Biomedical subjects

J Odle

Publications and source records attributed to J Odle.

At least 37 records · Page 2Linked to original sources

PubMed2000

Effects of dietary copper source and concentration on carcass characteristics and lipid and cholesterol metabolism in growing and finishing steers.

We conducted an experiment to determine the effects of dietary copper (Cu) source and level on carcass characteristics, longissimus muscle fatty acid composition, and serum and muscle cholesterol concentrations in steers. Sixty Angus and Angus x Hereford steers were stratified by weight and initial liver Cu concentration within a breed and randomly assigned to treatments. Treatments consisted of: 1) control (no supplemental Cu); 2) 20 mg Cu/kg DM from Cu sulfate (CuSO4); 3) 40 mg Cu/kg DM from CuSO4; 4) 20 mg Cu/kg DM from Cu citrate; 5) 20 mg Cu/kg DM from Cu proteinate; and 6) 20 mg Cu/kg DM from tribasic Cu chloride. A corn silage-soybean meal-based diet was fed for 56 d. Steers were then switched to a high-concentrate diet. Equal numbers (n = 5) of steers per treatment were slaughtered after receiving the finishing diets for either 101 or 121 d. Serum cholesterol was not affected by treatment during the growing phase but was decreased (P < .05) in steers supplemented with Cu by d 84 of the finishing period and remained lower (P < . 05) at subsequent sampling periods. Longissimus muscle cholesterol concentration tended to be reduced (P < .11) by Cu supplementation. Hot carcass weight and backfat were lower (P < .05) in animals receiving supplemental Cu. However, Cu-supplemented and control steers had similar marbling scores. Longissimus muscle polyunsaturated fatty acid concentrations (18:2 and 18:3) were increased (P < .07) and saturated fatty acid concentrations tended (P < . 11) to be reduced by Cu supplementation. These results indicate that as little as 20 mg of supplemental Cu/kg diet can reduce backfat and serum cholesterol and increase muscle polyunsaturated fatty acids in steers fed high-concentrate diets.

Animal Feed↗

PubMed1999

Dietary fat during pregnancy and lactation increases milk fat and insulin-like growth factor I concentrations and improves neonatal growth rates in swine.

Primiparous (n = 24) and multiparous (n = 24) sows were used to examine the effects of supplemental dietary fat and induction of parturition (d 112) on colostrum and milk composition and suckling piglet growth. Sows were assigned to one of eight treatments on d 90 of gestation that included variables such as parity (1 vs. >/=3), dietary fat (0 vs. 10%), and farrowing (natural vs. induction via lutalyse on d 112). Piglets suckling fat-supplemented dams grew up to 25% faster than control pigs nursing unsupplemented sows (250 vs. 200 g/d; P < 0.01). Improved growth was correlated with elevated milk fat and insulin-like growth factor (IGF) concentrations associated with fat supplementation. Dietary fat elevated milk fat concentration at 48 and 72 h postfarrowing by 21.6 and 22.6%, respectively (P < 0.05). Compared with nonfat-fed controls, multiparous sows fed 10% fat showed a more consistent rise in milk fat concentration, with 26% and 41% elevations for induced or naturally farrowing sows, respectively, vs. a 19% reduction or a 1% elevation in induced or naturally farrowing gilts (P < 0.01). The concentration of milk IGF-I tended to be lower in gilts than in multiparous sows (P < 0.2, 95.7 vs. 117.4 microg/L), and levels were particularly low in milk from induced gilts receiving no additional dietary fat (44.7 microg/L). However, fat supplementation elevated IGF-I to levels (110.6 microg/L) exceeding those measured in unsupplemented, naturally farrowing control sows and gilts (95.8 microg/L). In conclusion, supplemental dietary fat elevates milk fat in multiparous sows more than primiparous gilts regardless of farrowing treatment (induced vs. natural farrowing) and improves piglet growth throughout lactation irrespective of parity or farrowing treatment. The potential of supplemental dietary fat to reverse the reductions in milk IGF-I observed in first-parity females and in dams induced to farrow merits further investigation.

