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CVJ / VOL 57 / JUNE 2016 635
Article
Glucose intolerance in dairy goats with pregnancy toxemia: Lack of
correlation between blood pH and beta hydroxybutyric acid values
Miguel S. Lima, João B. Cota, Yolanda M. Vaz, Inês G. Ajuda, Rita A. Pascoal, Nuno Carolino,
Charles A. Hjerpe
Abstract — This study assessed the response to a glucose tolerance test in dairy goats with pregnancy toxemia (PT),
in healthy, pregnant, non-lactating dairy goats in the last month of gestation (HP), and in healthy, lactating, non-
pregnant, dairy goats in mid-lactation (HL). A 500 mL volume of a 5% glucose solution was administered by the
IV route. Blood glucose concentrations returned to pre-infusion levels by 90 min in all 8 HL goats, and by 180 min
in all 8 HP goats. In contrast, concentrations of blood glucose were still significantly above pre-infusion levels at
180 min post-infusion in all 8 PT goats. Thus, marked glucose intolerance was demonstrated in the PT goats, and
mild intolerance was noted in the HP goats. In 25 goats diagnosed with PT and having blood beta hydroxybutyric
acid (BHBA) values $ 2.9 mmol/L, the correlation coefficient for BHBA with blood pH was non-significant.
Résumé — Intolérance au glucose chez les chèvres laitières atteintes de toxémie gestationnelle : absence de
corrélation entre les valeurs du pH sanguin et de l’acide bêta-hydroxybutyrique. Cette étude a évalué la réponse
à un test de tolérance au glucose chez des chèvres laitières atteintes de toxémie gestationnelle (TG), chez des chèvres
laitières gravides en santé qui n’étaient pas en lactation durant le dernier mois de la gestation (HP) et chez des
chèvres laitières non gravides en santé en pleine lactation (HL). Un volume de 500 mL d’une solution de glucose
à 5 % a été administrée par voie IV. Les concentrations de glucose sanguin sont retournées à la normale dans un
délai de 90 minutes chez les huit chèvres HL et dans un délai de 180 minutes chez les huit chèvres HP. Par contraste,
les concentrations de glucose sanguin étaient toujours significativement supérieures aux niveaux de pré-infusion
180 minutes après l’infusion chez les huit chèvres TG. Par conséquent, une intolérance au glucose marquée a été
démontrée chez les chèvres TG et une intolérance légère a été observée chez les chèvres HP. Chez les 25 chèvres
diagnostiquées avec la TG qui présentaient des valeurs sanguines d’acide bêta-hydroxybotyrique (BHBA) de
$ 2,9 mmol/L, le coefficient de corrélation pour les BHBA avec le pH sanguin n’était pas significatif.
(Traduit par Isabelle Vallières)
Can Vet J 2016;57:635–640
Introduction
Several authors have recommended that dairy goats that
are acutely ill, pregnant, non-lactating and diagnosed
with pregnancy toxemia (PT), which is always accompanied
by hepatic lipidosis (1,2), should be treated with glucose by
the IV route (1,2). However, in our experience with obese PT
does, IV administration of glucose has provided little benefit, as
evidenced by either reduced severity of clinical signs or reduced
case fatality rates, whether the patients were hypoglycemic or
normoglycemic at the time of treatment (3). Because we had
previously demonstrated glucose intolerance in a few clinical
cases of PT in does that were not included in any formal study,
we decided to explore the possibility that glucose intolerance
might explain why our PT does fail to respond to glucose
therapy.
A glucose tolerance test (GTT) is used to assess the ability of
an animal to process a large glucose load that is administered
by either the IV or oral route. The IV route has been the route
utilized most often by veterinary clinicians in domestic animals
(4–6). In most species in which glucose tolerance testing has
been performed in normal, healthy individuals, blood glucose
values return to pre-treatment levels by 90 min following glucose
administration (4).
Glucose intolerance can result from an insufficient insulin
secretion response (5), insufficient effectiveness of insulin
(insulin resistance) (5), increased amounts of antagonistic
(counter-regulatory) hormones such as glucocorticoids (5), and
from liver dysfunction (resulting in reduced glucose uptake and
Faculdade de Medicina Veterinária, CIISA, DC, Universidade
de Lisboa, Portugal (Lima, Cota, Vaz, Ajuda); Barão e Barão,
Coutada Velha, Benavente, Portugal (Pascoal); INIAV, EUVG,
CIISA, Portugal (Carolino); School of Veterinary Medicine,
University of California, Davis, California 95616, USA
(Hjerpe).
Address all correspondence to Dr. Miguel Lima; e-mail:
mlmslima@fmv.ulisboa.pt
Use of this article is limited to a single copy for personal study.
Anyone interested in obtaining reprints should contact the
CVMA office (hbroughton@cvma-acmv.org) for additional
copies or permission to use this material elsewhere.
