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Highlights • Castration of bull calves increased pain indicator substance P. • Castration increased inflammation indicator haptoglobin. • A lidocaine-plus-flunixin (LF) treatment tended to reduce inflammation indicator. • LF treatment did not reduce elevated cortisol and substance P in castrated calves. • Additional treatment would be beneficial to pain relief in castrated calves. Abstract The aim of this study was to determine the effects of castration and a lidocaine-plus-flunixin (LF) treatment on growth and indicators of pain, inflammation, and liver function in Korean cattle bull calves. Forty Korean cattle bull calves (body weight 197.0 ± 2.94 kg and age 6.3 ± 0.09 months) were each assigned to one of four treatments (n = 10 heads/group): no castration with no LF injection (NC-NLF); no castration with LF injection (NC-LF); castration with no LF injection (C-NLF); and castration with LF injection (C-LF). LF treatment included a local anesthetic lidocaine hydrochloride injection (12 mL of 2% in the scrotum) and intravenous injection of a non-steroidal anti-inflammatory drug, flunixin meglumine (2 mg/kg body weight of 50 mg/mL solution), immediately prior to castration. For the NLF groups, a 0.9% NaCl placebo solution was used. Castration was performed surgically using a Newberry knife and a Henderson castrating tool. Blood was collected immediately before castration and at h 0.5, h 6, d 1, d 3, d 7, and d 14 after castration. Feed intake was recorded daily, and body weight was measured on the day prior to the experiment and at d 14 after castration. Castration tended (P = 0.07) to decrease average daily weight gain, but LF treatment did not affect weight gain. Castration increased both circulating cortisol concentrations (P < 0.001) at h 0.5 after castration and substance P (SP) concentrations (P = 0.001) at h 6 after castration. However, the LF treatment did not significantly reduce cortisol and SP concentrations in castrated animals. Castration increased (P < 0.001) circulating haptoglobin (Hp) concentrations on d 1 and d 3 after castration, and LF treatment tended (P = 0.09) to decrease Hp concentrations on d 1 and decreased (P = 0.02) Hp concentrations on d 3. Castration did not affect glutamic oxaloacetic transaminase (GOT) and glutamic pyruvate transaminase (GPT) concentrations. LF treatment increased GOT concentrations at h 6 (P < 0.001), d 1 (P < 0.001), and d 3 (P = 0.003). LF treatment also increased GPT concentrations on d 1 (P = 0.006) and d 3 (P = 0.003). In conclusion, castration of bull calves resulted in time-sequential increases in circulating concentrations of cortisol at h 0.5, SP at h 6, and Hp on d 1. LF treatment did not significantly reduce elevated cortisol and SP, but tended to decrease elevated Hp concentrations in castrated animals. Our study demonstrates that LF treatment is not sufficient for the reduction of the indicators of pain and inflammation in castrated calves, suggesting that additional alleviation methods are required. [ABSTRACT FROM AUTHOR]

This study was performed to compare expression of genes for extracellular matrix (ECM) components, ECM degrading factors, and integrin subunits in the longissimus thoracis (LT) between bulls and steers. Steers had lower ( P < 0.05) ECM component collagen type 1 α1 and collagen type 3 α1 mRNA levels than did bulls, but they had higher ( P < 0.05) thrombospondin 1 mRNA and protein levels. Steers had higher ( P < 0.01) matrix metalloproteinase (MMP) 9 mRNA levels than did bulls. Steers had higher ( P < 0.05) integrin α5 mRNA levels but lower ( P < 0.05) integrin β6 mRNA and protein levels; however, expression levels of several other integrin subunits were not different between steers and bulls. MMP9 mRNA levels were positively correlated ( P < 0.05) with intramuscular fat content in bull group. In conclusion, these results demonstrate that castration has moderate effects on expression of ECM components, ECM degrading factors, and integrin subunit genes in the LT. [ABSTRACT FROM AUTHOR]

Marbling score (MS) is related to beef auction price (AP) in Korea, but how these relate to marbling texture (i.e. number and distribution of marbling particles [MPs]) is not known. We examined relationships among carcass traits, carcass AP, and image analysis marbling texture traits. In experiment 1, carcass data and longissimus thoracis (LT) were obtained from Korean cattle steers reared under similar feeding conditions. MS, quality grade (QG), and AP were related (P < 0.001) to numbers of coarse MPs and fine MPs and fineness index. In experiment 2, LT images photographed at a slaughterhouse were used in regression analysis within individual QG classes (QGs: 1 [middle], 1+, and 1++ [best]). AP was related (P < 0.001) to numbers of coarse MPs and fine MPs and fineness index in both QGs 1+ and 1++ but not in QG 1. Overall, several marbling texture traits were related to AP, but both MS and QG were more strongly related to AP. • Computer image analysis (CIA) method could be used for marbling traits. • Beef quality grade had positive relationships with CIA traits in Korean cattle. • Auction price was positively related with some CIA traits in highly marbled beef. • CIA method could be used for determining the finely and highly marbled beef. [ABSTRACT FROM AUTHOR]