Animals↗

PubMed1999

Malnutrition modifies pig small intestinal inflammatory responses to rotavirus.

Infectious diarrheal diseases and malnutrition are major causes of child morbidity and mortality. In this study, malnutrition was superimposed on rotavirus infection in neonatal piglets to simulate the combined intestinal stress of viral enteritis in malnourished infants. Two-day-old piglets were assigned to three treatment groups as follows: 1) noninfected, fully nourished; 2) infected, fully nourished; and 3) infected, malnourished. Intestinal indices of inflammation were monitored over the subsequent 2-wk period. Intestinal damage and diarrhea were observed within 2 d of rotavirus infection and began to subside in nourished piglets by d 9 but persisted through d 16 postinfection in malnourished piglets. Rotavirus upregulated small intestinal expression of major histocompatibility complex (MHC) class I and class II genes; malnutrition intensified MHC class I gene expression and suppressed MHC class II expression. Jejunal CD4(+) and CD8(+) T-lymphocyte numbers were elevated for infected, nourished piglets on d 2, 9 and 16 postinfection. Malnutrition did not significantly affect the local expansion of T cell subsets in response to rotavirus. Intestinal prostaglandin E2 (PGE2) concentrations were elevated early after rotavirus infection independent of nutritional state. By d 9, PGE2 concentrations returned to baseline in infected, nourished piglets but remained elevated in malnourished piglets, corresponding to diarrhea observations. Together, the results identify intestinal indices of inflammation that are modulated by malnutrition and prompt reconsideration of current models of rotavirus pathophysiology.

Animals↗

PubMed1998

Food deprivation changes peroxisomal beta-oxidation activity but not catalase activity during postnatal development in pig tissues.

Peroxisomal beta-oxidation and catalase activity were investigated in liver, kidney and heart from pigs at the following timepoints: within 0.5 h after birth (0 h, unfed) and at 24 h (suckled or unsuckled), 10 d (suckled or 24-h food-deprived), 21 d (suckled or 24-h food-deprived) and 5 mo (overnight food-deprived). In liver, peroxisomal beta-oxidation increased about twofold at 24 h for suckled pigs (P < 0.001) but did not change for unsuckled pigs. The rate was further increased in 21-d-old pigs compared with 0- (P < 0. 001) or 24-h-old (P < 0.05) pigs, but was lower at 5 mo than at 10 or 21 d (P < 0.01). The rate was higher for food-deprived pigs than suckled pigs at 10 d (P < 0.001) of age. In kidney, peroxisomal beta-oxidation was unchanged during the first 24 h but was higher (P < 0.05) at 10 d for suckled pigs and at 21 d than at 0 h. Nutritional state did not influence renal peroxisomal beta-oxidation. In heart, peroxisomal beta-oxidation did not change with age or nutritional state. The developmental pattern of fatty acyl-CoA oxidase activity was similar to that of peroxisomal beta-oxidation in each tissue. Developmental increases of peroxisomal beta-oxidation were greater than those for first-cycle peroxisomal beta-oxidation reported earlier, suggesting that peroxisomal beta-oxidation became more complete in older pigs. Catalase activity did not change during the first 24 h after birth but then increased 10.5-, 2.9-fold and 33% at 10 d in liver, kidney and heart, respectively. The concentration of catalase mRNA was only 1.1- and 1. 3-fold higher at 10 d than at 24 h in liver and kidney, respectively. Catalase activity was not affected by food deprivation. We concluded the following: 1) peroxisomal beta-oxidation develops rapidly after birth and may be important for piglets to oxidize milk fatty acids; 2) food is required for the initial induction after birth; and 3) rapidly increased catalase activity during the first 10 d of life resulted from both pretranslational and post-translational regulation.

Aging↗

PubMed1998

Acetogenesis does not replace ketogenesis in fasting piglets infused with hexanoate.

