Hepatic Ketogenesis and Peripheral Ketone Body Utilization in the Ruminant

Abstract

Hepatic and alimentary ketogenesis occur at similar rates in fed, nonpregnant, nonlactating goats, sheep and dairy cows. Alimentary ketogenesis begins to diminish within 24 h after fasting but compensatory increases in hepatic ketogenesis maintain total splanchnic release and, therefore, no change in circulating concentrations of ketone bodies is observed. By the third day of fast the gut is utilizing acetoacetate and beta-hydroxybutyrate and alimentary ketogenesis has ceased. Hepatic ketogenesis of both ketone bodies accelerates rapidly due to portal-drained visceral and hindquarter lipolysis and subsequent hepatic fatty acid uptake and total circulating concentrations are doubled. During pregnancy and lactation in sheep and cows alimentary ketogenesis is maintained as long as digestible organic matter intake is constant. Hepatic and total splanchnic release of beta-hydroxybutyrate increases in late gestation and early lactation. Again, this is due to increased portal-drained visceral and hindquarter free fatty acid release and hepatic free fatty acid uptake. Hindquarter uptake of both ketones during late gestation is similar to the ratio observed in nonpregnant fed sheep but the percentage of utilization decreases, perhaps reflecting partitioning to uteroplacental tissues. Hindquarter uptake of both ketone bodies in sheep increases in early lactation due to increased circulating concentrations because extraction ratios are similar to those of fed animals. Ketosis during pregnancy in sheep and lactation in cows may be prevented by beta-hydroxybutyrate stimulation of pancreatic insulin production. However, an insulin-independent intrahepatic mechanism apparently occurs in sheep.(ABSTRACT TRUNCATED AT 250 WORDS)

Valores de referência e influência dos fatores etários, sexuais e da gestação no lipidograma de bovinos da raça Holandesa, criados no Estado de São Paulo

“…Os produtos finais da fermentação de carboidratos, acetato e butirato, podem ser convertidos em acetoacetato e β-HBO durante a absorção pelo epitélio ruminal, sendo assim denominada a cetogênese alimentar. Os corpos cetônicos circulantes no ruminante são 4-5 vezes maiores que o encontrado em animais não-ruminantes (HEITMANN et al, 1987).…”

“…Heitmann et al (1987), afirmaram que os ruminantes diferem, entre outros aspectos, dos demais monogástricos na medida em que grande quantidade de corpos cetônicos alimentares são liberados na veia porta devido à presença de fermentação bacteriana no rúmen. Os produtos finais da fermentação de carboidratos, acetato e butirato, podem ser convertidos em acetoacetato e β-HBO durante a absorção pelo epitélio ruminal, sendo assim denominada a cetogênese alimentar.…”

“…Os produtos finais da fermentação de carboidratos, acetato e butirato, podem ser convertidos em acetoacetato e β-HBO durante a absorção pelo epitélio ruminal, sendo assim denominada a cetogênese alimentar. Os corpos cetônicos circulantes no ruminante são 4 -5 vezes maiores que o encontrado em animais não-ruminantes (HEITMANN et al, 1987). A partir do momento em que ocorre a desmama aliado ao ativo desenvolvimento ruminal, há o aumento da concentração sérica de β-HBO devido à cetogênese alimentar, permanecendo fisiologicamente desta forma as faixas etárias subseqüentes.…”

Pregnancy toxaemia of ewes. A literature review

“…Στο τελικό στάδιο της κΰησης η έκκριση ινσουλίνης και η συγκέντρωση της στο πλάσμα μειώνονται 7 . Αντιθέτως, η συγκέντρωση της αυξητικής ορ μόνης, της προλακτίνης, της γαλακτογόνου ορμόνης του πλακοΰντα, των οιστρογόνων και της προγεστερόνης αυ ξάνεται 16 . Η αΰξηση της έκκρισης προλακτίνης και της αυ ξητικής ορμόνης προκαλεί αναστολή της δράσης της ιν σουλίνης στο λιπώδη ιστό επηρεάζοντας την κατανομή των αμινοξέων μεταξΰ ήπατος και εξωηπατικών ιστών 6 .…”

“…Τα ζώα σε φυσιολογικό ενεργειακό ισοζΰ-γιο επανεστεροποιοΰν τα NEFA στο ήπαρ και τα επανεκ-κρίνουν ως VLDL. Η γλυκόζη μετατρέπεται σε 1-φωσφο ρική γλυκερόλη, η οποία απαιτείται για την εστεροποίηση των NEFA εκτός των ηπατικών κυττάρων 16 . Όμως όταν συ νυπάρχει έλλειψη ενέργειας και αυξημένη παραγωγή NEFA, αυτά οξειδώνονται σε κετονικά σώματα 72930 .…”