• Dehorning of bull calves increased inflammation indicator haptoglobin. • Dehorning altered eating, head shaking, and lying frequencies. • Lidocaine-plus-flunixin treatment reduced head shaking frequency. • Head shaking frequency was associated with haptoglobin concentration. This study was performed to determine the effects of dehorning and lidocaine-plus-flunixin (LF) treatment on indicators of stress (cortisol) and acute inflammation [haptoglobin (Hp)] and behaviors in Korean cattle bull calves, and the associations among these parameters. A total of 36 Korean cattle bull calves (average body weight: 172 ± 3.6 kg; average age: 7.4 ± 0.2 months) were allocated among four treatments (n = 9 head/group) in a 2 × 2 factorial arrangement: no dehorning with no LF injection; no dehorning with LF injection; dehorning with no LF injection; and dehorning with LF injection. The LF treatment consisted of an anesthetic lidocaine hydrochloride injection in each horn and a non-steroidal anti-inflammatory drug, flunixin meglumine, injection immediately prior to dehorning. Dehorning was performed surgically using a Barnes dehorner. Blood was collected immediately before dehorning and at 0.5 and 5 hours and 1, 3, 7, and 14 days after dehorning. Rectal temperature was measured at the same time points, except hour 0.5. Dehorning did not affect the average daily gain and concentrate intake. Dehorning increased (P < 0.001) plasma cortisol concentrations at h 0.5 and increased plasma Hp concentrations at day 1 (P = 0.02) and day 3 (P = 0.03). Behavior frequencies were measured for 3 h from h 0.5 after dehorning. Dehorning decreased (P = 0.006) eating frequency, and a dehorning × LF treatment interaction was observed (P = 0.01) for head shaking frequency: dehorning increased (P < 0.05) head shaking frequency in the non-LF-treated groups, and LF treatment decreased (P < 0.05) head shaking frequency in dehorned animals. In correlation analyses, rectal temperature was positively correlated (0.37 < r < 0.50, P < 0.05) with Hp concentration at several time points (h 5, day 1, and day 3). Eating frequency was negatively correlated (r = –0.43, P < 0.05) with Hp concentration at day 1 and day 3. Head shaking frequency was positively correlated (r = 0.43, P < 0.05) with Hp concentration at day 1. In conclusion, dehorning caused temporal inductions of stress indicator cortisol and acute inflammation indicator Hp at h 0.5 and day 1 after dehorning, respectively. Dehorning altered eating, head shaking, and lying behavior frequencies. The LF treatment reduced head shaking frequency of dehorned animals. The increased head shaking and decreased eating following dehorning were closely associated with inflammation parameter Hp concentration, underscoring the potential benefit of controlling inflammation during the dehorning process to alleviate dehorning-associated stress and pain symptoms. [ABSTRACT FROM AUTHOR]

• Cold stress (CS) and fat supplementation may affect growth and rumen fermentation. • Mild or moderate CS does not affect growth performance of Korean cattle steers. • CS changes ruminal concentrations of total volatile fatty acid but RPF does not affect. • Rumen-protected fat (RPF) supplementation does not decrease nutrient intakes. • RPF supplementation does not improve growth performance. We investigated the effects of cold ambient temperatures and the supplementation of rumen-protected fat (RPF) on the growth performance, rumen fermentation parameters, and blood metabolic parameters of Korean cattle steers during the early fattening stage. Twenty Korean cattle steers (body weight = 356.5 ± 3.72 kg, age = 16.8 ± 0.34 months) were divided into two groups: 10 steers were fed a conventional concentrate (control), and 10 steers were fed a concentrate supplemented with 8 g/kg RPF (treatment). Steers were fed a concentrate at 1.6% body weight and 3 kg tall fescue hay daily for 12 weeks in 2016: January 8 to February 2 (P1), February 3 to March 3 (P2), and March 4 to April 1 (P3). Body weight was measured, and blood and rumen fluid were collected four times from each steer: at the start of the experiment, and then at 4-week intervals. The mean indoor temperatures during P1 (−7.37 ℃) and P2 (–2.96℃) were lower (P < 0.001) than the mean P3 temperature (6.22 ℃). These lower temperatures were within the range that causes mild to moderate cold stress (CS) in other cattle breeds. By contrast, the mean indoor temperature during P3 is considered thermoneutral. The average daily gain (P = 0.39 and P = 0.16) and gain-to-feed ratio (P = 0.26 and P = 0.57) were not affected by RPF supplementation or time-period. Total dry matter, crude protein, ether extract, neutral detergent fiber, and acid detergent fiber intakes per body weight were higher (all P < 0.001) in colder P1 or P2 compared to other time periods, but these variables were not affected (P ≥ 0.31) by RPF supplementation, except ether extract intake. Ruminal total VFA concentrations were higher (P = 0.001) in a colder January than in other months, but these were not affected (P = 0.26) by RPF supplementation. The ruminal propionate proportion was higher (P < 0.001) in a colder January than in other months, whereas the butyrate proportion was lower (P = 0.01). Serum triglyceride (P = 0.007), total cholesterol (P = 0.001), and high-density lipoprotein (P = 0.03) concentrations were lower during colder months. RPF supplementation increased (P = 0.008) serum cholesterol concentrations. Our results indicate that mild to moderate CS may not affect Korean cattle, as cattle growth performance was not affected by colder temperatures, although concentrate and forage intakes were increased, and some changes in blood metabolic and ruminal parameters were observed. The 8 g/kg RPF supplementation did not improve growth performance under cold conditions, although it did not decrease intake and ruminal total VFA concentration. [ABSTRACT FROM AUTHOR]

