Biomedical subjects

S M Innis

Publications and source records attributed to S M Innis.

At least 37 records · Page 2Linked to original sources

PubMed1999

Dietary canola oil alters hematological indices and blood lipids in neonatal piglets fed formula.

This study was undertaken to determine the effects of canola oil on platelet characteristics, blood lipids and growth in exclusively formula-fed piglets. Piglets were fed from birth to 10 or 18 d with formula containing 51% energy from fat, with 100% fat as canola or soybean oil; 26% soybean, 59% high oleic acid sunflower and 12% flax oil (canola mimic); or 26% canola (canola blend) or soybean (soybean blend) with high oleic acid sunflower, palm and coconut oil. The canola mimic provided similar carbon chain 16 and 18 fatty acids without the sterol or 20:1 and erucic acid (22:1) of canola oil. The oil blends provided formula resembling infant formulas but with higher 16:0 and lower unsaturated fatty acid levels than in canola or soybean oil. Body weight, weight gain and heart and liver weight were not different after 10 or 18 d feeding canola when compared to soybean oil alone or blended oil formulas. Piglets fed formulas with 100% canola oil had lower platelet counts than piglets fed formula soybean oil or the canola oil mimic. Platelet counts were lower, and platelet distribution width and volume were higher, when formulas with 100% canola or soybean rather than the blended oil formulas were fed. The results show that formula fat composition influences the developing hematological system and that canola oil suppresses the normal developmental increase in platelet count in piglets by a mechanism apparently unrelated to the formula 16:0, 18:1, 18:2(n-6) or 18:3(n-3), or plasma phospholipid 20:4(n-6) or 20:5(n-3).

Analysis of Variance↗

PubMed1998

Early diet influences hepatic hydroxymethyl glutaryl coenzyme A reductase and 7alpha-hydroxylase mRNA but not low-density lipoprotein receptor mRNA during development.

Plasma cholesterol levels increase after birth, and to a greater extent in breast-fed versus formula-fed infants. This increase is believed to be due to the high fat and cholesterol content of the infant diet, but little is known about the effects of early diet on the expression of proteins involved in regulating cholesterol metabolism. This study examined changes in the expression of hepatic proteins regulating cholesterol metabolism during development. Newborn piglets were fed sow milk or one of four formulas for 18 days. The formulas had similar levels of palmitic acid (16:0) as in milk, supplied as palm olein oil with 16:0 esterified predominantly to the sn-1,3 position or as synthesized triglyceride (TG) with 16:0 esterified mainly to the sn-2 position of glycerol, each with no cholesterol (<0.10 mmol/L) or 0.65 mmol/L cholesterol added. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis of mRNA levels was used to assess the effects of diet on hepatic hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase, low-density lipoprotein (LDL) receptor, and 7alpha-hydroxylase (C7H). LDL receptor mRNA levels showed no appreciable difference between milk- and formula-fed piglets. However, the levels of HMG-CoA reductase and C7H mRNA were higher (P < .05) in all formula-fed versus milk-fed piglets, irrespective of the formula TG source or cholesterol content. The lower levels of HMG-CoA reductase and C7H mRNA in milk-fed piglets were accompanied by higher (P < .05) plasma total, high-density lipoprotein (HDL), and apolipoprotein (apo) B-containing cholesterol. These studies show that the levels of hepatic HMG-CoA reductase and C7H mRNA, but probably not LDL receptor mRNA, are altered by early diet.

Animals↗

PubMed1998

Addition of triglycerides with arachidonic acid or docosahexaenoic acid to infant formula has tissue- and lipid class-specific effects on fatty acids and hepatic desaturase activities in formula-fed piglets.

