Stock-type mares (498 ± 9 kg BW; 12 ± 7 yr) were used in a completely randomized design for 56 d to test the hypothesis that concentrate fortification improves apparent digestion and enhances lean mass over the topline. Horses were stratified by age, BW, and BCS and randomly assigned to either a custom pelleted concentrate (CON; n = 13), or an iso-caloric, iso-nitrogenous pellet that included amino acid fortification, complexed trace minerals, and fermentation metabolites (FORT; n = 10). Concentrate was offered at a total 0.75% BW/d (as-fed) twice daily, and diets were designed to meet or exceed maintenance requirements for mature horses. Horses had ad libitum access to Coastal bermudagrass hay (7.4% CP, 67% NDF, and 40% ADF). Every 14 d BW and BCS were recorded, and ultrasound images were captured every 28 d. longissimus dorsi area (LDA) and subcutaneous fat thickness (FT) were measured between the 12th and 13th ribs (12th/13th) and 17th and 18th ribs (17th/18th). Intramuscular fat at the 17th/18th ribs and rump fat-thickness were also obtained. Horses were dosed with 10 g/d of titanium dioxide (TiO2) for 14 d to estimate forage dry matter intake (DMI). To account for diurnal variation, fecal samples were collected twice daily at 12-h intervals during the last 4 days, advancing by 3 h each day to represent a 24-h period. Fecal samples were composited by horse and analyzed for TiO2 to estimate fecal output and acid detergent insoluble ash was used to calculate forage DMI. To evaluate body composition, horses were infused with a 0.12 g/kg BW deuterium oxide (D2O) on d 0 and 56. Body fat percentage (BF) was determined by quantifying D2O in plasma samples collected at pre- and 4-h postinfusion via mass spectrometry. All data were analyzed using PROC MIXED (SAS v9.4). The model contained a fixed effect of diet; horse (diet) was a random effect. Horses receiving FORT gained 17th/18th FT (P < 0.01) and increased 17th/18th LDA from d 0 to 56 (P < 0.01) while 17th/18th FT and LDA were unchanged in CON. Regardless of diet, BF estimated by D2O infusion increased in all horses from d 0 to 56 (P < 0.01). Average hay DMI was 2.1% BW, but did not differ between diets. In this study, concentrate fortification did not significantly (P ≥ 0.27) affect apparent digestion. In conclusion, concentrate fortification may promote greater muscle development along the posterior topline.
Poor maternal nutrition can cause several maladaptive phenotypes in exposed offspring. While non-sex-specific and female-specific adaptations are well-documented, male-specific outcomes are still poorly understood. Of particular interest are the outcomes in bulls and rams, as developmental programming directly impacts long-term productivity of the animal as well as human food security. The following review discusses the impact of poor maternal dietary energy and protein on bull and ram developmental programming as it relates to growth, development, and reproductive capacity. The review also highlights the importance of the timing of maternal dietary insult, as early-, mid-, and late-gestational insults can all have varying effects on offspring.
Background: Gastrointestinal (GI) injury and dysbiosis are adverse events associated with nonsteroidal anti-inflammatory drug (NSAID) use in horses. Phenylbutazone has been shown to alter GI barrier function both in vitro and ex vivo, but its effects on barrier function have not been assessed in vivo. In addition, the ability of nutritional therapeutics to prevent these changes is not known. Objective: Our objectives were to determine whether (a) phenylbutazone affected barrier function in vivo and (b) if phenylbutazone-induced GI injury could be ameliorated by the use of a nutritional therapeutic. Animals: Thirty healthy horses were randomly assigned to 3 groups (n = 10 per group): control, phenylbutazone, or phenylbutazone plus nutritional therapeutic. Methods: This study was conducted as a blinded, randomized block design. All horses were managed identically throughout the study period. Samples were collected throughout the study period to monitor fecal microbiota changes and gastric ulcers before and after treatment. Quantification of the bacterial 16S rRNA gene in blood was used as a marker of intestinal permeability. Results: Phenylbutazone increased amounts of bacterial 16S rDNA in circulation 3.02-fold (95% confidence interval [CI], 0.1.89-4.17), increased gastric ulceration score by a mean of 1.1 grade (P = .02), and induced specific changes in the microbiota, including loss of Pseudobutyrivibrio of family Lachnospiraceae. These changes were attenuated by nutritional treatment.
Eighteen Quarter Horses were used in a randomized complete design for a 28-d experiment to evaluate age-related effects on inflammation and cartilage turnover after induction of a single inflammatory insult using lipopolysaccharide (LPS). Horses were grouped by age as yearlings (3 males and 3 females), 2 to 3 yr olds (2/3 yr old; 2 males and 4 females), and skeletally mature 5 to 8 yr olds (mature; 2 males and 4 females). On d 0, all horses were individually housed and fed diets that met or exceeded requirements. On d 14, horses were challenged with an intra-articular injection of LPS. Radial carpal joints were randomly assigned to receive 0.5 ng LPS solution obtained from O55:B5 or 0.8 mL sterile lactated Ringer's solution as a contralateral control. Synovial fluid was collected prior to LPS injection at h 0 before injection and at 6, 12, 24, 168, and 336 h after injection. Samples were analyzed using commercial ELISA kits for PGE, collagenase cleavage neoepitope (C2C), and carboxypropeptide of type II collagen (CPII). Heart rate (HR), respiratory rate (RR), and rectal temperature (RT) were monitored over the initial 24 h and carpal circumference and surface temperature were also recorded, with additional measurements at 168 and 336 h. Data were analyzed using PROC MIXED of SAS. Values for RT, HR, and RR were within the normal range for each age group. Heart rate and RT were influenced by age ( < 0.01), whereas RR was unaffected ( ≤ 0.21). Joint circumference was not influenced by age of horse ( = 0.84), but circumference and surface temperature increased ( < 0.01) over time across all age groups. Synovial PGE concentrations tended ( = 0.09) to be influenced by age, with yearlings having lower ( = 0.03) concentrations than mature horses. Concentrations of synovial C2C were affected by age of horse, with yearlings and 2/3 yr olds having lower ( < 0.01) concentrations than mature horses. Similarly, synovial CPII was influenced by age, with yearlings and 2/3 yr olds having lower ( ≤ 0.02) concentrations than mature horses. Ratios of anabolic CPII to catabolic C2C varied by age, with mature and 2/3-yr-old horses having greater ( < 0.01) values compared with yearlings. These results indicate that inflammation and the corresponding cartilage turnover in response to LPS administration vary with age.
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