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- Author or Editor: David S. Kronfeld x
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Abstract
Objective—To identify changes in folate status of mares and foals during lactation and growth, respectively.
Animals—20 Thoroughbred mares and foals.
Procedures—Pregnant mares, and following foaling the same mares with their foals, were maintained on mixed grass-legume pasture and fed either a traditional dietary supplement rich in sugar and starch (SS) or a dietary supplement high in fat and fiber (FF). Blood samples were collected monthly from mares and foals up to 6 months after foaling. Total folate concentration in feed and forage was determined. Analyses of plasma folate, RBC folate, plasma homocysteine (HCY), and milk folate concentrations were performed.
Results—Mare plasma folate concentrations declined moderately during 6 months of lactation. Mare RBC folate concentrations initially increased after foaling up to 3 months but declined toward the end of the study. Plasma HCY concentration was higher for mares fed the SS supplement, compared with mares fed the FF supplement from foaling to 6 months of lactation. Milk folate concentrations decreased during the first 3 months and then increased. Foal plasma folate initially declined but then increased. Stable concentrations of RBC folate were observed in foals. Plasma HCY concentrations in foals were unaffected by growth during the last 5 months. References range values for plasma folate, RBC folate, milk folate, and plasma HCY concentrations in healthy lactational mares and young growing foals were determined.
Conclusions and Clinical Relevance—Folate status was not impaired in lactating mares and growing foals under the conditions in our study. It appears that folate supplementation is not necessary. (Am J Vet Res 2005;66:1214–1221)
Abstract
Objective—To determine lactate breakpoint of horses and test for effects of training and dietary supplementation with corn oil on that breakpoint.
Animals—7 healthy Arabian horses.
Procedures—Horses received a control diet (n = 4) or a diet supplemented with 10% corn oil (4). A training program, which comprised two 5-week conditioning periods with 1 week of rest, was initiated. Submaximal incremental exercise tests (IET) were conducted before the first and after both conditioning periods. Blood samples for determination of blood lactate and plasma glucose concentrations were collected 1 minute before IET and during the 15 seconds immediately preceding each speed change. Data collected were fit to one- and twoslope broken-line models and an exponential model.
Results—Good fits were obtained by application of the broken-line models (adjusted R 2 > 0.92) to blood lactate concentration versus speed curves. Lactate breakpoints increased 41% after training but were not affected by diet. After training, slope 2 and peak blood lactate concentrations were greater in the corn oil group, compared with controls. Mean blood lactate concentration at the breakpoint was not affected by training or diet. Plasma glucose concentration versus speed curves also fit the broken-line models, and glucose breakpoints preceded lactate breakpoints by approximately 1 m/s in the second and third IET.
Conclusions and Clinical Relevance—Lactate breakpoints can be determined for horses, using blood lactate concentration versus speed curves generated during submaximal IET and may be useful for assessing fitness and monitoring training programs in equine athletes. (Am J Vet Res 2000;61:144–151)
Abstract
Objective—To develop proxies calculated from basal plasma glucose and insulin concentrations that predict insulin sensitivity (SI; L·min–1 ·mU–1) and beta-cell responsiveness (ie, acute insulin response to glucose [AIRg]; mU/L·min–1) and to determine reference quintiles for these and minimal model variables.
Animals—1 laminitic pony and 46 healthy horses.
Procedure—Basal plasma glucose (mg/dL) and insulin (mU/L) concentrations were determined from blood samples obtained between 8:00 AM and 9:00 AM. Minimal model results for 46 horses were compared by equivalence testing with proxies for screening SI and pancreatic beta-cell responsiveness in humans and with 2 new proxies for screening in horses (ie, reciprocal of the square root of insulin [RISQI] and modified insulin-to-glucose ratio [MIRG]).
Results—Best predictors of SI and AIRg were RISQI (r = 0.77) and MIRG (r = 0.75) as follows: SI = 7.93(RISQI) – 1.03 and AIRg = 70.1(MIRG) – 13.8, where RISQI equals plasma insulin concentration–0.5 and MIRG equals [800 – 0.30(plasma insulin concentration – 50)2]/(plasma glucose concentration – 30). Total predictive powers were 78% and 80% for RISQI and MIRG, respectively. Reference ranges and quintiles for a population of healthy horses were calculated nonparametrically.