The effects of including triglycerides with arachidonic [20:4(n-6)] or docosahexaenoic acid [22:6(n-3)] in formula on plasma chylomicron, LDL and HDL, liver, heart, kidney and brain (n-6) and (n-3) fatty acids were investigated in formula-fed piglets. Piglets were fed formula with (in % total fatty acids) 20% 18:2(n-6) and 2% 18:3(n-3) without or with 0.8% 20:4(n-6) or 0.3% 22:6(n-3) from birth to 18 d. The effects of adding 20:4(n-6) or 22:6(n-3) to the formula differed among different tissues and lipids, with the brain showing resistance to change. Piglets fed formula with 20:4(n-6) had significantly higher plasma, heart and kidney phospholipid and triglyceride, and liver triglyceride 20:4(n-6), but lower plasma and tissue phospholipid 18:2(n-6) than piglets fed formula without 20:4(n-6). Supplementation with 22:6(n-3), in contrast, had no effect on plasma or tissue 18:2(n-6). Higher 22:6(n-3) in liver phospholipid (30-92% greater) and triglyceride (200% greater) in piglets fed formula with 22:6(n-3) rather than without 22:6(n-3) was accompanied by lower 20:4(n-6) in liver phosphatidylethanolamine (mean +/- SEM, 8.6 +/- 0.4 and 10.5 +/- 0.4% fatty acids, respectively), but higher 20:4(n-6) in triglyceride (5.2 +/- 0.4 and 11.5 +/- 0.5%, respectively), and higher liver, heart and kidney phospholipid 20:5(n-3). These results indicate competitive interaction between dietary 20:4(n-6) and tissue 18:2(n-6), and between dietary 20:4(n-6) and tissue 20:5(n-3), rather than 22:6(n-3). The results also show that even at low intakes, dietary 22:6(n-3) or 20:4(n-6) supplementation alters the tissue phospholipid 20:4(n-6) to 20:5(n-3) balance. Studies on the physiologic effects of dietary 20:4(n-6) and 22:6(n-3) supplementation should consider the different sensitivity among tissues to dietary fatty acids.

Animals↗

PubMed1998

Effect of enteral nutritional products differing in carbohydrate and fat on indices of carbohydrate and lipid metabolism in patients with NIDDM.

Non-insulin dependent diabetes mellitus (NIDDM) is associated with chronic hyperglycemia, which increases the risk of developing microvascular and macrovascular complications. Elevated triglyceride (TG) and VLDL cholesterol levels and low levels of HDL cholesterol have also been frequently reported in NIDDM patients. A diet high in complex carbohydrate and low in fat is typically recommended for management of NIDDM, however, this has recently been challenged by scientific reports of the benefits of dietary intakes high in monounsaturated fat. Thirty-two individuals with NIDDM were randomized to receive either Ensure with Fibre (30% fat) or a high monounsaturated fatty acid product, Glucerna (50% fat). These products were consumed for 28 days at > 80% of daily energy intake. Post-treatment, dietary compliance was verified by a higher plasma TG 18:1 n-9 (p < 0.001) in the Glucerna group and a higher plasma TG 18:2 n-6 (p < 0.001) in the Ensure with Fibre group. The postprandial rise in blood glucose levels, determined by fingerprick samples, was significantly lower (p < 0.01) in the Glucerna group. Trends of clinical interest were greater mean decreases in the Glucerna group compared to the Ensure with Fibre group in: fructosamine, 9.13 umol/L vs 0.14 umol/L; glucose, 1.61 mmol/L vs 0.63 mmol/L; and insulin, 46.0 pmol/L vs 12.6 pmol/L; respectively. However, overall, fasting plasma glucose, fructosamine, TG and cholesterol levels were not significantly different between groups. Thus, in these patients, the high monounsaturated fat diet and the standard diet were similar with regard to usual indicators of carbohydrate and lipid metabolism. A high monounsaturated fat diet appears to pose no risk to lipoprotein metabolism in NIDDM patients.

Adolescent↗

PubMed1997

Visual acuity and blood lipids in term infants fed human milk or formulae.

This multicenter, parallel group study determined plasma phospholipid and red blood cell (RBC) phosphatidylcholine and phosphatidylethanolamine fatty acids, plasma cholesterol, apo A-1 and B, growth and visual acuity (using the acuity card procedure) in term infants fed from birth to 90 d of age with formula containing palm-olein, high oleic sunflower, coconut and soy oil (22.2% 16:0, 36.2% 18:1, 18% 18:2n-6, 1.9% 18:3n-3) (n = 59) or coconut and soy oil (10.3% 16:0 18:6% 18:1, 34.2% 18:2n-6, 4.7% 18:3n-3) (n = 57) or breast-fed (n = 56) with no formula supplementation. Different centers in North America were included to overcome potential bias due to differences in n-6 or n-3 fatty acids at birth or in breast-fed infants that might occur in a single-site study. Plasma and RBC phospholipid docosahexaenoic acid (DHA, 22:6n-3) and arachidonic acid (AA, 20:4n-6), cholesterol and apo B were significantly lower in the formula- than breast-fed infants. There were no differences in looking acuity or growth among the breast-fed and formula-fed infants. No significant relations were found between DHA and looking acuity, or AA and growth within or among any of the infant groups. This study provides no evidence to suggest the formula provided inadequate n-6 or n-3 fatty acids for growth and looking acuity for the first 3 mon after birth.

