The effect of exposure to, followed by consumption of, 10% flax chow from the 18th day of gestation to the 86th day after birth was examined in male and female Fischer 344 rats. Growth curves of the flax chow-fed rats were identical to those of regular chow-fed rats, as were such developmental milestones as pinna development, growth of hair and eye opening. Acoustical startle and the righting reflexes, developmental behavioural indices, were also the same. Blood glucose levels were comparable in flax chow-fed and regular chow-fed rats at all stages of development, indicating that flax is without effect on glucose balance. There were no signs of toxicity in the flax chow-fed rats since their plasma levels of alanine aminotransferase and gamma-glutamyltranspeptidase (gammaGT) were the same as those of regular chow-fed rats. The activity of gammaGT displayed an increase in the livers of flax chow-fed rats after puberty, more so in the male-four-fold-than in the female-1.38-fold. This is suggestive of an estrogenic effect which implicates an effect of an estrogenic flax lignan. An hepatobeneficial effect of the flax-induced increase in liver gammaGT is discussed. In summary, dietary 10% flax chow is without long-term effect on growth, development and behaviour, is non-toxic and may be hepatoprotective.
In Rana sylvatica, freeze-induced liberation of glucose from hepatic glycogen stores plays a critical role in conferring freeze tolerance. To determine whether an alteration in hepatic adrenergic receptor status, which dictates catecholamine-directed hepatic glycogenolytic responses, is involved in the glycemic response to freezing, hepatic alpha 1, alpha 2, and beta 2 adrenergic receptors and calcium transport were characterized by radioligand and radioisotopic techniques, respectively, in plasma membranes isolated from the livers of control, -2.5 degrees C-exposed, and frozen-thawed frogs. The three adrenergic receptors display marked and different patterns of changes in response to freezing, with two distinct receptor shifts clearly evident. In the control state, the beta 2 adrenergic receptor dominates over the alpha 1 receptor. At 12 h, beta 2 adrenergic receptor dominance intensifies by a receptor shift involving a decrease in the alpha 1 and alpha 2 adrenergic receptors. Coincident with the initiation of the glycemic response, this early shift may be causally related to it. At 24 h, the alpha 1 adrenergic receptor dominates, achieved by a receptor shift involving a decrease in the beta 2 adrenergic receptor and an increase in the alpha 1 and alpha 2 adrenergic receptors. This shift may be related to the maintenance of the glycemic response. Receptor shifts are associated with changes in calcium transport, which accentuate them. The thawed state is characterized by recovery of alpha, but not beta 2, receptor expression correlatable with, and perhaps allowing, a switch to hepatic glycogenesis. The role of thyroid hormone, whose levels are lower in the frozen state, in inducing receptor shifts is discussed.
Mitochondrial, endoplasmic reticular and plasma membrane fractions were isolated by a new method from control male Fischer 344 rats and rats given CCl4 by gavage. After 1 h of CCl4 treatment, rats were in glucose and pancreatic hormone balance but plasma levels of T3 and T4 were decreased 29 and 22%, respectively. After 24 hours of CCl4 treatment, rats were: hypoglycaemic and insulin and glucagon levels were increased 33- and 35-fold, respectively; total T4 levels were decreased 62%; while total T3 levels were normalized. In liver fractions from CCl4-treated rats, 1 h after CCl4 administration: (i) calcium binding was decreased 65% in the mitochondrial fraction, 66% in the endoplasmic reticular fraction and 46% in the plasma membrane fraction; (ii) calcium uptake was decreased 59% in the mitochondrial fraction, 46% in the endoplasmic reticular fraction and 37% in the plasma membrane fraction. After 24 h of CCl4 administration: (i) calcium binding was decreased 57% in the mitochondrial fraction, 50% in the endoplasmic reticular fraction and 71% in the plasma membrane fraction; (ii). calcium uptake was decreased 55% in the mitochondrial fraction, 17% in the endoplasmic reticular fraction and 53% in the plasma membrane fraction. In vitro studies indicated the plasma membrane calcium transport system to be rapidly (within a minute) and strongly (>90%) inhibited by CCl4. We conclude that CCl4 produces a differential inhibitory effect on the hepatocyte calcium pumps that are implicated with hepatocellular damage.
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