Objective—To identify changes in folate status of
mares and foals during lactation and growth,
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
Objective—To evaluate genetic and metabolic predis-positions and nutritional risk factors for development of pasture-associated laminitis in ponies.
Design—Observational cohort study.
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.
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
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
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 R2 > 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)
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
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)