Apolipoproteins↗

PubMed1997

Diet-induced changes in liver and bile but not brain fatty acids can be predicted from differences in plasma phospholipid fatty acids in formula- and milk-fed piglets.

The fatty acid composition of plasma phospholipids differs between infants fed formula and infants fed human milk, but the extent to which this is accompanied by differences in tissue phospholipid fatty acids is unclear. This paper describes analysis of plasma, liver and brain fatty acids from piglets fed one of seven formulas, varying in saturated, monounsaturated, (n-6) and (n-3) fatty acids or sow milk from birth for 18 d. Bile fatty acids were analyzed because they are secreted from liver and may be an important source of fatty acids for intestinal lipoprotein synthesis. The results were used to determine the relation between diet-related differences in plasma phospholipid fatty acids and those in brain, liver and bile. Where significant associations were found, prediction limits were constructed to assess the usefulness of analysis of plasma phospholipid fatty acids to predict diet-induced changes in tissue fatty acids. The proportions (g/100 g fatty acids) of 16:0, 18:0, 18:1, 18:2(n-6) and 20:4(n-6) in plasma phospholipids were significantly associated with the proportions of the same fatty acids in liver and bile, but not brain. The results show a reasonably precise, predictable association between plasma and liver, and plasma and bile fatty acids. Brain 20:4(n-6) and 22:6(n-3), in contrast, were not reliably associated with plasma phospholipid 20:4(n-6) and 22:6(n-3) for piglets fed milk or formula providing about 1.5% energy as 18:3(n-3).

Animal Feed↗

PubMed1997

Dietary triacylglycerols with palmitic acid (16:0) in the 2-position increase 16:0 in the 2-position of plasma and chylomicron triacylglycerols, but reduce phospholipid arachidonic and docosahexaenoic acids, and alter cholesteryl ester metabolism in formula-Fed piglets.

Milk triacylglycerols have an unusual fatty acid distribution, with palmitic acid (16:0) esterified predominately at the center (sn-2) position. Other dietary triacylglycerols contain 16:0 predominantly at the sn-1,3 positions. This study was designed to evaluate the effect of formula triacylglycerol fatty acid distribution on the composition and distribution of plasma lipoprotein fatty acids in piglets fed formula containing synthesized triacylglycerols or palm olein oil with about 32 or 4.2% 16:0, respectively, in fatty acids at the sn-2 position, with comparison to piglets fed sow's milk. Feeding formula with 16:0 at the triglyceride sn-2 position or sow's milk resulted in higher chylomicron triacylglycerol sn-2 16:0 than when palm olein was fed. This suggests that dietary triacylglycerol sn-2 position fatty acids are conserved during digestion, absorption and reassembly to chylomicron triacylglycerols. The increased chylomicron triacylglycerol sn-2 position 16:0 in piglets fed synthesized triacylglycerols was accompanied by lower chylomicron triacylglycerol arachidonic and docosahexaenoic acid than in piglets fed formula with palm olein, suggesting an interaction between dietary triacylglycerol saturated fatty acid distribution and (n-6) and (n-3) fatty acid transport.

Animals↗

PubMed1997

Formula containing randomized fats with palmitic acid (16:0) in the 2-position increases 16:0 in the 2-position of plasma and chylomicron triglycerides in formula-fed piglets to levels approaching those of piglets fed sow's milk.

