Post-Absorption:

1. Stored as fat in adipose tissue - (constant turnover)

2. Converted to acetyl - CoA via b -oxidation

acetyl CoA can be used for energy (NOT glucose), synthesis of fat, or formation of ketone body.

b -Oxidation - O₂ needed, so in the mitochondria.

Break down of fat to acetyl-CoA

One fatty acid goes through several cycles.

1 Cycle

1. takes off 2C - acetyl-CoA - 12 ATP

2. 1 FADH₂

3. 1 NADH

Takes 2 ATP to activate (initial investment)

Examples:

Caproic Acid C6:0 ® C₆H₁₂O₂

2 cycles of b -oxidation ®

3 acetyl CoA X 12 = 36 ATP

2 turns of cycle X 5 = 10 ATP

= 46 ATP - 2 ATP (initial investment) yields 44 ATP

Glucose only yields 36 ATP.

Stearic Acid C18:0

8 cycles of b -oxidation ®

9 acetyl CoA X 12 = 108 ATP

8 turns of cycle X 5 = 40 ATP

= 148 ATP - 2 ATP (initial investment) yields 146 ATP

Ketosis

General: Acetyl CoA can go to Krebs, Acetoacetate (then to acetone), or b -hydroxybutyrate.

Clinical Signs:

High blood ketone level

High urine ketone level

Low blood glucose

Breath smells like acetone, filtered through lungs

Causes:

1) body is dependant on gluconeogenesis (depletes OAA)

2) body mobilizing stored fat (b -oxidation ® increase acetyl-CoA)

3) Acetyl-CoA ® ketone bodies

When it occurs

1) starvation

2) high producing dairy cow (lactose - glu + gal), (no glu absorbed (glu)), (energy deficient - body fat - acetyl-CoA)

3) Late pregnant ewe with twins or triplets. Uterus increase - push against rumen, decrease DMI

Blood Changes: assume dairy cow

Treatment:

OAA precursors - enter Krebs as

- propionate - succinyl-CoA

- glutamate - a -ketogluterate

- aspartate - OAA