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Biomedical subjects

E L Lien

Publications and source records attributed to E L Lien.

At least 37 records · Page 2Linked to original sources
PubMed1996

Retinal fatty acids of piglets fed docosahexaenoic and arachidonic acids from microbial sources.

Docosahexaenoic acid (DHA, 22:6n-3) and arachidonic acid (AA, 20:4n-6) serve important roles in perinatal visual and neural development. A neonatal pig model was used to determine if dietary supplementation with DHA and AA at slightly greater concentrations than normally found in human milk would influence fatty acid accretion in retina. One-day-old piglets were assigned to one of four diets (n = 5/group): (i) STD, standard diet containing fat similar to infant formula; (ii) STD + DHA, 0.7% of fatty acids as DHA; (iii) STD + AA, 0.9% as AA; and (iv) STD + BOTH, 0.8% as DHA plus 1.0% as AA. After 25 d, fatty acids in retina phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were determined. Supplementation with DHA resulted in approximately twofold increases (P < 0.05) in PC-DHA (4.88% in STD vs. 10.03% in STD + DHA and 9.47% in STD + BOTH). Similarly, AA supplementation increased PC-AA 1.3-1.4-fold (4.47% in STD vs. 6.19% in STD + AA and 5.70% in STD + BOTH). For PE, supplementation with either fatty acid or in combination resulted in no significant increases, except for a 1.2-fold increase in DHA for STD + BOTH (32.66%) vs. STD (28.38%). Thus, PC responded to dietary supplementation, with addition of DHA, AA, or BOTH, resulting in increases in respective fatty acids; PE was less responsive, with only STD + BOTH resulting in increased DHA. No significant competition between DHA and AA in incorporation into phospholipids was observed. In conclusion, consumption of a combination of DHA and AA by neonatal pigs supported accretion of DHA in retina phospholipids, while simultaneously supplying the AA necessary for membrane phospholipids and eicosanoid biosynthesis.

Animals↗
PubMed1996

Short-term metabolic responses do not differ between neonatal piglets fed formulas containing hydrolyzed or intact soy proteins.

Hydrolyzed soy protein (SH) could be used as a protein source in formulas for infants with intolerance to cow's milk protein and may be preferable to intact soy protein (SI). However, metabolic responses to SH are poorly defined. Because of their partially hydrolyzed nature, nonphysiological elevations in either plasma amino acids or regulatory hormones may occur. Therefore, we evaluated effects of SH on plasma nutrient and pancreatic hormone (insulin, glucagon) concentrations. In Experiment 1, 24 newborn pigs were fitted with umbilical arterial and portal catheters, fed formula for 36 h and food deprived for 12 h. Pigs were then fed formula including either SH or SI with glucose polymers or casein-whey proteins (CW) containing lactose, and serial blood samples were taken for 2 h postprandially. Peak portal exceeded peak arterial amino acid concentrations within each treatment, and peak amino acid concentrations in CW-fed pigs exceeded those of SH- and SI-fed pigs. However, only SH formula-fed piglets had higher postprandial portal minus arterial amino acid concentrations (P < 0.05) throughout Experiment 1, suggesting that SH was well digested and absorbed. In Experiment 2, arterial catheters were inserted in 24 piglets. Previous procedures were followed except dietary carbohydrate was standardized to glucose polymers for all three diets, and sampling was extended to 3 h. Overall, portal or arterial nutrient and hormone concentrations were not different in the SI and SH groups (P > 0.05), indicating that hydrolyzed soy protein did not cause abnormal plasma concentrations. In conclusion, hydrolyzed soy protein did not result in elevated nutrient concentrations or hormone responses compared with intact soy or cow's milk protein.

Amino Acids↗
PubMed1996

Red blood cell and tissue phospholipid fatty acid profiles of weanling rats fed infant formula fat blends containing soy and/or corn oil.

Soy oil or corn oil may be employed to provide essential fatty acids in infant formulas. Both of these sources are high in linoleic acid; soy oil contains modest levels of alpha-linolenic acid, while corn oil contains very low levels of this essential omega 3 fatty acid. We examined the omega 3 long-chain polyunsaturated fatty acid (LCP) accretion in red blood cells, liver, and brain phospholipids of rats on diets containing infant formula fat blends with essential fatty acids provided from soy and/or corn oil. Although modest alterations occurred in the red blood cell omega 3 LCP fatty acid status, substantially larger changes were noted in liver LCP profiles. Due to the relatively mature nature of the rats employed in this experiment, no alterations were noted in brain fatty acid profiles. In conclusion, we have observed substantial tissue differences in animals fed soy or corn oil containing diets. It appears that corn oil is inappropriate for use in infant formulas.

Animals↗
PubMed1994

Effect of maternal dietary arachidonic or linoleic acid on rat pup fatty acid profiles.