Human and pig milk fat contains a high proportion of palmitic acid (16:0) which is largely esterified to the 2-position of the triglycerides. In contrast, the 16:0 in most nonmilk fats and in infant formulas is mainly esterified at the triglyceride 1,3 positions. Gastric and pancreatic lipases hydrolyze fatty acids from the dietary triglyceride 1- and 3-positions to produce unesterified fatty acids and 2-monoglycerides which are absorbed and re-esterified. In this study, we determined whether formula with chemically randomized oils, which equally distributes 16:0 among all the positions of triglycerides, influences growth or the distribution of fatty acids in plasma and liver lipid of formula-fed piglets compared with piglets fed formula with native oils or sow's milk. After feeding from birth to 18 d, piglets fed formula with palm olein randomized with canola oil (co-randomized) had higher weight gain per liter of formula intake and higher 16:0 in the chylomicron triglyceride 2-position than piglets fed formula with randomized or native palm olein oil blended with canola oil. The fatty acid distribution of formula triglycerides is an important determinant of pathways of 16:0 absorption, and consequently of plasma lipid fatty acids in formula-fed piglets.

Animals↗

PubMed1996

Dietary triacylglycerol structure and saturated fat alter plasma and tissue fatty acids in piglets.

Human and pig milk triacylglycerols contain a large proportion of palmitic acid (16:0) which is predominately esterified in the 2-position. Other dietary fats contain variable amounts of 16:0, with unsaturated fatty acids predominantly esterified in the 2-position. These studies determined if the amount or position of 16:0 in dietary fat influences the composition or distribution of liver, adipose tissue, lung, or plasma fatty acids in developing piglets. Piglets were fed to 18 d with sow milk or formula with saturated fat from medium-chain triglyceride (MCT), coconut or palm oil, or synthesized triacylglycerols (synthesized to specifically direct 16:0 to the 2-position) with, in total fatty acids, 30.7, 4.3, 6.5, 27.0, and 29.6% 16:0, and in 2-position fatty acids, 55.3, 0.4, 1.3, 4.4, and 69.9% 16:0, respectively. The percentage of 16:0 in the 2-position of adipose fat from piglets fed sow milk, palm oil, and synthesized triacylglycerols were similar and higher than in piglets fed MCT or coconut oil. Thus, the amount, not the position, of dietary 16:0 determines piglet adipose tissue 16:0 content. The effects of the diets on the plasma and liver triacylglycerols were similar, with significantly lower 16:0 in total and 2-position fatty acids of the MCT and coconut oil groups, and significantly higher 16:0 in the plasma and liver triacylglycerol 2-position of piglets fed the synthesized triacylglycerols rather than sow milk or palm oil. The lung phospholipid total and 2-position 16:0 was significantly lower in the MCT, coconut, and palm oil groups, but similar in the synthesized triacylglycerol group and sow milk group. The lung phospholipid total and 2-position percentage of arachidonic acid (20:4n-6) was significantly lower in all of the formula-fed piglets than in milk-fed piglets. The physiological significance of this is not known.

Adipose Tissue↗

PubMed1996

Effect of medium-chain triglycerides on calbindin-D9k expression in the intestine.

These studies determined the effect of the saturated fat source in infant formula on the expression of calbindin-D9k (CaBP-9k). Piglets were fed from birth to 8 d with milk or formula containing saturated fatty acids as medium-chain triglycerides (MCT), coconut oil, palm oil (Palm 1), or synthesized triglycerides with 16:0 directed to the sn-2 position (Palm 2). Levels of intestinal CaBP-9k mRNA were significantly (P < 0.01) higher in piglets fed formula with MCT than in piglets fed the other formula or milk; and higher in piglets fed the Palm-1 than in piglets fed Palm-2 formula. This is the first evidence that MCT alter piglet intestinal CaBP-9k mRNA.

Animals↗

PubMed1996

Blood lipid docosahexaenoic and arachidonic acid in term gestation infants fed formulas with high docosahexaenoic acid, low eicosapentaenoic acid fish oil.