The current studies were performed to better understand the physiological relevance of acetate in the poorly ketogenic piglet and to determine if endogenous acetogenesis rises with increased mitochondrial fatty acid beta-oxidation, analogous to ketogenesis. Plasma acetate concentration values in newborn, fasted, or suckled piglets (230-343 microM) were at least 10-fold higher than the ketone bodies, a pattern opposite to that in 24- to 48-h suckled rats (77-175 microM). Employing continuous infusion techniques with sodium [3H]acetate tracer in fasting approximately 40-h-old piglets, acetate rate of appearance (Ra) was found to be 34 +/- 4 micromol . min-1 . kg body wt-1. This basal Ra was double that observed in animals coinfused with sodium [1-14C]hexanoate (P < 0.001), despite active oxidation of the latter as determined by 14CO2 production. Active acetogenesis in vivo and relatively abundant acetate in piglet blood are consistent with the hypothesis that acetate plays an important physiological role in piglets. However, the negative impact of hexanoate oxidation upon acetate Ra and the lack of significant changes in circulating acetate in newborn, suckled, and fasted piglets draws into question the extent of analogy between acetogenesis and ketogenesis in vivo.

Acetates↗

PubMed1997

New insights into the utilization of medium-chain triglycerides by the neonate: observations from a piglet model.

Because of their unique digestive and metabolic properties, medium-chain triglycerides (MCT) are used in a variety of nutritional settings, including use as a readily digestible energy source for the neonate. This review examines recent findings from our laboratory related to MCT digestion and metabolism that are drawn from a neonatal piglet model, but which may be clinically relevant to human infants. We have shown that MCT utilization improves rapidly with postnatal age (within 24 h), which is likely due to the ontogeny of pancreatic lipase. Additional data delineate the dramatic effects of emulsification and fatty acid chain length (within the medium-chain family) on utilization, with the suggestion that triacylhexanoate is utilized at the highest rate. Again, these effects are likely mediated via an increase in the kinetics of digestion rather than metabolism. Indeed, using both in vitro and in vivo radiotracer techniques, we were unable to detect metabolic differences among even-chain fatty acid homologues. However, studies with isolated hepatocytes have shown greater oxidation rates of odd-chain fatty acids compared with even-chain homologues, in part as a result of the anaplerotic potential of propionyl-CoA arising from odd-carbon fatty acid oxidation. In vivo radiotracer studies also showed an improvement in octanoate oxidation to CO2, with a concomitant reduction in urinary dicarboxylic acid excretion when colostrum-deprived piglets were supplemented with L-carnitine. Further metabolic research led to the novel finding that piglets have a very limited hepatic capacity to synthesize ketone bodies, and that acetate may be a relatively important product of hepatic fatty acid oxidation in this species.

Animals↗

PubMed1997

Protein-energy malnutrition delays small-intestinal recovery in neonatal pigs infected with rotavirus.

Infectious diarrheal diseases and protein-energy malnutrition (PEM) are major causes of child morbidity and mortality worldwide. In the present study, PEM was superimposed on rotavirus infection in neonatal pigs to simulate chronic small intestinal stress in malnourished infants with viral gastroenteritis. Two-day-old cesarean-derived pigs (n = 39) were allotted to three treatment groups: 1) noninfected, full-fed; 2) infected, full-fed; and 3) infected, malnourished. Two days postinfection, severe diarrhea and weight loss (11%) were accompanied by reductions in villus height (60%) and lactase activity (78%) and increased crypt depth (32%) in infected full-fed compared with noninfected pigs (P < 0.05). Malnutrition blunted (P < 0.05) increases in crypt depth elicited by rotavirus. By 9 d postinfection, body weight was 59% less, villus height and lactase activity remained lower (50%), and crypt depth remained greater (62%) in infected full-fed compared with noninfected pigs (P < 0.05). However, diarrhea began to clear in infected full-fed, but not in infected malnourished pigs. Plasma insulin-like growth factor-I (IGF-I) was reduced 68% and crypt depth was reduced 19% in infected-malnourished compared with infected full-fed pigs (P < 0.05). Sixteen days postinfection, full-fed pigs had recovered from rotaviral infection; however, in infected-malnourished pigs, diarrhea and growth stasis persisted, and plasma IGF-I, villus height and alkaline phosphatase activity remained reduced compared with infected full-fed pigs (P < 0.05). Overall, PEM prolonged diarrhea and delayed small-intestinal recovery, indicating that nutritional status during diarrhea is essential for recovery from rotaviral enteritis.