Rapidly growing neonatal mammals accrete relatively large quantities of long chain (> or = C20) polyunsaturated fatty acids (LCP) in membrane phospholipids. We have examined accumulation of omega 6 LCP in suckling neonatal rat pups during the first 14 d of life when their dams received essential fatty acids in the form of triglycerides containing linoleic acid or arachidonic acid. Dietary levels of these fatty acids were either 1 or 5% of total dietary fatty acids. The fatty acid profile of pup stomach contents (composed solely of the dams' milk) and plasma lipids, as well as liver and brain phospholipids, were determined. Stomach linoleic and arachidonic acid levels reflected the diet of the dams. Pup plasma and liver arachidonic acid levels increased progressively from the group receiving 1% linoleic acid to 5% linoleic acid and from 1% arachidonic acid to 5% arachidonic acid. Interestingly, brain phosphatidylethanolamine and phosphatidylcholine arachidonic acid levels were more stable than plasma or liver levels. These results suggest that the brain may be capable of either selective transport of omega 6 LCP or chain elongation/desaturation of linoleic acid. These data indicate that care must be exercised when adding LCP to infant formula since widely divergent accretion rates of arachidonic acid may occur in various tissues.

Animals↗
PubMed1994

The role of fatty acid composition and positional distribution in fat absorption in infants.

Fat digestion and absorption in the infant is a multistep process. An initial gastric phase of lipolysis generates modest amounts of diglycerides, monoglycerides, and free fatty acids. These initial digestion products, as well as bile salts, are required for optimal activity of the intestinal phase of lipolysis. Colipase-dependent pancreatic lipase catalyzes the intraduodenal phase of triglyceride digestion in formula-fed infants; in breast-fed infants this process is also mediated by bile salt-stimulated lipase. Triglyceride fatty acid positional distribution may modulate the efficiency of nutrient absorption. Human milk contains palmitic acid (C16:0) primarily in the sn-2 position; infant formula fat blends contain palmitic acid predominantly in the sn-1 and sn-3 positions. Because pancreatic lipase selectively hydrolyzes triglycerides at the sn-1 and sn-3 positions, free fatty acids and 2-monoglycerides are produced. Free palmitic acid, but not 2-monopalmitin (which is efficiently absorbed), may be lost as a calcium-fatty acid soap in the feces. As a result, many infant formulas contain substantial levels of well-absorbed saturated fatty acids of shorter chain lengths (e.g., C12:0) in place of palmitic acid. Means of increasing the proportion of 2-palmitic acid in infant formula may make possible fat blends closer to that of human milk with acceptable absorption characteristics.

Animals↗
PubMed1993

Corandomization of fats improves absorption in rats.

Human milk fat is well absorbed despite its large concentration of long-chain saturated fatty acids (LCSFA), particularly palmitic acid. The superior absorption has been ascribed in part to the uncommonly high proportion of the palmitic acid in the sn-2 position of the triglycerides, 70% in human milk triglycerides compared with 10-15% in the fats and oils commonly used in infant formula blends. Colipase-dependent pancreatic lipase selectively hydrolyzes the fatty acids at the sn-1 and 3 positions, yielding free fatty acids and the 2-monoglyceride, which are absorbable. Free palmitic acid, but not monopalmitin, can be lost as calcium soaps in the feces. The present study demonstrated that mixtures of coconut oil and palm olein are better absorbed by rats if the proportion of LCSFA in the sn-2 position is increased by the process of chemical randomization, in which the fatty acids of the native oils are redistributed equally to all three positions in the rearranged triglycerides. The fecal excretion of total fatty acids, essentially LCSFA, from the mixtures in which the oils were randomized together (corandomized) was 30 to 60% less than from the mixtures of native oils.

Animals↗
PubMed1992

Oral hypoglycemic agents. Pyrimido[1,2-a]indoles and related compounds.

A series of pyrimido[1,2-a]indoles were synthesized and studied for their hypoglycemic activity following oral administration at a standard dose of 100 mg/kg to fed rats. The effect of 10-alkoxyalkyl, 10-alkyl, 10-aryl, and 3,3-dialkyl substitution on the activity of 10-hydroxypyrimido[1,2-a]indoles was investigated. Relative potencies of a number of the most active compounds were defined by three-point dose-response studies. The most potent compounds were those with either 3,3-dimethyl substituents, compounds 21, 22, and 38, or 3,3-spirocyclohexane substituents, compounds 39 and 49. 10-Aminopyrimido[1,2-a]indoles were in general less active than the 10-hydroxy analogues, and potency was further decreased by derivatizing the 10-amino group. The most potent 10-amino derivatives were 57 and 58.

Animals↗
PubMed1986

Alpha-2-adrenergic control of prolactin release.

