PubMed Health⌕ Search

Biomedical subjects

Hope A Weiler

Publications and source records attributed to Hope A Weiler.

At least 19 recordsLinked to original sources

Dietary arachidonic acid and docosahexaenoic acid elevate femur calcium and reduce zinc content in piglets.

Specific dietary polyunsaturated fatty acids (PUFAs) and long chain PUFAs (LCPUFAs) elevate femur calcium content and enhance calcium balance. Mother's milk is associated with enhanced calcium balance and contains LCPUFAs; arachidonic acid (AA), and docosahexanoic acid (DHA). However, the effect of AA and DHA on calcium metabolism and other bone minerals during infancy is unknown. Thus, piglets received one of four formulas (15 d): control or with AA:DHA (0.5:0.1 g, 1.0:0.2 g, or 2.0:0.4 g/100 g of fat). Calcium absorption, femur mineral composition, and urinary mineral excretion. Main effects identified using two-way analysis of variance (ANOVA) and post hoc analysis conducted using Duncan's multiple range test. Significant effects of diet were observed in femur calcium and zinc content, but not calcium absorption, urinary mineral excretion, femur ash weight, femur phosphorus, or femur magnesium content. The piglets receiving AA:DHA as 1.0:0.2 g/100 g of fat had 1.9% higher mg calcium/g of ash, but 8.6% lower mug zinc/g of ash compared with control. Thus, AA:DHA in a ratio of 5:1 does not affect mineral accretion, but AA plus DHA, in amounts similar to the upper limit of human milk, might be detrimental to bone mineralization over time due to lower zinc.

Absorptiometry, Photon↗

Marginal zinc deficiency exacerbates bone lead accumulation and high dietary zinc attenuates lead accumulation at the expense of bone density in growing rats.

Environmental lead exposure is associated with reduced bone growth and quality, which may predispose to osteoporosis. Zinc supplementation may reduce lead accumulation; however, effects on bone development have not been addressed. Our objective was to investigate the effects of marginal zinc (MZ) and supplemental zinc (SZ) intakes on bone lead deposition and skeletal development in lead-exposed rats. In a factorial design, weanling Sprague-Dawley rats were assigned to MZ (8 mg/kg diet); zinc-adequate control (CT; 30 mg/kg); zinc-adequate, diet-restricted (DR; 30 mg/kg); or SZ (300 mg/kg) groups, with and without lead acetate-containing drinking water (200 mg Pb/l) for 3 weeks. Excised femurs were analyzed for bone mineral density (BMD) by dual-energy x-ray absorptiometry, morphometry, and mineral content. MZ had higher femur lead and lower femur zinc concentrations and impaired skeletal growth and mineralization than CT. DR inhibited growth but did not result in higher femur lead concentrations than CT. SZ had higher femur zinc and lower femur lead concentrations than the other treatments. DR and SZ had impaired BMD versus CT and MZ. Lead also retarded skeletal growth and impaired BMD, but an interaction between lead and MZ was only found for femoral knee width, which was lower in MZ exposed to lead. In summary, while MZ deficiency exacerbated bone lead concentration, it generally did not intensify lead toxicity. SZ was protective against bone lead but was detrimental to BMD, suggesting that the optimal level of SZ to reduce lead absorption, while supporting growth and bone development, requires further investigation.

Animals↗

Plasma adipokines and body composition in response to modest dietary manipulations in the mouse.

