1. Investigación

1.8 or 25 µg of L-thyroxine/100 g body wt. were compared with intact controls (C). The appearance of radioacitvity in fatty acids 30 min after the i.p. injection•of (3-14C)pyruvate was reduced in adipose tissue and enhanced in liver of T+25, being no differences between the other groups and C. ( 14C)- Fatty acids are reduced with 3 h of fasting only in the adipose tissue of T+ 1.8 and C, while 24 h produces a reduction in liver in the T+ 1.8, T+25 and C, and in adipose tissue in the T+l.8 and C animals. The highest percentage of radioactivity was observed in the liver glyceride glycerol fraction, being greater in T+25 than in the other groups. Fasting produces an increment in the ( 14C)-glyceride glycerol fraction. being significant only in the hypothyroid animals in both liver and adipose tissue. The most sensitive parameter to fasting was the formation of ( 14C)-non-saponifiable lipid in both the C and T+ 1.8 animals, while it does not change in T+0 or T+0.I, but is enhanced within 24 h in the adipose tissue of T + 25. It is proposed that most of the observed changes are due to the other endocrine disfunction s which appear in hypo- and hyperthyroidism, as the in vivo results do not comply with in vitro effects of thyroxine on lipogenesis of others.

Three days after a single injection of streptozotocin rats showed hyperglycemia, hyperketonemia and hypoinsulinemia. Body and liver weights were reduced and the concentration of DNA-P, phospholipid-P, proteins and acetyl-CoA in the liver was augmented, while the concentration of glycogen and citric acid in these animals compared with the controls which did not receive the drug was decreased. After 48 h starvation, blood glucose remained higher in the streptozotocin-treated animals, while circulating ketones and insulin were not different from those in the controls. With the exception of body and liver weights, which were lower, and of liver DNA-P, which was higher than when fed, neither of the other parameters studied in the s:reptozotocin treated animals changed with fasting, while the response in the c0ntrols was normal; The incapacity of increasing the postprandial insulin secretion in these animals may contribute to the metabolic alterations found in the fed state.

A 24-h fast induced different patterns of change in the amino acid concentrations of liver, muscle, plasma and blood cells. Starvation produced generalized increases in blood amino acids despite decreases in plasma, thus increasing the blood cells amino acid pool. Muscle increased amino acid levels with fasting, while the changes were much more buffered in liver. The fraction of essential amino acids carried by the blood was considerably greater than that of muscle and liver. The size of muscle pool in the whole rat was much greater than that of liver and more than two orders of magnitude higher than that of the whole blood. Fasting-induced changes agree with the known transport of amino acids from muscle and other peripheral tissues towards the liver and other splanchnic organs.

Since during pregnancy the mother switches from an anabolic to a catabolic condition, the present study was addressed to determine the effect of 48 h food deprivation on days 7, 14 and 20 of pregnancy in the rat as compared to age matched virgin controls. Body weight, free of conceptus, decreased with food deprivation more in pregnant than in virgin rats, with fetal weight (day 20) also diminishing with maternal starvation. The decline of plasma glucose with food deprivation was greatest in 20 day pregnant rats. Insulin was highest in fed 14 day pregnant rats, and declined with food deprivation in all the groups, the effect being not significant in 7-day pregnant rats. Food deprivation increased plasma glycerol only in virgin and 20 day pregnant rats. Plasma NEFA and 3-hydroxybutyrate increased with food deprivation in all groups, the effect being highest in 20 day pregnant rats. Food deprivation decreased plasma triacylglycerols in 14 day pregnant rats but increased in 20 day pregnant rats. In 20-day fetuses, plasma levels of glucose, NEFA and triacylglycerols were lower than in their mothers when fed, and food deprivation caused a further decline in plasma glucose, whereas both NEFA and 3-hydroxybutyrate increased. Liver triacylglycerols concentration did not differ among the groups when fed, whereas food deprivation caused an increase in all pregnant rats and fetuses, the effect being highest in 20-day pregnant rats. Lipoprotein lipase (LPL) activity in adipose tissue was lower in 20 day pregnant rats than in any of the other groups when fed, and it decreased in all the groups with food deprivation, whereas in liver it was very low in all groups when fed and increased with food deprivation only in 20 day pregnant rats. A significant increase in liver LPL was found with food deprivation in 20 day fetuses, reaching higher values than their mothers. Thus, the response to food deprivation varies with the time of pregnancy, being lowest at mid pregnancy and greatest at late pregnancy, and although fetuses respond in the same direction as their mothers, they show a specific response in liver LPL activity

