex proportional to the concentration of cholesterol in the sample

18. S.Triglyceride test
Patient should be fast overnight for 12hr, only allowed water to drink.
Patient should be on usual diet for two weeks preceding the test.

19. Test Procedure

20. calculation
S.Triglyceride=Abs.Assay/Abs.standard  x conc.standard (200mg/dl)
Normal value TG mg/dl