The effect of fish oil high in docosahexaenoic acid (22:6n-3) and low in eicosapentaenoic acid (20:5n-3) in formula on blood lipids and growth of full-term infants was studied. Infants were fed formula with about 15% oleic acid (18:1), 32% linoleic acid (18:2n-6), 4.9% linolenic acid (18:3n-3) and 0, 0.10, or 0.22% 22:6n-3, or 35% 18:1, 20% 18:2n-6, 2.1% 18:3n-3 and 0, 0.11, or 0.24% 22:6n-3 from 3 d to 16 wk of age (n = 16,18,17,21,17,16, respectively). The formulae had < 0.1% 20:5n-3 and no arachidonic acid (20:4n-6). Breast-fed infants (n = 26) were also studied. Plasma phospholipid and red blood cell (RBC) phosphatidylcholine (PC) and phosphatidylethanolamine (PE) fatty acids were determined at 3 d and 4, 8, and 16 wk of age. These longitudinal analyses showed differences in blood lipid 22:6n-3 between breast-fed and formula-fed infants depending on the feeding duration. At 16 wk, infants fed formula with 0.10, 0.11% 22:6n-3, or 0.22% 22:6n-3 had similar 22:6n-3 levels in the plasma phospholipid and RBC PC and PE compared with breast-fed infants, and higher 22:6n-3 than infants fed formula without 22:6n-3. Formula with 0.24% 22:6n-3, however, resulted in higher plasma phospholipid 22:6n-3 than in breast-fed infants at 16, but not 4 or 8 wk of age. Plasma and RBC phospholipid 20:4n-6 was lower in formula-fed than breast-fed infants, but no differences in growth were found. Higher blood lipid C20 and C22 n-6 and n-3 fatty acids in infants fed formula with 20% 18:2n-6 and 2.4% 18:3n-3 compared with 32% 18:2n-6 and 4.9% 18:3n-3 show the increase in blood lipid 22:6n-3 in response to dietary 22:6n-3 depending on other fatty acids in the formula.

Arachidonic Acid↗

PubMed1996

Feeding formula without arachidonic acid and docosahexaenoic acid has no effect on preferential looking acuity or recognition memory in healthy full-term infants at 9 mo of age.

Preferential looking acuity and novelty preference (a test of recognition memory) were determined by using Teller Acuity Cards and the Fagan Test of Infant Intelligence, respectively, for 399-433 healthy full-term infants at 39 +/- 1 wk of age. Duration of breast-feeding and age of infant at introduction and amount and type of formula were determined by questionnaire. Seventy-four infants (17%) were never breast-fed; another 92 infants (21%) were still receiving breast milk as the milk source at 39 wk of age. There were no differences in visual acuity or novelty preference among the infants when they were stratified by incidence or duration of breast-feeding. The formulas met current Canadian guidelines with > or = 0.7% of energy as linolenic acid, but had no docosahexaenoic or arachidonic acid. The studies indicate that formulas containing adequate linoleic and linolenic acids, without arachidonic or docosahexaenoic acid, impose no measurable deficits in performance in these visual and cognitive developmental tests at 9 mo of age in healthy full-term infants.

Arachidonic Acid↗

PubMed1996

Plasma fatty acid responses, metabolic effects, and safety of microalgal and fungal oils rich in arachidonic and docosahexaenoic acids in healthy adults.

The effect of dietary supplementation with different amounts of a fungal oil containing arachidonic acid (AA, 20:4n--6) and a microalgal oil containing docosahexaenoic acid (DHA, 22:6n--3), blended to give a ratio of AA to DHA of 1.25:1.00, on plasma lipid AA, DHA, cholesterol, and triacylglycerols was evaluated in healthy men. Subjects (n = 8/group) were given 28.8 g fat/d containing 0 x (0 g AA, 0 g DHA), or 1 x (0.8 g AA, 0.6 g DHA), 3 x (2.2 g AA, 1.7 g DHA), or 5 x (3.6 g AA, 2.9 g DHA) the estimated intake of infants fed human milk with 0.5% AA and 0.4% DHA for 14 d. No clinically significant dose-related effects were seen on physical examination or from routine laboratory tests. The microalgal-fungal oil blend resulted in a significant, dose-dependent increase in plasma cholesterol and percentage phospholipid AA and DHA, and a decrease in percentage triacylglycerols and phospholipid linoleic acid. Plasma phospholipid AA and DHA increased approximately 18% and 50%, respectively, with the 1 x dose, similar to that expected at intakes provided by human milk. These oils appear to be safe dietary sources of AA and DHA for healthy adults at intakes equivalent to 0.8 g AA and 0.6 g DHA/d for > or = 2 wk.