Animals↗

PubMed1997

Rates of mitochondrial and peroxisomal beta-oxidation of palmitate change during postnatal development and food deprivation in liver, kidney and heart of pigs.

We measured total, mitochondrial and peroxisomal capacities for beta-oxidation of [1-14C]palmitate in homogenates of liver, kidney and heart from pigs within 0.5 h after birth (0 h, unfed) and at 24 h (suckled or unfed), 10 d (suckled or 24-h food-deprived), 21 d (suckled or 24-h food-deprived) and 5 mo (overnight food-deprived) of age. Assays were conducted in the absence (total beta-oxidation) or presence (peroxisomal beta-oxidation) of antimycin A and rotenone. Mitochondrial beta-oxidation was calculated as total minus peroxisomal beta-oxidation. Acid-soluble products (ASP) from incubation of tissue homogenates from 24-h-old unfed pigs with [1-14C]palmitate were analyzed by radio-HPLC. Total and mitochondrial beta-oxidation capacities were greater (P < 0.05) at 24 h after birth in liver, and at 10 d in kidney and heart, than at 0 or 24 h. Peroxisomal beta-oxidation capacity was increased (P < 0. 05) at 24 h after birth in liver and at 10 and 21 d in heart; in kidney, the capacity was higher during the preweaning period than in adults. Across ages, peroxisomal beta-oxidation capacity represented 37 to 51%, 28 to 41%, and 26 to 31% of total beta-oxidation capacity in liver, kidney, and heart, respectively. Food deprivation increased hepatic total beta-oxidation at 10 d and decreased peroxisomal beta-oxidation at 24 h but had no effect in kidney and heart. Regardless of the presence of respiratory inhibitors, 32%, 31 to 40%, and 45 to 50% of palmitate carboxyl carbon in acid-soluble products was accumulated in acetate in liver, kidney, and heart, respectively. We suggest that a high percentage contribution of peroxisomal beta-oxidation may act as a compensatory mechanism for piglets to oxidize milk fatty acids during postnatal development. Furthermore, acetogenesis may be an important fate of acetyl-CoA from beta-oxidation of fatty acids in various piglet tissues.

Animals↗

PubMed1997

Orally administered iodinated recombinant human insulin-like growth factor-I (125I-rhIGF-I) is poorly absorbed by the newborn piglet.

BACKGROUND: The purpose of the current study was to determine the degree to which milk-borne insulin-like growth factor-I (IGF-I) is absorbed. METHODS: Cesarean-derived piglets were fitted with umbilical arterial and venous catheters within 2 h of birth and were administered formula containing 21.7 +/- 1.8 microCi of iodinated recombinant human IGF-1 (125I-rhIGF-I) by orgogastric gavage. Blood samples were taken before administration of the 125I-rhIGF-I (t0) and for 4 h postgavage. Plasma was obtained by centrifugation and total and trichloroacetic acid precipitable radioactivity were determined. Immunoreactive 125I-rhIGF-I was assessed using a polyclonal antibody to human IGF-I. Four hours after feeding, intestines were removed, divided into 13 segments, and flushed with saline. Radioactivity within the small intestinal lumen and wall were measured. RESULTS: Radioactivity in portal blood was higher than t0 at all times points (p < 0.05), whereas arterial radioactivity did not differ from t0 until 30 min postgavage. On average 18-20% of total radioactivity in both portal and arterial blood was acid-precipitable, with the proportion decreasing over time (p < 0.001). Immunoprecipitable radioactivity averaged 3-5% of the total radioactivity and was higher in portal than arterial blood (p < 0.05). Based on a plasma volume of 0.062 +/- 0.005 L and a baseline plasma IGF-I concentration of 1.81 +/- 0.56 nmol/L, absorbed 125I-rhIGF-I represented 0.205% of the total plasma IFG-I pool, whereas 14% of the dose was associated with the lining of the intestine. CONCLUSIONS: Absorption of orally administered IGF-I does not contribute significantly to circulating IGF-I.

