Prolonged suppression of pituitary and pancreatic hormone release by a somatostatin analog.
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Biomedical subjects
Publications and source records attributed to E L Lien.
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Lipid accumulation is a hallmark of corpus luteum regression and we characterized lipids stored in rat corpora lutea of pregnancy between days 21 and 24 post coitum, the period of luteolysis. A 10-fold rise in lutein triglyceride concentrations occurred between days 21 and 24, which represented the major alteration in luteal lipid metabolism during luteolysis, coinciding with the appearance of numerous lipid droplets in the luteal cells. The fatty acid composition of luteal triglycerides was altered between days 20 and 23 in a pattern consistent with the influx of blood triglyceride fatty acids. No evidence for increased de novo fatty acid synthesis by luteal tissue between days 21 and 24 post coitum was obtained using in vitro methods. [14C]Acetate incorporation into lipids declined between days 16 and 24 and label was preferentially introduced into long chain polyunsaturated fatty acids. Rates of tritium incorporation into fatty acids from tritiated water were relatively low. [14C]Glucose was predominantly incorporated into the glycerol moiety of luteal lipids and incorporation of label into this fraction was augmented between days 21 and 23 post coitum. The incorporation of [14C]palmitate into triglycerides of luteal tissue during in vitro incubation also increased between days 21 and 23. In vitro lactate production, [14C]glucose oxidation, and [14C-palmitate oxidation to 14CO2 increased significantly during this time. We conclude that specific biochemical alterations occur in regressing corpora facilitating uptake and storage of blood glyceride fatty acids as triglycerides. The physiological significance of this triglyceride accumulation remains to be elucidated.
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The effects of an inhibitor of RNA synthesis, cordycepin, and an inhibitor of protein synthesis, cycloheximide, on aldosterone-induced changes in lipid metabolism and phospholipid fatty acid composition have been studied in the toad urinary bladder. At the concentrations employed, the inhibitors abolish the hormone-induced increases in total lipid synthesis, phospholipid fatty acid specific activities, and weight percentage of phospholipid long-chain polyunsaturated fatty acids as well as blocking the aldosterone-mediated increase in sodium transport.
A correlation study of the effects of two agents, 2-methyl-2-[p-(1,2,3,4-tetrahydro-1-naphthyl)phenoxy]propionic acid (TPIA) and amiloride, on aldosterone-induced alterations in Na+ transport, lipid synthesis, and phospholipid fatty acid composition has been carried out in the toad urinary bladder. TPIA, an inhibitor of acetyl-CoA carboxylase, inhibits aldosterone-stimulated Na+ transport as well as hormone-induced lipid synthesis and the increase in weight percentage of phospholipid long-chain polyunsaturated fatty acids. Amiloride, a diuretic which blocks sodium entry into the transporting epithelium, does not alter aldosterone's effects on lipid and fatty acid metabolism but prevents the hormone-induced increase in Na+ transport. These results support the conclusion that aldosterone increases Na+ transport in the toad urinary bladder by altering membrane fatty acid metabolism and that the lipid biosynthetic events following aldosterone treatment are a primary response to the hormone and not secondary to increased Na+ transport.
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BACKGROUND: Long chain polyunsaturated fatty acids (LCPUFAs) such as arachidonic acid (AA) and eicosapentaenoic acid (EPA) stimulate intestinal adaptation. Prostaglandins also enhance intestinal adaptation. The purpose of this study was to determine by which eicosanoid pathway dietary arachidonic acid enhances intestinal adaptation. Cyclo-oxygenase or lipoxygenase were selectively inhibited to determine whether either of them enhanced or inhibited adaptation. METHODS: Sixty Sprague-Dawley rats were divided into 2 groups, one receiving an 80% small bowel resection and the other receiving a sham operation. Rats were further divided into groups receiving either a placebo, a general lipoxygenase inhibitor (nordihydroguaiaretic acid [NDGA] at 40 mg/kg per day), or a cyclo-oxygenase-2 inhibitor (Etodolac at 3 mg/kg per day). Rats were pair-fed a diet containing 30% kcal from fat, primarily consisting of AA. RESULTS: After 14 days, mucosal mass, protein, DNA, and disaccharidase activity were measured in the remaining small intestine. There was a significant decrease in ileal mucosal mass in rats receiving Etodolac and a significant increase in mucosal mass in the duodenum in rats receiving NDGA (both p < .001). Mucosal DNA, protein, and disaccharidase data showed similar trends. CONCLUSIONS: These findings suggest that after small bowel resection, dietary arachidonic acid may facilitate the adaptation process by acting as a substrate for the synthesis of prostaglandins, and not through the derivatives of lipoxygenase such as leukotrienes or thromboxanes.
BACKGROUND: Efficacy of feeding hydrolyzed soy proteins to infants intolerant to cow milk proteins has not been determined fully. This study compared growth and intestinal responses of neonatal piglets fed formulas with hydrolyzed soy protein to piglets fed formulas with intact soy or cow milk (casein-whey) proteins. METHODS: Piglets (n = 40, day 2 postpartum) were fed commercial milk replacer until day 7 postpartum (designated day 0) and then were assigned randomly to casein-whey (CW) or soy (intact, SI; hydrolyzed SH) formulas to evaluate intestinal responses on days 0, 2, 5, and 10. RESULTS: Average daily gain was higher for CW (121 g/d; p < .05) compared with SI piglets 85 g/d); SH pig weight gain was intermediate (109 g/d). Villus height-to-crypt depth ratio in proximal jejunum was lower (p < .05) on day 2 than day 0 in soy-fed pigs and lower (p < .05) on day 5 than day 0 in CW pigs. Mucosal mast cells were generally higher in CW pigs compared with soy-fed pigs. Villus goblet cell numbers in the midjejunum of SH-fed piglets were lower (p < .05) on day 5 compared with day 0. On day 5, crypt goblet cell numbers were higher (p < .05) in the midjejunum of CW-fed piglets compared with SH-fed piglets with numbers intermediate for SI-fed piglets. Intestinal differences were not detected among dietary treatments for major histocompatibility complex class I and II gene expression, tissue concentrations of prostaglandin E2, or CD8+ T-cell numbers. CONCLUSIONS: Hydrolyzed soy proteins do not elicit intestinal inflammatory responses in piglets and may be viable alternatives to milk and intact soy proteins for feeding infants.
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