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Brachionus plicatilis are used as live prey for rearing winter flounder larvae at first feeding. This rotifer is grown between 20 and 25 °C (its optimal growth temperature) and then introduced into the 10 °C water in which larvae are reared. The rapid thermal difference between the two media is thought to reduce B. plicatilis quality and consequently affect larval rearing efficiency. In order to optimize larval rearing, a study was conducted to compare the effects of two different diets on larval growth performance and nutritional condition: (1) larvae fed B. plicatilis reared at 24 °C and (2) larvae fed B. plicatilis reared at 24 °C but acclimated overnight at 10 °C. Comparisons were undertaken using morphometric measurements, nucleic acid (RNA/DNA) ratios, total protein content, trypsin activity, and triacylglycerol/sterol ratios. Fatty acid composition of larvae was also studied with a focus on the levels and ratios of three essential fatty acids (docosahexaenoic acid or DHA, eicosapentaenoic acid or EPA, and arachidonic acid or AA). Unique information regarding trypsin activity and lipid components (phospholipid, triacylglycerol, and sterol) of winter flounder larvae is provided in this study. Trypsin activity was detected very early in larvae and was not affected by acclimation of prey. Phospholipid, triacylglycerol, and sterol composition showed no significant difference between the two diets tested and was characterized by high phospholipid content as well as low triacylglycerol and sterol contents. EPA, DHA, AA, DHA/EPA, and DHA/AA decreased from days 12 to 26. Interestingly, DHA content was significantly higher in larvae fed acclimated rotifers and AA content decreased significantly in 26-day-old larvae fed acclimated B. plicatilis . Overall results indicate that overnight acclimation of B. plicatilis at 10 °C is not important for optimizing the rearing of winter flounder larvae although it does influence the fatty acid composition.

The administration of norethindrone, a synthetic progestin, to female rats caused marked decreases in the cholesterol and protein contents of high-density lipoproteins (HDL), A 84% decrease in the total apolipoprotein (apo) E of HDL was associated with a 80% decrease in the proportions of apoE isoforms E1 and E2, whereas E3 and E4 were unchanged. This appears to be the first demonstration of hormonally-induced modification of the apoE phenotype.

Biological activities of estrogen molecules are altered by fluorination of ring A, and the resulting impairment to form catechols. 2-fluoroestradiol (2-F-E2) has been found to be devoid of carcinogenic action despite its high estrogenic potency; its metabolic effects are so far unknown. This study was designed to investigate the effects of 2-F-E2 on lipid metabolism, as compared to those of estradiol-17 beta(E2). Ovariectomized rats received E2 or 2-F-E2 by s.c. injection at a dose of 60 micrograms for three consecutive days. Parameters measured were weights of parametrial fat depots, fat cell volumes, levels of triacylglycerol and acylcholesterol in plasma, and enzymatic responses to the estrogens in isolated parametrial fat cells as evaluated in terms of lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL) activities. 2-F-E2 and E2 were found to produce comparable decreases in fat depots, cell volumes and plasma levels of acylcholesterol whereas plasma triacylglycerol was unchanged. Both estrogens decreased LPL, and increased HSL activities to the same extent. Thus, 2-F-E and E2 exhibited comparable effects on lipid metabolism. These effects appeared to depend mainly on the estrogenic potency of these molecules, and to be distinct from their carcinogenic action. Despite its high estrogenic potency, 2-F-E2 was found to be slightly less estrogenic than E2.

We investigated concomitantly the effects of ethinyl-estradiol (EE 2 ) at low dose (1.2 μg/animal for 10 days) and high dose (120 μg/animal for 3 days) on body weight, weight of fat stores, triglyceridemia and fat cell lipoprotein lipase and hormone-sensitive lipase activities in female rats. At low dose, EE 2 increased triglyceridemia and lipoprotein lipase activity, whilst high dose decreased both parameters. At low and high doses, and regardless of whether triglyceridemia and lipoprotein lipase activity were increased and decreased, EE 2 caused depletion in fat stores. Fat cells isolated from depleted fat tissue elicited marked increases in the response of hormone-sensitivelipase to epinephrine. Taken together, the data suggest that the potentiation of epinephrine-induced lipolysis in fat cells is likely to represent a major cause to estrogen-induced fat depletion.

The in vivo administration of ethinylestradiol to female rats causes dose-dependent decreases in tri-, di- and monoacylglycerol lipase activities in post-heparin heart effluents; monoacylglycerol lipase is less sensitive to estrogen than the other two.

We investigated the effects of ethinyl estradiol (EE2) on body weight, weights of fat depots, triglyceridemia and lipoprotein lipase (LPL) activity of fat cells isolated from the parametrial fat pads of female rats. LPL activity was assayed at the cell surface, using a suspension of intact fat cells as enzyme source. The cellular uptake of fatty acids liberated during hydrolysis was also evaluated. EE2 was administered daily for 10 days by s.c. injections of 0.06 0.6 6.0 and 60 μg of hormone per animal. EE2 at and above 0.6 jug/rat reduced body weight gain and weights of fat depots. Triglyceridemia increased at doses of EE2 up to 6 μg and showed a relative reduction at 60 μg. In parallel, LPL activity assayed both as cell-bound and heparin-released enzyme and expressed relative to cell DNA, responded to the hormone according to a biphasic pattern: EE2 increased LPL activity in the dose range 0.6-6.0 μg of EE2, whereas a decrease occurred at higher doses. Fat cells incorporated as acylglycerol 56.5 ± 6.2% (mean + SD) of the amount of fatty acid liberated enzymatically during incubation, and this percentage was essentially unchanged by EE2. EE2 at 60 μg/rat caused decreases in triglyceridemia and LPL activity and, as a consequence, decreases in fat depots. By contrast, EE2 at doses up to 6 μg created a paradoxical situation where concomitant increases in triglyceridemia and LPL activity, which should have favoured fat deposition, coexisted with fat depletion. Estrogen hormones at doses below toxicity increase the secretion of triglyceride-rich lipoproteins by liver. Whereas the increase in LPL activity oberved in this study at low doses of EE2 may reflect the LPL responses to liver-borne hypertriglyceridemia, the mechanism for the concomitant fat depletion is unclear. These data emphasize the complex effects of estrogen hormones on lipid metabolism.