The role of the alpha 2-adrenergic system in regulating prolactin release has been studied in vivo in male rats. Yohimbine administration alone, at doses ranging from 0.2 to 5.0 mg/kg, resulted in a dose-related elevation of plasma prolactin levels from a basal level of 8 +/- 2 to 65 +/- 6 ng/ml at the highest dose. In the same experiment clonidine, 0.2 mg/kg, suppressed basal prolactin levels to 4 +/- 1 ng/ml and returned prolactin levels of all animals receiving 0.2-5.0 mg/kg yohimbine to basal levels. Rats were treated with increasing doses of clonidine (0.05-1.0 mg/kg) in the presence or absence of a constant dose (1.0 mg/kg) of yohimbine. Clonidine alone at doses of 0.05 and 0.2 mg/kg again significantly suppressed prolactin levels, while a dose of 1.0 mg/kg did not (failure of high dose clonidine to suppress prolactin levels suggests an additional effect of clonidine on prolactin secretion unrelated to alpha 2-adrenergic agonist action). All three doses of clonidine completely reversed yohimbine-induced prolactin release. Basal prolactin levels were also significantly reduced by the selective alpha 2-adrenergic agonist UK-14,304 at a dose of 0.2 mg/kg. Yohimbine-induced prolactin release was reversed by UK-14,304 at doses of 0.2 and 1.0 mg/kg, but not at the lowest dose studied, 0.05 mg/kg. The lower potency of UK-14,304 than clonidine in this assay is consistent with the lower potency of UK-14,304 as an alpha 2-adrenergic-agonist antihypertensive agent. Several alpha 2-antagonists in addition to yohimbine were studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Anorectic drugs which stimulate thermogenesis.

Two anorectic drugs commonly prescribed as adjuncts in weight control and a third experimental drug were studied in rats for their anorectic and possible thermogenic activities. Diethylpropion, a congener of amphetamine, mazindol, which is chemically unrelated to amphetamine, and ciclazindol, an experimental drug structurally similar to mazindol, were given in graded doses to determine their effect on food and oxygen consumption (VO2). Anorectic effects exhibited by diethylpropion and mazindol were similar and more potent than ciclazindol. Both resting and anesthetized VO2 measurements were done to assess the thermogenic activity of the drugs. Anesthetized VO2 was performed in an attempt to separate peripheral from centrally-mediated actions of the drugs. Amphetamine was also tested at 1.0 mg/kg in order to correlate relative potencies. Mazindol, but not diethylpropion or ciclazindol, produced a dose response increase in resting VO2. At the 1.0 mg/kg dose, amphetamine produced a greater increase in resting VO2 than mazindol. At this dose, both drugs elicited centrally-induced alertness, although amphetamine elicited greater activity than mazindol. Mazindol and diethylpropion, but not ciclazindol, caused a dose-related increase in anesthetized VO2. The anesthetized VO2 response to amphetamine at 1 mg/kg was greater than the responses of mazindol and diethylpropion at 3.0 mg/kg. These findings confirm the previously recognized anorectic effects of mazindol and diethylpropion and also demonstrate that mazindol and diethylpropion but not ciclazindol (at the doses used) produced dose-related increases in VO2 (energy expenditure) by stimulating directly peripheral mechanisms and in the case of mazindol central mechanisms as well.

Amphetamine↗
PubMed1981

Route of administration as a factor in the selectivity of hormone suppression of a somatostatin analog in rats.

The method of administration of [D-Ala5,D-Trp8] somatostatin is of central importance in determining the degree and duration of suppression of insulin and glucagon release. The analog decreased insulin levels in rats when injected by s.c. or i.v. routes, with a nadir 15 minutes following injection. After i.v. injection, insulin levels rapidly returned to basal values while s.c. injection produced significant suppression for 60 minutes. Neither type of injection altered glucagon levels. Intravenous infusion resulted in inhibition of both insulin and glucagon release, with rebound hyperglucagonemia, but not hyperinsulinemia in the post-infusion period. Plasma glucose levels reflected these hormonal changes. Thus, dramatic alterations in the specificity of this somatostatin analog may be achieved by employing different methods of administration.

Animals↗
PubMed1978

Effect of somatostatin and a glucagon-specific analog on glucose homeostasis during arginine infusion.

The glucose response to arginine infusion in normal rats was studied during insulin and glucagon deficiency (somatostatin infusion, 1 mg/kg/hr) or selective glucagon deficiency ([D-Cys14]-somatostain infusion, 1 mg/kg/hr). In control studies, plasma glucose levels rose 14 mg/dl in response to arginine and returned to basal levels at the termination of the infusion. Insulin levels increased 136 +/- 12 muU/ml and glucagon increased 76 +/- 12 pg/ml during the infusion. Infusion of somatostatin resulted in supression of both arginine-induced insulin and arginine-induced glucagon release, and marked hyperglycemia ensued. The administration of [D-Cys14]-somatostatin during arginine infusion produced no associated hyperglycemia. It resulted in suppression of glucagon secretion and a modest rise in insulin release. These results demonstrate that the hyperglycemic effects of somatostatin in arginine-treated animals do not arise in animals treated with glucagon-specific somatostatin analogs.

Animals↗
PubMed1978

Prolonged suppression of insulin release by a somatostatin analog.

A somatostatin analog, [D-Ala5, D-Trp8]-somatostatin, has been found to selectively inhibit insulin and GH release in rats. The release of these hormones is inhibited by an analog dose of 5 microgram/kg in short term experiments (15 min from analog administration to blood sampling), while glucagon levels are not lowered by analog doses as high as 500 microgram/kg. The lowered insulin to glucagon ratio results in hyperglycemia. [D-Ala5, D-Trp8]Somatostatin is also long acting; a 1 mg/kg dose results in hypoinsulinemia for 2 h and hyperglycemia for 3 h.

Alanine↗