This document summarizes lipid catabolism and metabolic pathways. It defines lipids and describes their functions. It then explains that catabolism breaks down nutrients into energy through ATP or heat. Specific pathways covered include digestion and absorption of lipids, free fatty acid mobilization, lipid activation, beta-oxidation of fatty acids in the mitochondria, and ketogenesis. Clinical correlations are discussed for conditions related to defects in these lipid catabolic pathways such as weight loss, steatorrhea, hypoglycemia, neurological disorders, metabolic acidosis, and bad breath.
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lipidcatabolism2016431008-190412173810.pptx
1. Lipid Catabolism
Metabolic Pathways & Clinical Correlations
Kazi Tarmeem Noor
#2016431008
Department of Genetic Engineering & Biotechnology
Shahjalal University of Science & Technology, Sylhet
2. Definition & Function
LIPID
Non polar
Water insoluble
Carbonyl containing
Organic compound
Membrane
structural
component
Storage depot
& transport
form of
metabolic fuel
Nerve ending
receptors &
neuro-
transmitters
Bacterial
membrane &
exoskeleton
Enzyme
co-factor
3. Metabolism
Catabolism
Breakdown of nutrient
molecules
Energy stored as ATP or
yielded as heat
Bioenergetic applications Clinical approaches
Anabolism
Biosynthesis of
macromoleculesfrom
catabolic products
Energy absorbed
Cell structure
maintenance
4. Digestion, Absorption & Metabolic Fate
Lingual Lipase degrades
TG to free FA & glycerol
Gastric Lipase
Hydrolyzes TG to
micelles
Intestinal Mucosa forms
chylomicrons
Chylomicrons travel
through blood & Lymph
Lipoprotein Lipase &
apo-C II releases FA &
Glycerol
Free FA & Glycerol enter
cell to be oxidized
6. Free Fatty Acid Mobilization
Receptors activated by hormones
(glucagon, epinephrine)
cAMP from activated receptor
activates Protein Kinase
PKA then activates Hormone
Sensitive Lipase (HSL)
PKA phosphorylates perilipin (blocks
access to fat globules when not
phosphorylated)
HSL then hydrolyses TAGs in adipose
storage to release FFA
FFA then enters blood stream
Transported to tissues like myocytes
bound to albumin
7. Lipid Activation
Glycerol produced from hydrolysis of TAG is
converted to Dihydroxy Acetone Phosphate
DAH is isomerized to Glyceraldehyde-3-
Phosphate
G-3-P moves through Glycolysis and then
into Krebs Cycle to produce Energy by
Lipolysis
8. β oxidation
Fatty Acid Activated to Fatty Acyl Co-A
FA Co-A dehydrogenated to make
double-bond between α and β carbon
Double bond hydration
Β-hydroxyl group dehydrogenated to
ketone
Co-A added & acetyl Co-A Produced
9. β oxidation energetics
Each β-oxidation cycle
C(n)Acyl-CoA + CoA-SH + FAD + NAD+ + H2O → C(n-2)Acyl CoA + Acetyl CoA + FADH2 + NADH + H+
Complete oxidation of Palmitoyl CoA
Palmitoyl CoA + 7CoA-SH + 7FAD + 7NAD++ 7H2O → 8Acetyl CoA + 7FADH2+ 7NADH + 7H+
Converting NADH and FADH2 to their corresponding ATP equivalents
Palmitoyl CoA + 7CoA-SH + 7O2 + 28Pi + 28ADP → 8Acetyl CoA + 28ATP + 7H2O
After Acetyl CoA molecules enter Krebs cycle and Electron Transport System
8Acetyl CoA + 16O2 + 80Pi + 80ADP → 8CoA + 80ATP + 16CO2 + 16H2O
Thus complete energy release
Palmitoyl CoA + 23O2 + 108Pi + 108ADP → CoA + 108ATP + 16CO2 + 23H2O
There is utilization of ATP during the conversion
of palmitic acid to palmitoyl-CoA
the net gain is ≈106 ATP.
All the above calculations are done considering
one molecule of NADH gives 2.5 molecules of ATP
and
one molecule of FADH2 gives 1.5 molecules of ATP
in the Electron Transport System.
