The effects of weaning and milk on mammary fatty acid synthesis

• 1.

  1. A mechanism is proposed to account for the rapid cessation of fatty acid synthesis in the lactating mammary gland following weaning. It is suggested that milk contains an inhibitor which accumulates with the retained milk and serves to shut off fatty acid synthesis.

• 2.

  2. Extracts of lactating rat mammary glands were prepared at various time intervals from 3 to 24 h following weaning. During this period there is a rapid accumulation of milk in the gland, measured by the lactose concentration in the extract and a concomitant diminution of fatty acid synthesis, measured by the incorporation of [¹⁴C]acetate into long-chain fatty acids. Fatty acid synthesis is partially restored in such extracts if the rat, whose young were removed 24 h previously, is sucked by another litter for 3–18 h, resulting in the removal of all the accumulated milk from the gland.

• 3.

  3. When access to some of the rat's mammary glands is prevented for 9 h while the other glands are suckled, milk accumulates in the obstructed glands. Extracts from such glands incorporate only one-tenth as much [¹⁴C]acetate into fatty acids as extracts from the suckled glands.

• 4.

  4. The addition of rat milk to an extract of actively lactating rat mammary gland results in severe inhibition of fatty acid synthesis.

• 5.

  5. Acetyl-CoA carboxylase (acetyl-CoA:CO₂ ligase (ADP), EC 6.4.1.2) was measured in (NH₄)₂SO₄-treated mammary extracts by the incorporation of NaH¹⁴CO₃ into malonyl-CoA. This enzyme is profoundly inhibited by the addition of rat milk.

• 6.

  6. The inhibitory activity is located in the particulate fraction of milk.