Administration, Oral↗

PubMed1997

Hepatic fatty acid metabolism in pigs and rats: major differences in endproducts, O2 uptake, and beta-oxidation.

Models of mammalian hepatic lipid metabolism are based largely on observations made in adult rats, emphasizing ketogenesis as a primary adjunct to mitochondrial beta-oxidation. Studies using piglets have illustrated the divergent nature of intermediary metabolism in this model, wherein ketogenesis and beta-oxidation are small and acetogenesis is an important route of fuel carbon flux. To clarify potential species differences in hepatic lipid metabolism and its control, we compared O2 consumption and metabolic end products in fasted pig and rat liver homogenates treated with 1-[14C]C16:0. Carboxyl carbon accumulation in acid-soluble products (ASP) plus CO2 was threefold greater and O2 consumption was twofold greater in rats (P < 0.05). Unlike rats, pigs showed negligible carboxyl carbon accumulation in ketone bodies (3-7% of ASP), whereas acetate was a carboxyl carbon reservoir in both animals (17-31% of ASP in pigs). Malonate increased (approximately 2-fold) and antimycin/rotenone decreased (40-60%) radiolabel accumulation in acetate. These data concur with the hypotheses that comparatively low hepatic beta-oxidative flux in piglets is partially related to a smaller metabolic rate and that substantial acetogenesis occurs intramitochondrially in both pigs and rats.

Animals↗

PubMed1997

Response of hepatic mitochondrial and peroxisomal beta-oxidation to increasing palmitate concentrations in piglets.

Responses of total, mitochondrial, and peroxisomal beta-oxidation to increasing [1-14C]-palmitate concentrations (0.02-1.0 mM) were measured in liver homogenates from neonatal pigs. Incubations were conducted in the absence (total beta-oxidation) or presence (peroxisomal beta-oxidation) of antimycin A and rotenone; mitochondrial beta-oxidation was calculated as total minus peroxisomal oxidation. Total and mitochondrial beta-oxidations were maximized at a palmitate concentration of 0.05 mM, whereas peroxisomal beta-oxidation was maximized at 0.50 mM palmitate. Across concentrations, peroxisomal beta-oxidation contributed 40-47% of total beta-oxidation. An increased rate of CO2 production and a greater ratio of CO2 production to total mitochondrial beta-oxidation as palmitate concentration increased suggested that the limited capacity for mitochondrial beta-oxidation was attributable primarily to limited ketogenic capacity. Comparative observations in liver from adult rats showed that peroxisomal beta-oxidation was maximized at 0.1 mM palmitate, but total and mitochondrial beta-oxidation rates were not maximized even at 1 mM palmitate. At 1 mM palmitate, peroxisomal beta-oxidation was 20% of total beta-oxidation in adult rats and 37% in adult pigs. Therefore, the contribution of peroxisomal beta-oxidation to total beta-oxidation is highly dependent on substrate concentration and appears to be greater in adult pigs than in adult rats. The greater proportional contribution of peroxisomal beta-oxidation in piglet liver might act as a compensatory mechanism for piglets to oxidize milk fatty acids.

Animals↗

PubMed1997

Small intestinal disaccharidase activity and ileal villus height are increased in piglets consuming formula containing recombinant human insulin-like growth factor-I.