Background: Routine total parenteral nutrition (TPN) in neonatal care can result in hepatic dysfunction in 40–60% of patients, most commonly as fatty liver, but little work has been conducted on the underlying mechanisms causing hepatic dysfunction. Objective: To use a piglet model for the premature human neonate on TPN, supplemented with lipid emulsions, to investigate hepatic responses. Method: Piglets were delivered 2 days prematurely. Six control piglets were fed enterally (E), whilst twelve animals were maintained on TPN. TPN piglets received the standard TPN solution plus the lipid emulsion as either ClinOleic (C, n = 6) or Intralipid (I, n = 6). Hepatic lipid content and the fatty acid composition of liver triacylglyercol (TAG) as well as hepatic lipase (HL) activity were determined. Lipoprotein lipase (LPL) activity was measured in the liver, muscle and adipose tissue. The plasma concentrations of choline, bilirubin, TAG and non-esterified fatty acids (NEFA) were also measured. Results: Liver lipid was significantly increased in piglets on TPN and the tissue fatty acid profiles reflected the lipid emulsion. HL and LPL activities were reduced in liver but LPL increased in adipose tissue during TPN. Plasma concentrations of choline, bilirubin, TAG and NEFA were similar across the treatments. Conclusions: The results suggest fatty liver occurs in neonates receiving TPN and the source of the accumulated lipid appears to be the lipid emulsion used. The factors regulating lipase activity during TPN require further study. The piglet can be used as a model for neonatal TPN.

To study the effect of diabetes on hepatic protein synthesis and polysomal aggregation in pregnant rats, female rats were treated with streptozotocin prior to conception. Some animals were mated. and studied at day 20 of pregnancy, whereas. others were studied in parallel under non pregnant conditions. The protein synthesis rate measured with an "in l'ITTO .. cell-free system was higher in pregnant than in virgin control rats. It decreased with diahetes in both groups. although values remained higher in diabetic pregnant rats than in the virgin animals. The fetuses of diabetic rats had a lower protein synthesis rate than those from controls, although they showed a higher protein synthesis rate than either their respective mothers or virgin rats. Liver R~A concentration was higher in control and diabetic. pregnant rats than in virgin rats, and the effect of diabetes decreasing this parameter was only significant for pregnant rats. Liver RNA concentration in fetuses was lower than in their mothers, and did not differ between control and diabetic animals. The decreased protein synthesis found in d1ahe11c animals was accompanied by disaggregation of hea,·y polysomes into lighter species, indicating an impairment in peptide-chain initiation.

1) Thyoridectomized rats were fed with a low iodine diet, injected daily with 0, 0.1, 1.8 or 25 µg of L-thyroxine/100 g body wt., and compared with intact controls. 2) Plasma protein-bound iodine was decreased in the rats given the 0 and 0.1 µg doses, unchanged in those given the 1.8 µg doses, unchanged in those given the 1.8 µg dose increased in those given the 25 µg one. 3) The liver content of DNA-P, phospholipid-P, proteins and fatty acids was decreased in the rats that did not receive thyr.oxine, practically recuperated in those receiving 0.1 µg and normal in those given 1.8 or 25 µg of thyroxine. 4) 3 h of starvation produced a reduction in the liver content of total fatty acids that disappeared after 24 h. 5) When fod, liver glycogen concentration was low in the rats given 25 µg of thyroxine. 6) With starvation, the fall in liver glycogen and blood glucose, and the rise in liver acetylCoA and citrate and blood glycerol concentrations were faster in the thyroidectomized rats that did not receive thyroxine than in the other groups. 7) The rise in plasma free fatty acid and blood ketone bodies concentrations were similar in all the groups, the greater level of the first parameter being observed after 6 h of starvation in the rats given 25 µg of thyroxine and in the second one after 24 h in the rats given either 0.1, 1.8 or 25 µg of thyroxine. 8) The rapid decrease in the availability of carbohydrate stores with starvation in the thyroidcctomized rats could be responsible for their fast call for lipid utilization. The slower response to fasting in the hyperthyroid animals is probably a consequence of their reduced amount of endogenous substrates to be mobilized.