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 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)