OBJECTIVE: The relationship between adipokine levels and body composition has not been carefully examined. Most studies in humans are cross-sectional, and the few studies in mice have been restricted to a comparison of control animals with markedly obese, insulin-resistant mice. Our objective was to study changes in adipokine levels and body composition in response to modest dietary intervention. RESEARCH METHODS AND PROCEDURES: Plasma resistin, adiponectin, and leptin levels were examined in mice fed ad libitum, a 75% restricted diet, or a diet supplemented with 10% sucrose. Body composition was determined by whole-body DXA. RESULTS: The percentage body fat was reduced in mice subjected to the restricted diet and increased in mice supplemented with 10% dextrose. Adipokine levels were not different in either of these groups compared with the control mice. A significant inverse correlation was observed between resistin levels and total body fat, whereas there was no significant correlation between body fat and adiponectin levels. Positive correlations were observed between leptin levels and percentage body fat, total body fat, and abdominal fat. Leptin levels correlated with plasma glucose, but multivariate analysis revealed that this correlation was the result of a strong positive correlation between leptin and insulin levels. There were no correlations between glycemia and resistin or glycemia and adiponectin levels, and no correlation was observed between any of the adipokine levels and bone mineral content or density. DISCUSSION: These data suggest that in the mouse, modest dietary perturbations have little effect on resistin and adiponectin levels despite significant effects on glycemia, insulin levels, and bone parameters.

Adiponectin↗

Minimal enteral feeding within 3 d of birth in prematurely born infants with birth weight < or = 1200 g improves bone mass by term age.

BACKGROUND: Evidence-based practice guidelines for aggressive nutritional intervention by using parenteral amino acids (AAs) and minimal enteral feeding (MEF) as early as the first day of life have not been tested for benefits to bone mass. OBJECTIVE: We investigated whether early introduction of parenteral AAs and MEF improves growth and bone mass achieved by term age in infants born prematurely. DESIGN: Twenty-seven infants who were < or = 1200 g and < or = 32 wk gestation at birth were randomly assigned by using a 2 x 2 design to treatment of either 1 g AAs/kg within the first 24 h or 12 mL MEF x kg(-1) x d(-1) within the first 72 h of life. Nutrition and growth were documented during hospitalization, and bone mineral content (BMC) of lumbar spine 1-4, femur, and whole body was measured at term age. Biomarkers of bone metabolism were measured at weeks 1, 3, and 5 and at discharge. Statistical analysis was conducted by using 2 x 2 analysis of variance for intent to treat and for infants receiving protocol nutrition. RESULTS: Over the first 14 d of life, a main effect of early AAs elevated total intake of protein, and a main effect of early MEF was a higher frequency of MEF volumes exceeding > 12 mL x kg(-1) x d(-1). Main effects on growth were not evident. An interaction effect was observed for osteocalcin whereby early AAs or MEF alone elevated osteocalcin. A main effect of early MEF yielded higher BMC of spine and femur. CONCLUSION: Early aggressive nutrition support with MEF enhances BMC in premature infants, but early MEF or AAs do not improve growth.

Absorptiometry, Photon↗

Dietary conjugated linoleic acid does not adversely affect bone mass in obese fa/fa or lean Zucker rats.

Conjugated linoleic acid (CLA) elevates body ash in healthy animals. The objective of the present study was to determine if single or mixed CLA isomers improve bone mass in an obese and hyperinsulinemic state. Male (n = 120) lean and obese fa/fa Zucker rats (age, 6 weeks) were randomized to 8 weeks on a control diet or to 0.4% (w/w) cis-9, trans-11 CLA (Group 1); 0.4% (w/w) trans-10, cis-12 CLA (Group 2); 0.4% (w/w) cis-9, trans-11 CLA and 0.4% (w/w) trans-10, cis-12 CLA (Group 3); 0.4% (w/w) cis-9, trans-11 CLA, 0.4% (w/w) trans-10, cis-12 CLA, and traces of other CLA isomers (Group 4); and 0.4% (w/w) cis-9, trans-11 CLA, 0.4% (w/w) trans-10, cis-12 CLA, and 0.3% (w/w) other CLA isomers (Group 5). Bone area (BA), bone mineral content (BMC), and bone mineral density (BMD) of the whole body, spine, and femur were measured at baseline (6 weeks) and at 14 weeks of age. Effects of genotype, diet, and genotype x diet interactions were assessed using factorial analysis of variance. At 6 and 14 weeks, whole-body BA and BMC were lower in lean rats compared with fa/fa rats. Similarly, at 14 weeks, fa/fa rats had a higher spine and femur BMD despite a lower femur weight. The fa/fa rats in Groups 4 and 5 had higher adjusted whole-body BMC compared with Group 3, but not with Group 1, Group 2, or the control. In lean rats, Group 3 had a greater adjusted whole-body BMC than Groups 1 and 2, but not Group 4, Group 5, or the control. Thus, commercially available CLA mixtures and single CLA isomers do not affect bone mass in a hyperinsulinemic, obese state.

