L11: Fatty Acid Catabolism Flashcards
what is the difference between glucose metabolism & fatty acid metabolism in terms of energy yield
- glucose metabolism yields ATP
- but F.A metabolism yields higher levels of ATP while regenerating glucose
the bulk of stored metabolic fuels is in what form & how long will this keep you alive for
stored metabolic fuel in the form of triacylglycerols in adipose tissue, sufficient to prolong life for 3 months
when does melting point increase
melting point increases with chain length (& decreases with number of double bonds)
when does melting point decrease
melting point decreases with the number of double bonds (increases w chain length)
when do fatty acids yield increased energy (in terms of structure)
the more carbons in the structure, the more energy is yielded
what enzyme causes serious defects
Acyl-CoA Dehydrogenase
symptoms of acyl-CoA dehydrogenase deficiency
- low energy
- fat accumulation
- vomiting
- sleeplessness
- coma
tx of acyl-CoA dehydrogenase deficiency
low fat and high carb diet
eating a little, but often
what is the most common acyl-CoA dehydrogenase deficiency
MCAD (Medium Chain Acyl-CoA Dehydrogenase Deficiency)
affects 1:66,000
what is the feature of NAFLD
deposition of excess TAGs in liver
5 causes of NAFLD
- Hep B
- Poisoning by excess lipid: less removal & breakdown = fatty infiltration into cells
- Modern malnutrition: less cofactors & AAs for proteiin synthesis
- Mobilisation of non esterified F.As from adipocytes - increase in fatty acids being synthesised
- Decreases oxidation of fat by hepatic cells
resuts of NAFLD
liver scarring & disease
Long term: liver failure
what is wolman’s disease a deficiency of
lysosomal acid lipase defiency
feature of wolman’s disease
certain fats abnormally accumulate in tissues & organs
symptoms of wolman’s disease
- swelling of stomach (abdominal distension)
- vomiting
- enlargement of liver/spleen (hepatosplenomegaly)
when does ketone body formation occur
to provide energy when carbohydrates unavailable - low card diet, starvation, fasting, untreated diabetes (conditions that support gluconeogenesis)
what is synthesised into ketone bodies in the liver
acetyl-CoA from beta oxidation synthesised into ketone bodies mainly in liver
2 common ketone bodies
acetoacetate & beta-hydroxybutyrate
where are acetoacetate & beta-hydroxybutyrate exported to & what do they do
they are blood soluble amalgamations of acetyl-CoA
exported in blood to organs that need energy where they reconvert to acetyl-CoA to give energy
what is exhaled as a result of ketone body formation
acetone
why does decreased food intake slow citric acid cycle
as oxaloacetate used for essential glucose synthesis
(oxaloacetate (OAA) — a critical molecule in the citric acid cycle — gets diverted away from the cycle to support gluconeogenesis)
why does acetyl-CoA accumulate after ketone body formation
Acetyl-CoA from beta oxidation cant enter TCA cycle & so accumulates
what does ketogenic diet do to body
forces it to burn/oxidise fats rather than carbs
what is keto diet used to treat
epilepsy
