Answers are grounded in this paper and cite their sources.
These data would indicate that crude “toxic fat” has a marked effect on testicular development without appreciably affecting the development of secondary sex characters or growth rate. At levels of 0.5 and 1.0% “toxic fat,” reduced testicular development usually occurred in conjunction with hydropericardium and ascites. When the level of fat was reduced to 0.25%, hydro-pericardium and ascites was markedly reduced, whereas, retarded testicular development persisted. It would appear that in immature chickens testicular hypoplasia resulting from consumption of crude “toxic fat” is a more sensitive index of toxicity than is hydropericardium or ascites.
No takes yet. Share an insight, caveat, or question.
Allen et al. (1962) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: