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Setchell KD, Gosselin SJ, Welsh MB, Johnston JO, Balistreri
WF, Kramer LW, Dresser BL, Tarr MJ Gastroenterology 1987 Aug 93:2
225-33
Abstract
The cheetah in the wild is ''racing towards extinction''
mostly due to habitat destruction. Its survival will probably depend
on accelerated captive breeding. At this time, however, reproductive
failure and liver disease threaten the future of the captive cheetah
population. Histopathological evaluation of more than 100 cheetah
livers identified venocclusive disease as the main hepatic lesion
responsible for liver disease in this species. Analysis of the commercial
feline diet by high-performance liquid chromatography and gas-liquid
chromatography-mass spectrometry revealed large amounts of two phytoestrogens
identified as daidzein and genistein. These compounds were found
to be derived from a soybean product that was a component of the
cheetah diet, and their concentrations both ranged from 18 to 35
micrograms/g diet. The adult cheetah consequently consumes approximately
50 mg/day of these weak estrogens. When extracts of the diet were
tested for estrogenicity using a bioassay, a dose-related increase
in uterine weight was observed. In 4 cheetahs studied, withdrawal
of this feline diet by substitution with a chicken diet resulted
in an improvement in conventional liver function tests and a normalization
in the appearance of hepatic mitochondria. We conclude that the
relatively high concentrations of phytoestrogens from soybean protein
present in the commercial diet fed to captive cheetahs in North
American zoos may be one of the major factors in the decline of
fertility and in the etiology of liver disease in this species.
The survival of the captive cheetah population could depend upon
a simple change of diet by excluding exogenous estrogen.
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