636 CVJ / VOL 57 / JUNE 2016
ARTICLE
storage in the liver) (5,7). The authors postulate that glucose
intolerance observed in PT goats and healthy, pregnant, non-
lactating dairy goats, in the last month of gestation (HP goats)
was caused (at least in part) by insulin resistance, which has
been consistently demonstrated in pregnant sheep (8) and cattle
(9–13). Reduced insulin secretion could also have been a con-
tributing factor (14), and impaired hepatic function might also
have played a role (15), in view of the marked hepatic lipidosis
that was observed in 6 of the fatal PT cases.
Obesity in sheep is associated with a decrease in insulin
sensitivity (16,17) which was suggested to be consistent with
decreased insulin receptors in peripheral tissues (17). Insulin
resistance during late gestation might possibly be an etiologic
factor in PT in ewes (8).
Pregnancy toxemia appears to be related to the glucose
demands of the fetal-placental unity, due to the rapid growth of
large or multiple fetuses during the last month of gestation (18).
The pregnant female must cope with this negative energy bal-
ance through metabolic adaptations (19). The consequences of
this negative energy balance for the dam are hypoglycemia, lipid
mobilization, and accumulation of ketone bodies (20). With
lipid mobilization, large amounts of non-esterified fatty acids
are delivered to the liver. A certain percentage of these fatty acids
are esterified in the cytosol, forming triglycerides and favoring
fat accumulation in the liver (19). At least in ewes, however, it
is still uncertain whether the increase in energy demands of late
gestation can fully explain the appearance of PT (21).
During late gestation, ewes have reduced ability to metabolize
BHBA, thereby promoting hyperketonemia (21) which exerts
adverse effects on energy balance and glucose metabolism (21).
It appears that impaired ketone body utilization in late preg-
nancy facilitates development of PT, especially in ewes carrying
twins (21). Insulin resistance has also been documented in dairy
cows with induced or spontaneous hepatic lipidosis and ketosis
(9–13), and in humans with spontaneous hepatic lipidosis and
ketosis (22).
Pregnancy toxemia occurs during the last month of gestation
in ewes and does (1,2). Obese goats that are pregnant with mul-
tiple fetuses are particularly vulnerable to PT (23). It is believed
that large amounts of accumulated intra-abdominal fat and rapid
expansion of the uterus during late gestation combine to reduce
the space available for ruminal expansion. As a result, these
animals are unable to consume the volumes of feedstuffs needed
to meet their energy requirements (20,23,24). A decrease in the
plane of nutrition during the latter half of pregnancy, coupled
with a short period of food deprivation, are also very important
risk factors, especially in ewes bearing twins and triplets (20).
Excessively thin ewes are also at high risk (20).
The primary objective of this study was to assess the response
to an IV glucose load in goats diagnosed with PT, and to com-
pare that response to responses in HP goats, and in healthy,
non-pregnant goats in mid lactation (more than 100 days
in milk) (HL goats). A physical examination was performed
and biochemical blood values were determined in all goats. A
second objective was to determine the extent to which values
for blood BHBA and blood pH might be correlated in 25 does
diagnosed with PT.
Materials and methods
This study was done on a 2000-head dairy goat farm, located
48 km northeast of Lisbon, Portugal. The goats were of 2 breeds,
Alpine (1200 animals) and Saanen (600 animals) with some
animals being crosses of these 2 breeds (200 animals). All
goats were continually housed in confinement, and all adult
lactating does had access to free stalls and were fed a complete
ration, ad libitum. Their Total Mixed Ration (TMR) consisted
of corn silage (30%), alfalfa hay (22%), brewer’s grains (22%),
rye-grass hay (8%), and a concentrate mix (18%). The TMR
was offered once per day. All the adult goats had free access to
mineral blocks containing NaCl, magnesium, and trace amounts
of iron, iodine, cobalt, manganese, zinc, and selenium.
There were 3 kidding seasons per year, beginning in January,
April, and October. Each kidding season began on the first day
of the month, and continued for 45 d. Daily milk production
in this herd averaged approximately 3 L/doe. Machine milking
was performed twice daily. One month before their estimated
kidding dates, lactating pregnant does were moved to a separate
dedicated pen, the TMR was withdrawn, milking ceased, and
wheat straw was fed, ad libitum. In addition, 1 kg/head per day
of a different concentrate mix was provided, split into 4 feed-
ings, equally distributed throughout each 24-hour period. This
ration change was intended to reduce the rate of occurrence of
PT (which ranged from 2.0% to 6.9% during this study), by
reducing overconsumption of calories, excessive weight gain, and
abdominal fat accumulation, during the last 30 d of gestation.
A second study involved 25 PT goats, whose blood BHBA
values were compared with their blood pH values. This study
included 8 PT goats that were enrolled in the glucose tolerance
test (GTT) study, plus 17 PT goats not previously involved in
any formal study.