Animals↗

(n-3) fatty acids reduce the release of prostaglandin E2 from bone but do not affect bone mass in obese (fa/fa) and lean Zucker rats.

Childhood obesity is prevalent and linked to the development of Type 2 diabetes mellitus (DM) and poor bone health. Some PUFA enhance bone mass and thus may improve bone health in obese children. The study objective was to determine the effects of dietary (n-6) compared with (n-3) essential PUFA and long-chain PUFA (LCPUFA) on bone in an obese and insulin-resistant state. Male fa/fa (n = 48) and lean Zucker rats (n = 48) were fed diets containing safflower oil [SO, high (n-6) PUFA], flaxseed oil [FXO, high (n-3) PUFA], or menhaden oil [MO, high (n-3) LCPUFA] for 9 wk. Measurements included the following: femur bone area (BA), mineral content (BMC), density (BMD), morphometry and ex vivo release of prostaglandin E(2) (PGE(2)); plasma osteocalcin and C-terminal telopeptides of type I collagen. Differences among groups were detected using 2-way ANOVA. Genotype effects in the fa/fa rats included lower femoral weight, length, BA, and BMC, as well as femoral head and proximal epiphysis widths compared with the lean rats, but BMD was not affected. Femur BA, BMC, and BMD did not differ among the dietary groups, but diaphysis width was elevated in the MO group and PGE(2) release was reduced by the FXO and MO diets. No genotype x diet interactions were observed. These data indicate that the fa/fa Zucker rat is at risk for low bone mass and that dietary (n-3) FA effectively reduce PGE(2) release. Whether reduced PGE(2) will support optimal peak bone mass during childhood and conserve bone mass with aging warrants investigation.

Animals↗

Low levels of dietary arachidonic and docosahexaenoic acids improve bone mass in neonatal piglets, but higher levels provide no benefit.

In piglets, feeding arachidonic acid (AA) and docosahexaenoic acid (DHA) in a 5:1 ratio leads to elevated bone mass, but the optimal total quantity requires clarification. We studied bone mass and modeling of piglets that were randomized to receive 1 of 4 formulas for 15 d: control formula or the same formula with various levels of AA:DHA (0.5:0.1 g, 1.0:0.2 g or 2.0:0.4 g AA:DHA/100 g of fat). Measurements included: bone area (BA), mineral content (BMC), and density (BMD) of whole body, lumbar spine, and excised femurs; biomarkers of bone modeling were plasma osteocalcin and urinary cross-linked N-telopeptides of type 1 collagen (NTx), tibial ex vivo release of prostaglandin E(2) (PGE(2)), plasma insulin-like growth factor-1 (IGF-1), and tissue fatty acids. Main effects were identified using ANOVA and post hoc Bonferroni t tests. In supplemented piglets, relations among liver fatty acid proportions and bone mass were assessed using Pearson correlations. Whole body (P = 0.028) and lumbar spine (P = 0.043) BMD were higher in the group supplemented with 0.5:0.1 g AA:DHA/100 g of fat than in controls. Tissue AA and DHA increased in proportion to diet levels. Liver eicosapentaenoic acid (EPA) correlated positively (r > or = 0.38, P < or = 0.05) with whole body and femur BMC and BMD and lumbar spine BMC. Liver AA:EPA ratio correlated negatively (r > or = -0.039, P < or = 0.05) with whole body, femur, and lumbar spine BMC plus whole body and femur BMD. Dietary 1.0:0.2 g AA:DHA/100 g reduced NTx relative to 2.0:0.4 g AA:DHA/100 g of fat (P = 0.039). The diets did not affect the other biochemical variables measured. Low levels of dietary AA:DHA (0.5:0.1 g/100 g of fat) elevate bone mass, but higher amounts are not beneficial.