Adult↗

PubMed1995

Palmitic acid is absorbed as sn-2 monopalmitin from milk and formula with rearranged triacylglycerols and results in increased plasma triglyceride sn-2 and cholesteryl ester palmitate in piglets.

Milk fatty acids contain 20-30% palmitic acid (16:0), with approximately 70% of the 16:0 esterified to the sn-2 position of the milk triacylglycerol. Formulae containing vegetable and oleo oils contain different amounts of 16:0, but all have unsaturated fatty acids esterified to the triacylglycerol sn-2 position. Intraluminal triacylglycerol hydrolysis by endogenous lipases produces sn-2 monoacylglycerols and free fatty acids, which are absorbed and re-esterified in the enterocyte for secretion to plasma. The extent of absorption and re-esterification of sn-2 monoacylglycerols from milk or formula fats in infants is unknown. This was studied by feeding piglets sow milk or formulae containing similar total saturated fat, 18:1, 18:2(n-6) and 18:3(n-3) with unsaturated fatty acids at the sn-2 position or with rearranged triacylglycerols containing approximately 30% 16:0, with 70% 16:0 in fatty acids at the sn-2 position. Feeding milk or 16:0 on the sn-2 position of formula with rearranged triacylglycerols resulted in higher 16:0 esterified to the plasma triacylglycerol sn-2 position and in cholesteryl esters than feeding formulae with 0.4 to 4.4% 16:0 in the sn-2 position fatty acids. The absorption of 16:0 as monopalmitin from milk and any metabolic importance in human infants has yet to be determined.

Animals↗

PubMed1995

Marine and freshwater fish oil varying in arachidonic, eicosapentaenoic and docosahexaenoic acids differ in their effects on organ lipids and fatty acids in growing rats.

Arachidonic acid [20:4(n-6)] and docosahexaenoic acid [22:6(n-3)] are important to normal neurodevelopment and visual function. Infants fed formula often have low blood lipid 20:4(n-6) and 22:6(n-3). Consumption of fish oils high in eicosapentaenoic acid [20:5(n-3)] and 22:6(n-3) with no 20:4(n-6) increases tissue 20:5(n-3) and 22:6(n-3) but decreases 20:4(n-6). Some freshwater fish oils contain higher 20:4(n-6) and lower 20:5(n-3) than usual marine fish oils, but their effects on tissue fatty acids are not well known. Therefore, the effects of feeding weaning rats 30 d with 12% (wt/wt) soybean oil [0.0% 20:4(n-6), 20:5(n-3) and 22:6(n-3)], 2% safflower oil with 10% marine fish oil [0.9% 20:4(n-6), 15.1% 20:5(n-3), 7.3% 22:6(n-3)] or 10% freshwater fish oil [3.3% 20:4(n-6), 5.9% 20:5(n-3), 8.0% 22:6(n-3)] on plasma, tissue and brain fatty acids was determined. Levels (g/100 g) of 20:4(n-6) were significantly higher and 20:5(n-3) lower in plasma, liver, kidney and brain of rats fed freshwater fish oil rather than marine fish oil. Marine fish oil, but not freshwater fish oil resulted in a higher brain 20:5(n-3) and 22:6(n-3), and lower 20:4(n-6) than soybean oil. Plasma and liver triglyceride concentrations were significantly lower in rats fed marine fish oil, but not in rats fed soybean oil when compared with those fed freshwater fish oil. The results indicate dietary 20:4(n-6) prevents the decline in plasma and tissue 20:4(n-6) caused by dietary 20:5(n-3) and/or 22:6(n-3). Oils with 20:4(n-6) may affect cholesterol and triglyceride metabolism differently than usual fish oils.

Animals↗

PubMed1994

Evidence that palmitic acid is absorbed as sn-2 monoacylglycerol from human milk by breast-fed infants.