The effect of orally administered IGF-I on intestinal development was assessed in piglets. Cesarean-derived, colostrum-deprived piglets received formula alone or formula containing 65 nM (500 microg/L) of recombinant human IGF-I. IGF-I intake averaged 200 microg/kg/d. On d 7 and 14 postpartum, piglets were killed, organs were removed and weighed, and tissue and blood samples were collected. The small intestine was divided into 13 segments that were weighed and measured. A sample of each segment was fixed in formalin, and the mucosa was scraped for enzyme analyses. Food intake, body and organ weights, intestinal weight, length, protein, DNA and RNA content did not differ between the treatment groups. Serum IGF-I, IGF-II, and IGF-binding protein profiles and tissue IGF-binding protein mRNA expression were also comparable between the treatment groups. In contrast, intestinal enzymes and villus height were increased by oral IGF-I. Lactase was approximately 2-fold higher (p < or = 0.05) in the jejunum and proximal ileum, and sucrase was approximately 50% higher (p < or = 0.05) in the jejunum of IGF-I-treated animals than in controls. Villus height in the terminal ileum was approximately 50% greater in IGF-I-treated animals than in controls (p = 0.03). In conclusion, orally administered IGF-I at 200 microg/kg did not affect whole body or organ growth or serum IGF-I concentrations; however, intestinal disaccharidase activity and ileal villus growth were responsive to orally administered IGF-I, supporting a potential role for milk-borne IGF-I in neonatal intestinal development.

Animals↗

PubMed1996

Acetate represents a major product of heptanoate and octanoate beta-oxidation in hepatocytes isolated from neonatal piglets.

An experiment was conducted to explore the nature of the radiolabel distribution in acid-soluble products (ASPs) resulting from the oxidation of [1-14C]C7:0 or C8:0 by isolated piglet hepatocytes. The differences between odd and even chain-length and the impacts of valproate and malonate upon the rate of beta-oxidation and ASP characteristics were tested. A minor amount of fatty acid carboxyl carbon (< or = 10% of organic acids identified by radio-HPLC) accumulated in ketone bodies regardless of chain-length or inhibitor used. In all cases, acetate represented the major reservoir of carboxyl carbon, accounting for 60-70% of radiolabel in identified organic acids. Cells given [1-14C]C7:0 accumulated 85% more carboxyl carbon in Krebs cycle intermediates when compared with C8:0, while accumulation in acetate was unaffected. The results are consistent with the hypothesis that anaplerosis from odd-carbon fatty acids affects the oxidative fate of fatty acid carbon. The piglet appears unique in that non-ketogenic routes of fatty acid carbon flow (i.e. acetogenesis) predominate in the liver of this species.

Acetates↗

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

The riboflavin requirement of adult dogs at maintenance is greater than previous estimates.

A study was conducted to determine the riboflavin requirement of adult dogs at maintenance. Twenty adult mixed breed dogs were fed a semipurified meal with one of five riboflavin concentrations: Diet 1, 1.7 mg/kg; Diet 2, 2.7 mg/kg; Diet 3, 3.7 mg/kg; Diet 4, 4.7 mg/kg; and Diet 5, 5.7 mg/kg. The erythrocyte glutathione reductase activity coefficient (EGRAC) was used to determine biochemical riboflavin deficiency. Dogs fed Diet 1 had a greater (P < 0.05) EGRAC (1.24) on d 56 of the trial compared with that of dogs fed Diet 5 (1.11), indicating marginal riboflavin deficiency in dogs fed Diet 1. On d 84 the mean EGRAC for dogs fed Diet 1 (1.36) was different from EGRAC obtained for dogs fed the other diets (1.19, P < 0.05). The difference in mean EGRAC was still present of d 112 (1.59 vs. 1.27; P< 0.01). There was no difference in d 112 mean EGRAC for dogs fed Diets 2, 3, 4 and 5 (P < 0.05). The broken line requirement estimate for the adult dog at maintenance was determined to be 66.8 microgram riboflavin x kg body wt(-1) x d(-1) using the d 112 EGRAC as the basis for assessing biochemical riboflavin deficiency.

Animal Nutritional Physiological Phenomena↗

PubMed1996

Intestinal effects of milkborne growth factors in neonates of agricultural importance.

