Effect of sea buckthorn berries and pulp in a liquid emulsion on gastric ulcer scores and gastric juice pH in horses.

BACKGROUND: Sea buckthorn berries (Hippophae rhamnoides) are rich in vitamin C and E, carotenoids, flavonoids, fatty acids, plant sterols, lignans, and minerals. A feed supplement containing sea buckthorn berries might have efficacy in treatment and prevention of gastric ulcers in horses. OBJECTIVES: To test the efficacy of a commercially available formulation of sea buckthorn berries and pulp (SeaBuck SBT Gastro-Plus) for treatment and prevention of gastric ulcers in stall-confined horses. ANIMALS: Eight Thoroughbred and Thoroughbred-cross horses (3-10 years of age, 5 geldings and 3 mares, 380-600 kg body weight). METHODS: This study was a 2-period crossover in which all horses received no treatment (untreated controls; n = 8) and treatment (SeaBuckSBT Gastro-Plus, 4 ounces [35.6 g berries and pulp], twice daily; n = 8) mixed with a pelleted complete feed (18% crude fiber; 9% starch; 14% crude protein). Horses were treated for 4 weeks followed by a 1-week (d28-d35) alternating feed-deprivation period to induce or worsen existing ulcers. Gastroscopic examinations were performed on days 0, 28, and 35. Gastric juice pH was measured and gastric ulcer number and severity scores were assigned by a masked investigator. RESULTS: Mean nonglandular gastric ulcer scores significantly (P < .05) increased in all horses after day 28, as a result of intermittent feed deprivation. Mean nonglandular gastric ulcer number (P = .84) and severity (P = .51) were not significantly different between SBT-treated and untreated control horses. However, mean glandular ulcer number (P = .02) and glandular ulcer severity (P = .02) were significantly lower in the SBT-treated horses compared with the untreated control at week 5. CONCLUSIONS AND CLINICAL IMPORTANCE: SeaBuck SBT Gastro-Plus liquid fed to horses did not show efficacy in treatment or prevention of naturally occurring nonglandular ulcers in horses; however, glandular ulcer scores were significantly lower in SBT-treated horses after feed deprivation. Thus, SBT might have efficacy in prevention of glandular ulcers in horses housed in stalls and undergoing intermittent feeding.

Hyperleptinemia in horses: responses to administration of a small dose of lipopolysaccharide endotoxin in mares and geldings.

Mares and geldings in good body condition selected for hyperleptinemia vs. normal leptin concentrations were studied to determine whether the hyperleptinemic condition affected various characteristics of the hematologic and hormonal systems after a challenge with lipopolysaccharide endotoxin. Four mares and 4 geldings that were determined to be hyperleptinemic (mean plasma leptin concentrations of 10.0 to 15.5 ng/mL) and 4 mares and 4 geldings with mean plasma leptin concentrations between 2.4 and 5.5 ng/mL were administered Escherichia coli O55:B5 endotoxin (35 ng/kg of BW in 500 mL of saline over a 30-min infusion), or saline only, in pairs in a single-switchback design, with horses and treatments randomly assigned for the first infusion. Physiological variables and blood components were monitored for 24 h after the onset of infusions. Treatments were switched and the second infusions were administered 8 d later. Relative to vehicle infusion, endotoxin infusion increased (P < 0.01) the rectal temperature, heart rate, respiration rate, plasma total protein concentration, and blood packed cell volume; there was an interaction of leptin status, endotoxin treatment, and time for heart rate (P = 0.039), respiration rate (P = 0.018), and plasma total protein concentration (P = 0.054). Blood concentrations of leukocytes, lymphocytes, and neutrophils all decreased (P < 0.001) after endotoxin infusion; there was an interaction (P = 0.0057) between sex and leptin status for blood platelet concentration. Plasma leptin concentrations increased (P = 0.013) after endotoxin infusion in both hyperleptinemic horses and those with reduced leptin concentrations. There were interactions (P < 0.037) of sex with endotoxin treatment and time for plasma concentrations of cortisol and prolactin, whereas plasma GH concentrations were affected (increased; P < 0.001) only by time after infusion. Given that the effects of hyperleptinemia were generally minor, it was concluded that the hyperleptinemic condition, and its associated type-2 diabetic symptoms, has a minimal impact on the components of the hematologic and hormonal systems studied.

Effect of dexamethasone, feeding time, and insulin infusion on leptin concentrations in stallions.

