Multiparous sows (n = 307) were used to evaluate the effects of added dietary L-carnitine, 100 mg/d during gestation and 50 ppm during lactation, on sow and litter performance. Treatments were arranged as a 2 (gestation or lactation) x2 (with or without L-carnitine) factorial. Control sows were fed 1.81 kg/d of a gestation diet containing .65% total lysine. Treated sows were fed 1.59 kg/d of the control diet with a .23 kg/d topdressing of the control diet that provided 100 mg/d of added L-carnitine. Lactation diets were formulated to contain 1.0% total lysine with or without 50 ppm of added L-carnitine. Sows fed 100 mg/d of added L-carnitine had increased IGF-I concentration on d 60 (71.3 vs. 38.0 ng/mL, P<.01) and 90 of gestation (33.0 vs. 25.0 ng/mL, P = .04). Sows fed added L-carnitine had increased BW gain (55.3 vs 46.3 kg; P<.01) and last rib fat depth gain (2.6 vs. 1.6 mm; P = .04) during gestation. Feeding 100 mg/d of added L-carnitine in gestation increased both total litter (15.5 vs. 14.6 kg; P = .04) and pig (1.53 vs 1.49 kg; P<.01) birth weight. No differences were observed in pig birth weight variation. Added L-carnitine fed during gestation increased litter weaning weight (45.0 vs. 41.3 kg, P = .02); however, no effect of feeding L-carnitine during lactation was observed. No differences were observed in subsequent days to estrus or farrowing rate. Compared to the control diet, feeding added L-carnitine in either gestation, lactation, or both, increased (P<.05) the subsequent number of pigs born alive, but not total born. In conclusion, feeding L-carnitine throughout gestation increased sow body weight and last rib fat depth gain and increased litter weights at birth and weaning.

Two experiments were conducted to evaluate the effect of dietary L-carnitine on growth performance and body composition of early-weaned pigs. In Exp. 1, 120 weanling pigs (initially 5.6 kg and 19 +/- 2 d of age) were allotted in a 3 x 2 factorial with four pigs per pen and five replications (pens) per treatment. Main effects from d 0 to 14 after weaning included dietary L-carnitine (0, 500, or 1,000 ppm) and soybean oil (0 to 10%). From d 14 to 35 after weaning, levels were reduced to 0, 250, or 500 ppm L-carnitine and 0 or 5% soybean oil. No L-carnitine x soybean oil interactions were observed (P > .10). From d 0 to 14, L-carnitine and soybean oil had no effect (P > .10) on pig performance. From d 14 to 35 and d 0 to 35, gain:feed ratio (G/F) improved (linear, P < .05) with increasing dietary L-carnitine; however, ADG and ADFI were not affected. Soybean oil improved ADG and G/F (P < .05) from d 14 to 35 and ADG from d 0 to 35. In Exp. 2, 180 weanling pigs (initially 6.0 kg and 22 +/- 2 d of age) were allotted in a 2 x 3 factorial. Pigs were fed either 0 or 1,000 ppm L-carnitine from d 0 to 14 after weaning and then pigs fed each of these diets were fed diets containing 0, 250, or 500 ppm L-carnitine from d 14 to 35. No interactions occurred between feeding L-carnitine from d 0 to 14 and performance observed from d 14 to 35. From d 0 to 14 after weaning, L-carnitine increased ADG (P < .08) and ADFI (P < .02). From d 14 to 35, ADFI decreased (linear, P < .05) and G/F increased (quadratic, P < .05) as dietary L-carnitine increased. Cumulative (d 0 to 35) ADFI decreased (linear, P < .05) and G/F increased (linear, P < .05) with increasing L-carnitine. On d 35, 14 pigs from each of four selected treatments (0 or 1,000 ppm L-carnitine from d 0 to 14 followed by either 0 or 500 ppm from d 14 to 35) were slaughtered, and carcass composition was recorded. Carcass moisture and CP percentages were not influenced (P > .10) by dietary L-carnitine. However, pigs fed 1,000 ppm L-carnitine from d 0 to 14 had less (P < .05) carcass lipid and daily lipid accretion on d 35 whether they were fed L-carnitine from d 14 to 35 or not. These results suggest that dietary L-carnitine improves G/F and reduces carcass lipid accretion in early-weaned pigs.

The objectives of this experiment were to determine long-term responses to supplemental fat (from whole soybeans and liquid animal fat) and to determine whether the supplementation of nicotinic acid would enhance milk protein content or yield. From wk 4 through 43 postpartum, 44 multiparous Holstein cows (10 to 12 per treatment) were assigned to one of four dietary treatments: 1) control, 2) control plus 12 g/d of nicotinic acid, 3) supplemental fat, and 4) supplemental fat plus 12 g/d of nicotinic acid. The dry matter intake of cows did not differ among dietary treatments. Yields of milk, solids-corrected milk, and 3.5% fat-corrected milk were increased by nicotinic acid; the yield of fat-corrected milk during wk 4 to 25 was increased by supplemental fat. Contents of crude protein (CP) and true protein in milk were less for cows fed diets supplemented with fat or nicotinic acid; casein content was decreased by nicotinic acid. Intake of net energy for lactation was greater for cows fed supplemental fat; energy balance was greater during wk 4 to 25 for cows fed diets supplemented with fat. Body condition score and body weight were less when nicotinic acid was added to the control diet than when it was added to the diet supplemented with fat. Supplemental fat increased the concentration of nonesterified fatty acids (NEFA) in plasma; nicotinic acid increased NEFA when it was added to the control diet but decreased NEFA when it was added to the diet supplemented with fat. Nicotinic acid did not prevent the decrease in milk CP content that was induced by dietary fat, but it did increase milk yield and tended to increase the yield of milk CP.

No abstract

A recent comparative transcriptomic study of Müller glial (MG) in vertebrate retinas revealed that Fatty Acid Binding Proteins (FABPs) are among the most highly expressed genes in chick (Hoang et al., 2020). Herein we investigate how FABPs and fatty acid synthase (FASN) influence glial cells in the chick retina. During development, FABP7 is highly expressed by retinal progenitor cells and maturing MG, whereas FABP5 is upregulated in maturing MG. PMP2 (FABP8) is expressed by oligodendrocytes and FABP5 is expressed by non-astrocytic inner retinal glial cells, and both of these FABPs are upregulated by activated MG. In addition to suppressing the formation of Müller glia-derived progenitor cells (MGPCs), we find that FABP-inhibition suppresses the proliferation of microglia. FABP-inhibition induces distinct changes in single cell transcriptomic profiles indicating transitions of MG from resting to reactive states and suppressed MGPC formation, with upregulation of gene modules for gliogenesis and decreases in neurogenesis. FASN-inhibition increases the proliferation of microglia and suppresses the formation of MGPCs. We conclude that fatty acid metabolism and cell signaling involving fatty acids are important in regulating the reactivity and dedifferentiation of MG, and the proliferation of microglia and MGPCs.