Signal transducers and activators of transcription 5 (STAT5) mediates growth hormone signals, which may control hepatic cholesterol uptake and bile acid metabolism. Deregulation of liver cholesterol homeostasis and bile acid metabolism may cause liver damage and cholesterol gallstone development. The purpose of this study was to understand the role of local STAT5 signaling in cholesterol and bile acid metabolism using liver-specific STAT5 knock-out (STAT5 LKO) mice on a normal diet and a cholesterol- and bile acid-containing lithogenic diet. STAT5 LKO mice showed significant down-regulation of STAT5 and insulin-like growth factor-1 genes. STAT5 gene deletion had a minor effect on cholesterol metabolism, as evidenced by a minor change in circulating cholesterol levels and no changes in expression of hepatic low-density lipoprotein receptor and cholesterol synthesis genes in STAT5 LKO mice. In contrast, bile acid synthesis and uptake genes were profoundly down-regulated and bile acid detoxification genes were up-regulated in STAT5 LKO mice. In STAT5 fl/fl mice, a lithogenic diet induced liver damage, as evidenced by moderate increases in liver ballooning, inflammation and fibrosis. However, STAT5 deletion ameliorated the degree of liver damage induced by the lithogenic diet. In STAT5 LKO mice, a lithogenic diet did not alter the incidence or severity of cholesterol gallstones. In conclusion, local STAT5 signaling does not have a significant role in cholesterol metabolism. In contrast, hepatic STAT5 signaling has significant roles in regulating transcription of genes for synthesis, transport and detoxification of bile acids, but it has only a minor role in bile acid metabolism. [ABSTRACT FROM AUTHOR]

Growth hormone (GH) signal is mediated by signal transducer and activator of transcription 5 (STAT5), which controls hepatic lipid metabolism. Nonalcoholic fatty liver disease (NAFLD) is clinically associated with a deficiency in GH. This study was performed to understand the role of local STAT5 signaling on hepatic lipid and glucose metabolism utilizing liver-specific STAT5 gene deletion (STAT5 LKO) mice under both normal diet and high-fat diet (HFD) feeding conditions. STAT5 LKO induced hepatic steatosis under HFD feeding, while this change was not observed in mice on normal diet. STAT5 LKO caused hyperglycemia, hyperinsulinemia, hyperleptinemia and elevated free fatty acid and cholesterol concentrations under HFD feeding but induced only hyperglycemia on normal diet. At the molecular level, STAT5 LKO up-regulated the expression of genes involved in lipid uptake (CD36), very low-density lipoprotein receptor (VLDLR), lipogenic stearoyl-CoA desaturase and adipogenic peroxisome proliferator-activated receptor gamma, in both diet groups. In response to HFD feeding, further increases in CD36 and VLDLR expression were found in STAT5 LKO mice. In conclusion, our study suggests that low STAT5 signaling on normal diet predisposes STAT5 LKO mice to early development of fatty liver by hyperglycemia and activation of lipid uptake and adipogenesis. A deficiency in STAT5 signaling under HFD feeding deregulates hepatic and body glucose and lipid metabolism, leading to the development of hepatic steatosis. Our study indicates that low STAT5 signaling, due to low GH secretion, may increase a chance for NAFLD development in elderly people. [ABSTRACT FROM AUTHOR]