Three experiments tested the hypotheses that daily cortisol rhythm, feeding time, and/or insulin infusion affect(s) leptin secretion in stallions. Ten mature stallions received ad libitum hay and water and were fed a grain concentrate once daily at 0700. In Exp. 1, stallions received either a single injection of dexamethasone (125 microg/kg BW i.m.; n = 5) or vehicle (controls; n = 5) at 0700 on d -1. Starting 24 h later, blood samples were collected every 2 h for 36 h via jugular venipuncture. Cortisol in control stallions varied (P < 0.01) with time, with a morning peak and evening nadir; dexamethasone suppressed (P < 0.01) cortisol concentrations. Leptin and insulin were greater (P < 0.01) in the treated stallions, as was the insulin response to feeding (P < 0.01). Leptin in control stallions varied (P < 0.01) in a diurnal pattern, peaking approximately 10 h after onset of eating. This pattern of leptin secretion was similar, although of greater magnitude (P < 0.01), in treated stallions. In Exp. 2, five stallions were fed the concentrate portion of their diet daily at 0700 and five were switched to feeding at 1900. After 14 d on these regimens, blood samples were collected every 4 h for 48 h and then twice daily for 5 d. Cortisol varied diurnally (P = 0.02) and was not altered (P = 0.21) by feeding time. Insulin and leptin increased (P < 0.01) after feeding, and the peaks in insulin and leptin were shifted 12 h by feeding at 1900. In Exp. 3, six stallions were used in two 3 x 3 Latin square experiments. Treatments were 1) normal daily meal at 0700; 2) no feed for 24 h; and 3) no feed and a bolus injection of insulin (0.4 mIU/kg BW i.v.) followed by infusion of insulin (1.2 mIU.kg BW(-1).min(-1)) for 180 min, which was gradually decreased to 0 by 240 min; sufficient glucose was infused to maintain euglycemia. Plasma insulin increased (P < 0.01) in stallions when they were meal-fed (to approximately 150 microIU/mL) or infused with insulin and glucose (to approximately 75 microIU/mL), but insulin remained low (10 microIU/mL or less) when they were not fed. The increases in insulin were paralleled by gradual increases (P < 0.01) in leptin concentrations 3 to 4 h later in stallions fed or infused with insulin and glucose. When stallions were not fed, leptin concentrations remained low. These results demonstrate that feeding time, and more specifically the insulin increase associated with a meal, not cortisol rhythm, drives the postprandial increase in plasma leptin concentrations in horses.

Endocrine responses in mares and geldings with high body condition scores grouped by high vs. low resting leptin concentrations.

Previous observations from this laboratory indicated that horses with high BCS could have resting plasma leptin concentrations ranging from low (1 to 5 ng/mL) to very high (10 to 50 ng/mL). To study the possible interactions of leptin secretion with other endocrine systems, BCS and plasma leptin concentrations were measured on 36 mares and 18 geldings. From mares and geldings that had a mean BCS of at least 7.5, five with the lowest (low leptin) and five with the highest (high leptin) leptin concentrations were selected. Jugular blood samples were collected twice daily for 3 d from the 20 selected horses to determine average resting hormone concentrations. Over the next 12 d, glucose infusion, injection of thyrotropin-releasing hormone (TRH), exercise, and dexamethasone treatment were used to perturb various hormonal systems. By design, horses selected for high leptin had greater (P < 0.0001) leptin concentrations than horses selected for low leptin (14.1 vs. 2.8 +/- 0.92 ng/mL, respectively). In addition, mares had greater (P = 0.008) leptin concentrations than geldings. Horses selected for high leptin had lower (P = 0.027) concentrations of GH but higher (P = 0.0005) concentrations of insulin and thriiodothyronine (T3) than those selected for low leptin. Mares had greater (P = 0.0006) concentrations of cortisol than geldings. There was no difference (P > 0.10) in concentrations of IGF-1, prolactin, or thyroid-stimulating hormone (TSH). Horses selected for high leptin had a greater (P = 0.0365) insulin response to i.v. glucose infusion than horses selected for low leptin. Mares had a greater (P = 0.0006) TSH response and tended (P = 0.088) to have a greater prolactin response to TRH than geldings; the T3 response was greater (P = 0.047) in horses selected for high leptin. The leptin (P = 0.0057), insulin (P < 0.0001), and glucose (P = 0.0063) responses to dexamethasone were greater in horses selected for high leptin than in those selected for low leptin. In addition, mares had a greater (P < 0.0001) glucose response to dexamethasone than geldings. Cortisol concentrations were decreased (P = 0.029) by dexamethasone equally in all groups. In conclusion, differences in insulin, T3, and GH associated with high vs. low leptin concentrations indicate a likely interaction of these systems with leptin secretion in horses and serve as a starting point for future study of the cause-and-effect nature of the interactions.