17A02: Exam Report

Outline the components of dietary fat (20% of marks). Describe their possible metabolic fates (80% of marks).

21% of candidates passed this question.

Almost all candidates interpreted “metabolic fate” to mean absorption, digestion and transport of fat. Hence a lot of time was spent on this and little on the fate of fat once it enters the blood stream. The processes of neither beta oxidation, nor lipogenesis were not well understood. Ketone body production was better understood.

14B09: Exam Report

Outline the fate of the triglyceride component of orally ingested fat

8% of candidates passed this question.

Triglycerides (TGs) consist of a 3 carbon glycerol backbone with 3 fatty acids attached. It was expected candidates would detail the fate from digestion and absorption, through distribution to storage and metabolism. Most candidates knew the absorptive processes very well but knowledge of TGs fate once it was packaged into a chylomicron was lacking. Some detail was expected on the passage to the liver via the portal circulation, packing and unpacking and distribution to the body. Very few candidates mentioned appropriate hormones and enzymes, target cells or ketogenesis. Some discussion was expected on the possible fate of acetyl Co A. Comment on the synthesis of lipids and the existence of essential fatty acids gained additional marks.

Pi / 17A02 / 14B09: Outline the components of dietary fat (20 marks). Describe their possible metabolic fates (80 marks)

Dietary Fat

  • Lipids are available to body from 3 sources
    1. Food
    2. Stored in AT tissue
    3. Synthesised in liver
  • Lipids from food:
    1. Triglycerides = 1 glycerol + 3 FAs
      • Fatty Acids = long hydrocarbon chain with a carboxyl group (COOH)
        • COOH is what makes it an acid
        • Saturated/unsaturated
        • Short/medium/long chain
        • 2 essential FAs: omega 3 FA & omega 6 FA
    1. Phospholipids
    2. Cholesterol


Fat from diet

Broken down by pancreatic lipase

absorbed & packaged


Absorbed in lacteal vessels (lymph caps)

Chylomicrons do not enter liver

Chylomicrons are transported & via Thoracic Duct empty into venous circulation at junction of jugular & subclavian veins




Broken down by LIPOPROTEIN LIPASE which hydrolyses TAGs → releasing Glycerol & FAs

Lipoprotein lipase is synthesised by skeletal m. & AT

  • ↑ [Insulin] after meal stimulates AT to ↑lipoprotein lipase secretion
  • FAs/Glycerol then taken up by other tissue


  • Muscles: oxidised to produce E
  • Adipose tissue: re-esterified & stored as TAGs (adipocytes are 95% TAG by volume)
  • Liver:

a. oxidised to provide E

b. precursors to ketone bodies

c. converted to VHDL for storage



  • To obtain E from fat, TAGs must be hydrolysed into FAs + glycerol
  • Occurs in cytoplasm
  • Stimulated by Hormone Sensitive Lipase (HSL)
  • Activated by ↓[insulin], ↑[cholesterol]
  • FAs then oxidised by β-oxidation into Acetyl CoA
  • Acetyl CoA enters Krebs
  • Glycerol enters glycolysis


    • Occurs in cytoplasm
    • FAs converted → Fatty Acyl CoA
    • FA combines with Carnitine
    • FA-Acyl-Carnitine can be transported across mitochondrial membrane
    • In mitochondrial matrix, Fatty-Acyl-Carnitine is converted back → Fatty Acyl CoA → Acetyl CoA → Kreb’s → ATP


  • Ketones are an alternative E source
  • Oxidised to produce E for brain
  • Excess acetyl CoA/extreme starvation stimulates ketone production:

Acetyl CoA + Acetyl CoA

Acetoacetyl CoA




(1° ketone in blood)

Ketones are freely diffusible

Oxidised to provide E for brain




Acetoacetyl CoA

Acetoacetyl CoA + Acetoacetyl CoA

Enters Krebs

  • If ketones are produced faster than they’re used → broken down to CO2 + acetone → exhaled


  • Excess acetyl CoA → converted to TAGs → stored in adipose tissue
  • Occurs in cytoplasm of adipocytes & hepatocytes
  • Most Acetyl CoA formed from glycolysis
  • One Acetyl CoA has 2-C added to it from another Acetyl CoA
  • Process repeats until you have FA of appropriate length → storage