Conclusions and Clinical Relevance—Proxies for screening SI and pancreatic beta-cell responsiveness in horses from this study compared favorably with proxies used effectively for humans. Combined use of RISQI and MIRG will enable differentiation between compensated and uncompensated insulin resistance. The sample size of our study allowed for determination of sound reference range values and quintiles for healthy horses. (Am J Vet Res 2005;66:2114–2121)
Abstract
Objective—To evaluate genetic and metabolic predis-positions and nutritional risk factors for development of pasture-associated laminitis in ponies.
Design—Observational cohort study.
Animals—160 ponies.
Procedures—A previous diagnosis of laminitis was used to differentiate 54 ponies (PL group) from 106 nonlaminitic ponies (NL group). Pedigree analysis was used to determine a mode of inheritance for ponies with a previous diagnosis of laminitis. In early March, ponies were weighed and scored for body condition and basal venous blood samples were obtained. Plasma was analyzed for glucose, insulin, triglycerides, nonesterified fatty acids, and cortisol concentrations. Basal proxies for insulin sensitivity (reciprocal of the square root of insulin [RISQI]) and insulin secretory response (modified insulin-to-glucose ratio [MIRG]) were calculated. Observations were repeated in May, when some ponies had signs of clinical laminitis.
Results—A previous diagnosis of laminitis was consistent with the expected inheritance of a dominant major gene or genes with reduced penetrance. A prelaminitic metabolic profile was defined on the basis of body condition, plasma triglyceride concentration, RISQI, and MIRG. Meeting ≥ 3 of these criteria differentiated PL-from NL-group ponies with a total predictive power of 78%. Determination of prelaminitic metabolic syndrome in March predicted 11 of 13 cases of clinical laminitis observed in May when pasture starch concentration was high.
Conclusions and Clinical Relevance—Prelaminitic metabolic syndrome in apparently healthy ponies is comparable to metabolic syndromes in humans and is the first such set of risk factors to be supported by data in equids. Prelaminitic metabolic syndrome identifies ponies requiring special management, such as avoiding high starch intake that exacerbates insulin resistance.
Abstract
Objective—To compare effects of oral supplementation with an experimental potassium-free sodiumabundant electrolyte mixture (EM-K) with that of oral supplementation with commercial potassium-rich mixtures (EM+K) on acid-base status and plasma ion concentrations in horses during an 80-km endurance ride.
Animals—46 healthy horses.
Procedure—Blood samples were collected before the ride; at 21-, 37-, 56-, and 80-km inspection points; and during recovery (ie, 30-minute period after the ride). Consumed electrolytes were recorded. Blood was analyzed for pH, PvCO2, and Hct, and plasma was analyzed for Na+, K+, Cl–, Ca2+, Mg2+, lactate, albumin, phosphate, and total protein concentrations. Plasma concentrations of H+ and HCO3–, the strong ion difference (SID), and osmolarity were calculated.
Results—34 (17 EM-K and 17 EM+K treated) horses finished the ride. Potassium intake was 33 g less and Na+ intake was 36 g greater for EM-K-treated horses, compared with EM+K-treated horses. With increasing distance, plasma osmolarity; H+, Na+, K+, Mg2+, phosphate, lactate, total protein, and albumin concentrations; and PvCO2 and Hct were increased in all horses. Plasma HCO3–, Ca2+, and Cl– concentrations were decreased. Plasma H+ concentration was significantly lower in EM-K-treated horses, compared with EM+K-treated horses. Plasma K+ concentrations at the 80-km inspection point and during recovery were significantly less in EM-K-treated horses, compared with EM+K-treated horses.
Conclusions and Clinical Relevance—Increases in plasma H+ and K+ concentrations in this endurance ride were moderate and unlikely to contribute to signs of muscle fatigue and hyperexcitability in horses. (Am J Vet Res 2005;66:466–473)
