Glucose Turnover and Hepatocyte Glucose Production of Starved and Toxaemic Pregnant Sheep

Abstract

Ewes bearing twins were starved for 10 days during the last month of gestation to induce ovine pregnancy toxaemia (OPT). Glucose turnover was measl,lred by a primed continuous infusion of [U_ '4C]_ and [6-3 HJglucose at the end of 10 days of starvation (non-susceptible), or earlier when ewes became recumbent with OPT (susceptible). All ewes were slaughtered at the end of the infusion and hepatocytes were prepared in order to measure glucose production from different substrates. Many of the ewes had dead foetuses when slaughtered. Glucose production rates by hepatocytes with the substrates propionate, lactate or alanine were significantly less from the susceptible ewes than were those from non-susceptible ewes. These low rates were not stimulated by incubation with glucagon (10-8 M), glutamine or glycerol. Rates of glucose turnover and of hepatic glucose production from all substrates were higher for ewes with dead than with live foetuses. The data support the hypothesis that pathogenesis of OPT is related to an impairment of hepatic gluconeogenesis, and further suggest that, in starved pregnant ewes, maternal glucose production may be restrained in the presence of a live foetus.

Altered plasma triglyceride-rich lipoproteins and triglyceride secretion in feed-restricted pregnant ewes

“…This finding is in agreement with previous reports (Wastney et al, 1983;Remesy et al, 1986;Emery et al, 1992). The observed metabolic response during pregnancy results from a higher lipid mobilisation in response to high energy needs (Christie, 1981).…”

Selected serum biochemical parameters and acute phase protein levels in a herd of Saanen goats showing signs of pregnancy toxaemia

“…In this study all goats with high serum glucose concentrations and which were in the last four weeks of the gestation period (Group 3), had two dead foetuses and these results are similar to previous reports. Hyperglycaemia occurs because foetal death removes the suppressing effect of the foetus on hepatic gluconeogenesis (Wastney et al 1983). Compared with the control (Group 1), glucose values were decreased significantly (P < 0.001) in Group 2 and only three of them delivered dead foetuses.…”

Indicadores bioquímicos e hormonais de casos naturais de toxemia da prenhez em ovelhas

“…Nas ovelhas acometidas por TP os valores encontrados para glicose apresentando três variações, , contradiz alguns relatos sobre o comportamento desta variável na patogenia da doença, em que a hipoglicemia é a anormalidade inicialmente mais detectada (Kranfield 1972, Wastney et al 1983, Scott et al 1995, Andrews 1997, Barakat et al 2007). Entretanto, em alguns casos naturais de TP relatados, a hipoglicemia parece ser consequência da hipercetonemia e da inapetência, antes de ser considerada a causa dessas mudanças (Andrews et al 1996, Henze et al 1998.…”

“…As alterações nos índices da creatinina e uréia caracterizando um quadro de azotemia foram relatadas, em cabras e ovelhas com TP em diferentes intensidades, por Wastney et al (1983), Andrews et al (1996), Sargison et al (1994), Van Saun (2000), Barakat et al (2007) e Yarin & Ciftci (2009), que relataram a má função renal e o catabolismo protéico como causa da elevação nos valores destes indicadores da função renal. Esta alteração pode ser explicada por observações feitas por Ferris et al (1969) e Marteniuk & Herdt (1988), que encontraram inϐiltração excessiva de gordura no epitélio tubular acarretando modiϐicações estruturais glomerulares, provocando uma degeneração dos rins em ovelhas com a doença, e que podem prejudicar a função renal.…”