Reduction of postnatal morbidity and mortality of mammalian neonates poses a significant challenge to agricultural and medical sciences. Because nutritional insufficiency and diarrhea represent major stressors, an understanding of factors mediating postnatal growth and development of the gastrointestinal tract is essential. This review explores the role that milkborne growth factors may play in stimulating functional development of the neonatal intestine, with emphasis on the porcine, bovine, and ovine species. Studies reporting milk concentrations and intestinal effects are reviewed, with emphasis on epidermal growth factor, insulin, and the insulin-like growth factors. Collectively, these studies suggest that milkborne growth factors may provide important regulatory signals to the neonatal intestine under both normal and pathophysiological states.

Animals↗

PubMed1996

Effect of feeding a milk replacer to early-weaned pigs on growth, body composition, and small intestinal morphology, compared with suckled littermates.

Feeding of milk replacer to early-weaned pigs was evaluated in two experiments. In Exp. 1, 18 litters of pigs were either weaned conventionally (d 21), split-weaned and fed milk replacer plus starter diet (d 14 and 21), or weaned and fed milk replacer plus starter diet (d 21). Split weaning combined with feeding a milk replacer increased ADG 22% from d 14 and d 28 compared to conventional weaning (P < .05). Feeding a milk replacer plus starter diet after weaning increased ADG 30% between d 21 and 28 compared to conventional weaning (P < .01). In Experiment 2, four litters of 12 pigs each were divided at d 18 into six heavy and six light pigs and randomized across sow-suckled, milk replacer, or starter diet groups. After 1 wk, pigs fed milk replacer weighed 20% more (P < .001), contained 10% more protein (P < .01) and 17% more fat (P < .05), and had 74% longer villi in the proximal small intestine (P < .001) than suckled pigs. In contrast, pigs fed starter diet weighed 19% less (P < .001), contained 20% less protein and fat (P < .001), and had 28% shorter villi in the proximal small intestine (P < .05) than suckled pigs. Therefore, milk replacer feeding the 1st wk after weaning stimulates pig development, both locally in the small intestine and on a whole-body basis, most likely by an increased energy and nutrient intake. Suckling beyond 18 d postnatally inhibits pigs to reach maximal potential weight gain. In conclusion, milk replacer feeding might be beneficial to reach maximal pig weight gain at weaning.

Aging↗

PubMed1995

Carnitine palmitoyltransferase modulation of hepatic fatty acid metabolism and radio-HPLC evidence for low ketogenesis in neonatal pigs.

A neonatal piglet model was used to study hepatic fatty acid metabolism during the early postnatal period. Hepatocytes were isolated from pigs at birth or after 24 h, in fed or unfed states (n = 4 pigs/group). Cells were incubated with 1 mmol/L [1-(14)C]-octanoate (C8) or -palmitate (C16) in the presence or absence of 1 mmol/L L-carnitine, carnitine plus tetradecylglycidic acid (TDGA; 10 mumol/L) or carnitine plus glucagon (0.5 microgram/L). Accumulation of radiolabel [nmol/(h. 10(6) cells)] in CO2 and acid-soluble products (ASP) was higher (3.5- and 4.5-fold, respectively) from C8 than from C16 (P < 0.0001). Glucagon, carnitine and TDGA had no effect on the oxidation of C8 (P > 0.1). Carnitine addition tended to increase C16 flux to ASP [from 5.3 to 7.6 nmol/(h. 10(6) cells); P < 0.1], whereas carnitine plus TDGA decreased flux (from 7.6 to 2.1; P < 0.001). Esterified products accounted for 70% of metabolized label in control C16 incubations; this was reduced to 62% by carnitine (P < 0.05) and increased to 80% by the addition of carnitine plus TDGA (P < 0.0001). The 1-(14)C flux to CO2 in cells from 24-h-old unfed piglets was 47% lower than from fed pigs (P < 0.01) but 28% higher than in pigs at birth. Radiolabel contained in ASP and total metabolized label were 48% lower from unfed pigs compared with the piglets at birth and 24-h-old fed pigs (P < 0.01) and were paralleled by changes in oxygen consumption.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