Animals↗

Proximal intestinal absorption of calcium is elevated in proportion to growth rate but not bone mass is small for gestational age piglets.

During the first year of life, body calcium content increases faster in relation to body size than any other time during growth. Studies have shown postnatal growth and bone mineralization differences between appropriate for gestational age and small for gestational age infants. The objective of this study was to compare duodenal calcium transport using intestinal ligated loop technique in 21-day-old small for gestational age (birth weight of <1.2 kg) and appropriate for gestational age piglets (birth weight of > or =1.4 kg). Piglets were fed liquid formula between day 5 and 21 of life and monitored daily for weight gain. At day 21 calcium absorption was measured followed by measurement of bone mass using dual energy x-ray absorptiometry. Small for gestational age piglets had greater calcium absorption and growth rate than appropriate for gestational age piglets. Birth weight was negatively related to weight gain and calcium absorption. Weight gain was positively related to calcium absorption. Appropriate for gestational age piglets had significantly higher whole body bone mineral content than small for gestational age piglets even after correction for body size. Whole body bone mineral content was positively correlated with birth weight and negatively correlated with calcium absorption. These observations suggest that small for gestational age piglets are capable of absorbing elevated amounts of calcium in the proximal intestine in support of compensatory growth. However, at 21 days of age small for gestational age piglets are similar in size but have lower bone mass compared to appropriate for gestational age piglets.

Absorptiometry, Photon↗

The effect of dietary n-3 long-chain polyunsaturated fatty acids on femur mineral density and biomarkers of bone metabolism in healthy, diabetic and dietary-restricted growing rats.

INTRODUCTION: Dietary fish oil promotes bone formation in healthy states, but its effect during insulin deficiency or nutrient restriction is unclear. METHODS: Eighty weanling male rats were randomized to receive an injection of streptozotocin to induce insulin deficiency (diabetes) or saline (control) and a diet containing soy oil or corn + fish oil for 35 days. Half of the saline-injected rats were randomized to 20% dietary restriction. Measurements were growth, biomarkers of bone metabolism and femur bone mass. RESULTS: Density of femur was elevated in the corn + fish group and reduced in the diabetes group. Plasma osteocalcin and bone prostaglandin E2 (PGE2) were reduced by the corn + fish diet. N-telopeptide, IGF-1, bone PGE2 and urinary Ca were highest and calcitriol lowest in the diabetes group. CONCLUSIONS: These data suggest that the benefit of a diet high in n-3 long-chain polyunsaturated fatty acid is most advantageous to long bone density in healthy states.

Animals↗

Dose response of bone mass to dietary arachidonic acid in piglets fed cow milk-based formula.

BACKGROUND: The addition of arachidonic acid (AA) and docosahexaenoic acid (DHA) to infant formula was recently approved in North America. In piglets, dietary AA is linked to elevations in bone mass. OBJECTIVE: The objective was to investigate the effects of varied amounts of dietary AA on bone modeling and bone mass with the use of the piglet model for infant nutrition. DESIGN: Male piglets (n = 32) were randomly assigned to receive 1 of 4 formulas supplemented with AA (0.30%, 0.45%, 0.60%, or 0.75% of fat) plus DHA (0.1% of fat) from days 5 to 20 of life. Measurements included biomarkers of bone modeling, fatty acid status, and whole-body and femur bone mineral content; bone area was measured by dual-energy X-ray absorptiometry. Differences among groups were detected with two-factor analysis of variance. Regression analyses were used to determine factors responsible for bone mineral content after dietary AA was accounted for. RESULTS: Proportions of AA in plasma, liver, and adipose were modified by the dietary treatments, but bone modeling was not affected. Liver AA was positively related to plasma insulin-like growth factor 1 and calcitriol and urinary N-telopeptide. Whole-body bone mineral content was elevated in the piglets fed 0.60% and 0.75% AA and was best predicted by dietary AA and bone resorption. CONCLUSIONS: This study confirms that dietary AA alters bone mass and clarifies the best amount of AA to add to the diet of pigs born at term. Because the amount of dietary DHA was held constant, whether other amounts of DHA are related to bone mass requires investigation.

