Tg estimation practical for mbbs, bds, nursing, bmlt

1. ESTIMATION OF
TRIACYLGLYCEROL/TRIGLYC
ERIDE FROM GIVEN SAMPLE
Binaya Tamang
UCMS-Bhairahawa

2. INTRODUCTION
• The fats and oils are chemically triacylglycerols.
• Esters of glycerol with 3 F.A.
• non-polar in character
• neutral fats.
• Synth; In all tissue ( major: adipose tissue, liver)
• Function.
– Stored in adipose tissue as fuel reserve.
– Reserve as essential F.A.
– Precursors of eicosanoids

3. TRIGLYCERIDES / TRIACYLGLYCEROLS
(TGs / TAGs)

4. Properties of TGs
Properties
Hydrolysis By Lipase into FFA and glycerol
Saponification By alkali into glycerol and soaps
Rancidity Deterioration of TG to unpleasant taste and ordour
Lipid peroxidation Oxidation of lipids in living cells to produce peroxides and
free radicals

5. Types of TGs.
• Simple triacylglycerols contain the same type of fatty acid
residue at all the three carbons e.g. Tristearoyl glycerol or
tristearin.
• Mixed triacylglycerols: They contain 2 or 3 different types of
fatty acid residues. more common. E.g., 1,3 palmitoyl 2
linolenoyl glycerol.
• In general, fatty acid attached to C1 is saturated, that
attached to C2 is unsaturated while that on C3 can be
either.

7. REFERENCE RANGE IN SERUM:
• Normal: < 150 mg/dl
• Borderline high: 150 -199 mg/dl
• High: 200 -499 mg/dl
• Very high: > 500 mg/dl

8. CLINICAL SIGNIFICANCE
HYPERTRIGLYCERIDEMIA
– Primary : familial/ genetic
– Secondary: acquired/ medical condition AND drugs

9. Secondary: acquired/ medical condition
- Obesity
- Diabetes Mellitus
- Nephrotic syndrome
- Hypothyroidism
- Alcoholism
- Estrogen administration
- Various drugs: β blockers, thiazides etc.

10. • HYPOTRIGLYCERIDEMIA
- Large dose of ascorbic acid
- Drugs: Oral hypoglycemics, heparin etc.
- Hyperthyroidism
- Malnutrition
- Malabsorption
- Liver failure
NOTE: In clinical context, it is
hypertriglyceridemia, or rather dyslipidemia, that
is more relevant

11. • OBESITY
- High carb. and fat diet leading to increased synthesis.
- Less utilization related to lifestyle and genetic factors.
• DIABETES MELLITUS
Decreased amount &/or activity of insulin
↓ed LPL activation in vessel ( ↓ed clearance TG rich lipoproteins)
↑ed lipolysis (HSL)in adipose tissue ( ↑ed influx of FFA to liver
hepatic TG ↑es)
As a result high TG in blood.

12. Alcoholism
Change in redox potential (↑ed
NADH/NAD+ ratio) high energy
level
↓ed TCA cycle and β oxidation of fatty
acid.
favors lipogenesis ( acetyl coA to FA
synthesis TG )
- High TG
fatty liver

13. • Nephrotic syndrome
- Loss of albumin  compensatory increase of lipoprotein by
liver (Apo B-100)↑es VLDL and IDL.
- Also, in nephrotic patient the Lipoprotein lipase and hepatic
lipase activity is ↓ed clearance of TG.
• Hypothyroidism
- Decreased LPL activity low clearance of VLDL in blood.
- ↑ed TSH ↑es HSL activity in adipose tissue more FFA in
serum esterification  ↑ TAG in blood.
- various other factors (many genes of FA/Chol. synthesis and
breakdown are affected).

14. Some clinical signs
Arcus senilis
Lipemia
retinalis
Eruptive
xanthomas
White ring
White
blood
vessel of
retina

15. QUANTITATIVE ESTIMATION OF TG
(GPO METHOD)
PINK/RED
Sample: serum/fasting: to reduce effect of
chylomicron TAG.

16. B S T
Reagent (ml) 1 1 1
Standard
(μl)(200mg%)
- 10 -
Sample (μl) - - 10
-Incubate at 370C for 10 min.
-After the reaction is complete, measure the absorbance of S and T
against reagent blank (B) at 520 nm.