Milk fatty acids consist of about 20-25% palmitic acid (16:0), with about 70% of 16:0 esterified to the sn-2 position of the milk triacylglycerols. Hydrolysis of dietary triacylglycerols by endogeneous lipases produces sn-2 monoacylglycerols and free fatty acids, which are absorbed, reesterified, and then secreted into plasma. Unesterified 16:0 is not well absorbed and readily forms soaps with calcium in the intestine. The positioning of 16:0 at the sn-2 position of milk triacylglycerols could explain the high coefficient of absorption of milk fat. However, the milk lipase, bile salt-stimulated lipase, has been suggested to complete the hydrolysis of milk fat to free fatty acids and glycerol. These studies determined whether 16:0 is absorbed from human milk as sn-2 monopalmitin by comparison of the plasma triacylglycerol total and sn-2 position fatty acid composition between breast-fed and formula-fed term gestation infants. The human milk and formula had 21.0 and 22.3% of 16:0, respectively, with 54.2 and 4.8% 16:0 in the fatty acids esterified to the 2 position. The plasma triacylglycerol total fatty acids had 26.0 +/- 0.6 and 26.2 +/- 0.6% of 16:0, and the sn-2 position fatty acids had 23.3 +/- 3.3 and 7.4 +/- 0.7% of 16:0 in the three-month-old exclusively breast-fed (n = 17) and formula-fed (n = 18) infants, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Breast Feeding↗

PubMed1994

Plasma and tissue lipids of piglets fed formula containing saturated fatty acids from medium-chain triglycerides with or without fish oil.

Addition of fish oil (FO) with carbon chain 20 and 22 (long-chain polyunsaturated fatty acids; LCPs) n-3 fatty acids to formula has been considered as a method to provide 22:6n-3 to preterm infants. These studies determined the effects of including 0.73% n-3 LCPs from FO in formula containing saturated fatty acids as medium-chain triglyceride (MCT) oil on plasma and organ triglyceride (TG), phospholipid (PL), and cholesterol ester (CE) contents and compositions in piglets. Reference piglets were fed their own mother's milk. Piglets fed the formula with FO had significantly lower liver and kidney, but not plasma, TG concentrations; lower liver PL 20:4n-6; and higher plasma, liver, and kidney TG, PL, and CEn-3 LCPs than piglets fed the formula without FO. The increase in liver and kidney lipid n-3 LCPs and the decrease in kidney lipid content shows that inclusion of FO in formula with a high content of MCTs and 18:2n-6 does not promote tissue lipid metabolism similar to natural milk feeding. Piglets fed formula with FO had similar brain 20:4n-6 and 20:5n-3 but higher 22:6n-3 than did piglets fed sow milk. Diet-related differences in plasma and red blood cell PL were not reliable predictors of differences in brain LCP.

Animals↗

PubMed1994

Development of visual acuity in relation to plasma and erythrocyte omega-6 and omega-3 fatty acids in healthy term gestation infants.

The development of preferential looking acuity was studied prospectively to 3 mo of age in exclusively breast-fed and formula-fed term gestation infants. The formula contained (% of total fatty acids) 17.9% linoleic acid (18:2 omega-6) and 2.1% alpha-linolenic acid (18:3 omega-3) but no docosahexaenoic acid (22:6 omega-3) or arachidonic acid (20:4 omega-6). The breast milk contained (mean +/- SEM) 13.4 +/- 0.8% 18:2 omega-6, 1.5 +/- 0.1% 18:3 omega-3, 0.51 +/- 0.03% 20:4 omega-6, and 0.22 +/- 0.02% 22:6 omega-3. Preferential looking acuity, assessed by the acuity-card procedure, and plasma phospholipid and erythrocyte phosphatidylcholine and phosphatidylethanolamine fatty acids were determined at 14 d and 3 mo of age. There were no significant differences in acuity at 14 d or 3 mo, despite substantial differences in erythrocyte and plasma lipid 22:6 omega-3. Visual acuity was [mean (cycles/degree) +/- SD (octaves)] 3.93 +/- 0.54 and 4.77 +/- 0.48 and erythrocyte phosphatidylethanolamine %22:6 omega-3 was (mean +/- SE) 7.6 +/- 0.5 and 4.0 +/- 0.2 in the 3-mo-old breast-fed and formula-fed infants, respectively. These studies show that feeding formula containing 2.1% 18:3 omega-3 (approximately 1.0% energy) results in development of visual acuity similar to breast-feeding in term infants to > or = 3 mo of age.

Breast Feeding↗