Animals↗

Dietary soy protein attenuates renal disease progression after 1 and 3 weeks in Han:SPRD-cy weanling rats.

Compared with casein, dietary soy protein slows disease progression in animal models of chronic renal injury. To determine whether dietary soy protein feeding can alter early disease progression, male Han:SPRD-cy rats (n = 87) in a very early stage of chronic kidney disease were fed soy protein compared with casein-based diets for 1 or 3 wk. Kidneys were assessed for fibrosis, cyst growth, fatty acid composition and prostaglandin E(2) (PGE(2)) production. Soy protein feeding significantly reduced renal fibrosis by 22% (P = 0.0347) and 38% (P = 0.0102) after 1 and 3 wk of diet, and cyst growth was 34% lower after 3 wk (P < 0.0001). Kidney 18:2(n-6) levels were reduced in normal and diseased rats after as little as 1 wk of consuming the soy protein diet. Dietary soy protein also partially ameliorated the suppression of PGE(2) production observed in diseased kidneys. Compared with diseased kidneys from casein-fed rats, ex vivo PGE(2) release was 31-32% higher after 1 (P = 0.0281) and 3 (P = 0.0189) wk of dietary soy protein consumption. Hence, the first signs of a beneficial soy protein effect were observed after 1 wk of feeding, with further improvements evident after 3 wk. These data demonstrate that dietary soy protein compared with casein delays disease progression in an early stage of chronic kidney disease.

Animals↗

Zinc-deficient rats have more limited bone recovery during repletion than diet-restricted rats.

The objective of this study was to investigate the effects of dietary zinc deficiency and diet restriction on bone development in growing rats, and to determine whether any adverse effects could be reversed by dietary repletion. Weanling rats were fed either a zinc-deficient diet ad libitum (ZD; <1 mg zinc/kg) or nutritionally complete diet (30 mg zinc/kg) either ad libitum (CTL) or pair-fed to the intake of the ZD group (DR; diet-restricted) for 3 weeks (deficiency phase) and then all groups were fed the zinc-adequate diet ad libitum for 3, 7, or 23 days (repletion phase). Excised femurs were analyzed for bone mineral density (BMD) using dual-energy x-ray absorptiometry, and plasma was analyzed for markers of bone formation (osteocalcin) and resorption (Ratlaps). After the deficiency phase, ZD had lower body weight and reduced femur BMD, zinc, and phosphorus concentrations compared with DR; and these parameters were lower in DR compared with CTL. Femur calcium concentrations were unchanged among the groups. Reduced plasma osteocalcin in ZD and elevated plasma Ratlaps in DR suggested that zinc deficiency limits bone formation while diet restriction accelerates bone resorption activity. After 23 days of repletion, femur size, BMD, and zinc concentrations remained lower in ZD compared with DR and CTL. Body weight and femur phosphorus concentrations remained lower in both ZD and DR compared with CTL after repletion. There were no differences in plasma osteocalcin concentrations after the repletion phase, but the plasma Ratlaps concentrations remained elevated in DR compared with CTL. In summary, both ZD and DR lead to osteopenia during rapid growth, but the mechanisms appear to be due to reduced modeling in ZD and higher turnover in DR. Zinc deficiency was associated with a greater impairment in bone development than diet restriction, and both deficiencies limited bone recovery during repletion in growing rats.

