No abstract

Medium‐chain fatty acids (MCFA) are often included in neonatal milk formulas as a more readily oxidized source of energy compared with long‐chain fatty acids (LCFA). This rapid oxidation of MCFA is thought to enhance growth. Thus, the objectives of this study were to evaluate the effect of energy supplementation and fat source on growth and body composition, and determine the rate of Krebs Cycle substrate utilization in neonatal pigs. Eleven three‐day‐old pigs were allocated to one of three sow milk replacer formulas: a control (CONT) and diets rich in either LCFA or MCFA. The CONT formula provided 80%, whereas the MCFA and LCFA formulas provided 120%, of the metabolizable energy requirements of neonatal pigs. Pigs were fed for 20 days and body composition measured by DXA before initiation and on day 20 of feeding. At the end of the study, pigs were euthanized and muscles and organs collected and weighed. Livers were digested with collagenase and isolated hepatocytes were incubated in media containing all amino acids, glucose, and short‐chain fatty acids in the presence of [U13C] labeled alanine, glucose, propionate, and glutamate for 90 min. The enrichment of Krebs Cycle intermediates was determined using gas chromatography/mass spectrometry. Body weight of pigs in the LCFA group was greater than those in the MCFA and CONT groups on days 18 and 20. In addition, percent fat measured by DXA was greater for MCFA (8%) and LCFA (7%) than those in the CONT (4%) group, and this increase in fat deposition occurred at the expense of lean tissue (P < 0.05). Longissimus dorsi and heart weights as percent of body weight were similar for all groups; however, soleus weight was less for MCFA compared with those in the CONT and LCFA groups. In addition, liver and kidney weights as a percentage of body weight were greater for pigs in the MCFA group compared with those in the CONT group with LCFA being intermediate (P< 0.05). There was no effect of formula feeding on glucose and alanine contribution to lactate synthesis in isolated hepatocytes, but this contribution was greater for glucose (36%) than for alanine (15%) (P<0.05). Conversely, the contribution of alanine (35%) carbon to pyruvate was greater than the contribution of glucose (7%) (P<0.05). Furthermore, in hepatocytes of pigs fed CONT formula 39% of pyruvate carbon was derived from alanine and 31–34% for pigs in the LCFA and MCFA groups (P<0.05). Lastly, glutamate contributed 64% of α‐ketoglutarate carbon in hepatocytes of CONT and MCFA and only 40% for LCFA pigs. These data suggest that dietary MCFA increase body fat without increasing lean tissue accretion compared with CONT. In addition, anaplerosis from glutamate was greater for pigs fed MCFA and CONT than for those fed LCFA.