Animals↗

Dietary arachidonic acid suppresses bone turnover in contrast to low dosage exogenous prostaglandin E(2) that elevates bone formation in the piglet.

This study was designed to compare the effects of dietary arachidonic acid (AA) versus prostaglandin E(2) (PGE(2)) on bone cell metabolism and bone mass. Twenty-eight piglets from 7 litters were randomized to 1 of 4 treatments for 15 days: fatty acid supplemented formula (FA: 0.8% of total fatty acids as AA and 0.1% of total fatty acids as DHA)+PGE(2) injections (0.1mg/kg/day), FA+saline injections, standard formula (STD: n-6:n-3 of 8:1) + PGE(2) injections or STD+saline injections. PGE(2) resulted in elevated osteoblast activity as indicated by plasma osteocalcin and also reduced urinary calcium excretion. Dietary FA resulted in reduced bone resorption as indicated by urinary N-telopeptide and reduced bone PGE(2). Both PGE(2) and FA treatments independently lead to elevated femur mineral content, but the combined treatment caused a reduction. Thus the mechanisms by which PGE(2) and FA lead to enhanced bone mass are distinct.

Animals↗

Dietary conjugated linoleic acid reduces PGE2 release and interstitial injury in rat polycystic kidney disease.

BACKGROUND: Conjugated linoleic acid (CLA) describes positional isomers of linoleic acid (LA). Experimental health benefits of CLA include amelioration of malignancy and inflammatory disease and reduction of adiposity. The Han:SPRD-cy rat model of polycystic kidney disease (PKD) features prominent renal interstitial inflammation and fibrosis that is amenable to dietary modification. We studied CLA supplementation in the modification of inflammatory outcomes in the Han:SPRD-cy rat. METHODS: Male offspring of Han:SPRD-cy heterozygotes were fed diets, using corn oil or corn oil with a CLA enriched oil (1% of diet by weight as CLA). After 8 weeks, measurements included renal function and morphometry, ex vivo release of renal prostaglandin E2 (PGE2), and renal and hepatic tissue fatty acid profiles. RESULTS: Urine creatinine was significantly higher in PKD animals fed CLA (P = 0.004), but differences in serum creatinine and creatinine clearance did not quite reach significance in PKD animals. CLA feeding reduced interstitial inflammation (P < 0.001), fibrosis (P = 0.03), and renal PGE2 release (P = 0.02). Cystic change and oxidized low-density lipoprotein (LDL) staining did not change significantly. CLA feeding produced increased renal and hepatic CLA isomers. Hepatic, but not renal, LA proportion was reduced on the CLA diet. The renal proportion of the PGE2 precursor, arachidonic acid (AA), was not changed by diet, but hepatic AA proportion increased significantly with CLA feeding (P= 0.009). CONCLUSION: CLA reduces renal production of PGE2, without reduced availability of the precursor fatty acid, AA. Short-term feeding of CLA to Han:SPRD-cy rats also has significant renal anti-inflammatory and antifibrotic effects. As inflammation and fibrosis are important components of the progression of chronic renal injury, CLA may be a useful agent in dietary amelioration of renal disease.

Animals↗

Dietary flax oil reduces renal injury, oxidized LDL content, and tissue n-6/n-3 FA ratio in experimental polycystic kidney disease.

As whole flaxseed is beneficial in the treatment of experimental renal disease, we undertook a study to determine whether previously documented benefits of whole flaxseed could be reproduced with dietary low-lignan flax oil (FO), a rich source of alpha-linolenic acid, in experimental polycystic kidney disease. Male offspring of Han:SPRD-cy heterozygous rats were fed a synthetic diet containing FO or corn oil (CO) for 8 wk from the time of weaning. Renal inflammation, fibrosis, proliferation, cystic change, and oxidized-LDL were assessed morphometrically. Hepatic and renal lipid composition was assessed using GC. FO feeding produced hepatic and renal enrichment of n-3 PUFA and an increase in C18:>C18 PUFA ratios (18-carbon PUFA compared to longer-chain PUFA), with a reduction in proportion of hepatic long-chain PUFA. The FO-based diet was associated with lower mean cystic change by 29.7% (P = 0.018), fibrosis by 21.7% (P = 0.017), macrophage infiltration by 31.5% (P < 0.0001), epithelial proliferation by 18.7% (P = 0.0035), and ox-LDL detection by 31.4% (P < 0.0001) in Han:SPRD-cy heterozygotes. Serum creatinine was significantly lower in FO-fed diseased animals. A small hypocholesterolemic effect was noted in all animals fed FO. FO feeding moderates renal injury, modifies the profile of substrates available for elongation to eicosanoid precursors, and inhibits the elongation of C18 PUFA in this model. The consumption of FO-based products may prove a more practical way of obtaining health benefit than attempts to increase dietary content of unrefined seed.

Animals↗

Modulation of essential (n-6):(n-3) fatty acid ratios alters fatty acid status but not bone mass in piglets.

Dietary (n-6) and (n-3) fatty acids have been implicated as important regulators of bone metabolism. The main objective of this research was to define the response of whole-body growth, fatty acid status and bone mass to a reduced dietary (n-6):(n-3) fatty acid ratio. A secondary objective was to determine whether there is an amount of fat x fatty acid ratio interaction for these outcomes. Piglets (n = 32) were randomized to 1 of 4 diets: group 1: [30 g fat/L + (n-6):(n-3) ratio 4.5:1]; group 2: [30 g fat/L + (n-6):(n-3) ratio 9.0:1]; group 3: [60 g fat/L + (n-6):(n-3) ratio 4.5:1]; and group 4: [60 g fat/L + (n-6):(n-3) ratio 9.0:1]. After 21 d, outcomes assessed included growth, fatty acid status and bone mass and metabolism. Growth and bone mass did not differ among the four groups nor did arachidonic acid (AA as g/100 g fatty acids) in plasma, adipose and brain. Piglets fed diets 1 and 3 with the lower (n-6):(n-3) ratio had lower liver AA (P < 0.001). Those fed diets 1 and 2 containing 30 g fat/L had lower docosahexaenoic acid (DHA as g/100 g fatty acids) in liver (P < 0.001), plasma (P = 0.019) and adipose tissue (P = 0.045). However, piglets fed diets 1 and 3 had higher (P < 0.001) brain DHA than those fed diets with a higher (n-6):(n-3) ratio. Higher plasma DHA was associated with less bone resorption (r = -0.44, P = 0.01). Therefore, elevation of dietary (n-3) fatty acids supports growth and fatty acid status while not compromising bone mass. The results may be of relevance to the nutritional management of preterm infants whose DHA status is often too low and bone resorption too high.

Adipose Tissue↗

Sows' milk attenuates dexamethasone-induced reductions in liver docosahexaenoic acid.

The objective was to determine the effects of dexamethasone (Dex) on growth and arachidonic (AA) and docosahexaenoic (DHA) acid status. Piglets were randomized to suckling or formula feeding plus Dex or placebo treatment for 15 days. Weight and length at the beginning and end of study was used to assess growth. After 15 days, AA and DHA in phosphatidylethanolamine (PE) and phosphatidylcholine (PC) were measured in liver and plasma and total AA and DHA in forebrain and brainstem. Dex treatment significantly reduced weight and length. Dex reduced liver PC and PE DHA in the formula group, but the reduction in the suckled group was not significant. PC AA and DHA were positively related in liver and plasma. A main effect of Dex to reduce AA and DHA was observed in forebrain but not in brainstem. Sows' milk attenuated the Dex-induced reduction in liver DHA but not forebrain AA and DHA or somatic growth.

Animals↗