Experiment 1 involved 24 does, divided into 3 groups of 8
(PT, HP, and HL). Three PT does gave birth in April/May 2013,
2 in October/November 2013 and 3 in January/February 2014.
The rates of PT occurrence (number of cases of PT divided by
the number of does kidding) during each of these 3 kidding
periods were 22/415 (5.3%), 7/356 (2.0%), and 29/418 (6.9%),
respectively.
Any doe in the dry doe pen that did not show normal interest
in eating when fresh concentrate mix was offered was considered
to be a PT suspect, and was tested for urine ketone bodies (if a
urine sample could be obtained). Ketonuria and aciduria were
confirmed in 4 does. A blood sample was obtained from every
PT suspect, and tested for BHBA on a day when the veterinar-
ian was present on the farm. All 25 of the PT does enrolled in
this study had individual blood BHBA values between 2.9 and
8.0 mmol/L. Additional (more definitive) clinical signs of PT,
such as persistent recumbency, depression, swollen limbs, rapid
respirations (polypnea), inability to rise, stand and walk, and/or
neurological signs would also trigger a request for the patient
to be examined by a veterinarian, and for the blood BHBA
concentration to be determined.
The following clinical signs were observed in the 8 PT does
in this study: anorexia (n = 8 does), absence of ruminal motil-
ity (n = 7 does), sternal recumbency, but able to rise upon
CVJ / VOL 57 / JUNE 2016 637
ARTICLE
stimulation (n = 6 does), swollen limbs (n = 5 does), neurologi-
cal abnormalities, such as “star gazing” (opisthotonus) (n = 2
does), and abnormally drooped ears (n = 2 does). Six of the 8 PT
does died, even though kidding was induced using dexametha-
sone (Vetacort; Vétoquinol, Barcarena, Portugal), 1 mg/10 kg
body weight (BW), IM, and dexcloprostenol (Gestavet-Prost®;
Hipra, Lisbon, Portugal), 125 mL, IM), (n = 5 does) or a cesar-
ean section was performed (n = 3 does).
Each HP (control) goat was picked from the same pen from
which its cohort PT goat came, on the same day that the PT case
was enrolled in the study, and selected to mirror, as closely as
possible, its cohort PT goat with respect to age, body condition
score (BCS), body weight, and breed (in that approximate order
of importance).
The 5 criteria used in selection of the HL does are: . 100 days
in milk (DIM), milk production . 1.5 L/d, BCS, age, and breed.
Most of the HL does were thin, so BCS were weighted more
heavily in the selection process than were ages or breeds. An
attempt was made to select HL goats whose BCS most closely
approximated those of the PT goats.
At the time that each doe was being selected and enrolled in
this study, its weight and BCS were determined. A blood sample
was obtained from the jugular vein of each of the 24 does, on
the side opposite that subsequently used for glucose infusion.
The following devices were used on-farm: a validated electronic
on-farm test (Precision Xceed; Abbott, UK) to quantify BHBA
(25) and a portable analyzer (i-Stat; Sensor Devices, Waukesha,
Wisconsin, USA) to measure Na1, K1, Cl2, HCO3
2, glucose,
pH, base excess, pCO2, anion gap and urea nitrogen.
Subsequently, an 18-gauge 2-inch catheter (Introcan; W.B.
Braun, Rohrdorf, Germany) was introduced into the appropriate
jugular vein, and 500 mL of a 5% glucose solution was admin-
istered to each of the 24 experimental does, over an average
time of 10 min (about 0.37g of glucose/kg BW). Blood samples
were then collected from all PT, HP, and HL does at 30 and
90 min after completion of glucose infusion, from the same
vein previously used for this purpose, and blood glucose values
were determined. A third blood glucose value was determined
at 180 min post-infusion, in does in which the 90-min blood
glucose concentration exceeded that doe’s pre-infusion level.
In Experiment 2, the objective was to determine the extent to
which the blood values for BHBA and pH in individual goats
with PT might be correlated. The criteria for inclusion of PT
goats in this experiment were that i) there was a compatible case
history, ii) characteristic clinical signs of PT were present, and
iii) blood concentrations of BHBA were $ 2.9 mmol/L.
Blood samples were obtained from the jugular vein of 17
additional PT does making a total of 25 does with clinical signs
of PT in which blood BHBA values were determined with the
electronic on-farm test (Precision Xceed) and blood pH values
were measured with a portable analyzer (iStat). Of these 25 PT
goats, 5 were Saanen, 9 were Alpine and 11 were Saanen-Alpine
cross-breds.
Statistical analysis
Data from the three 8-goat groups were analyzed with statistical
software (IBM SPSS Statistics V.19, Armonk, New York, USA)
for descriptive statistics and for hypothesis testing. Due to the
small sample size, the non-parametric Mann Whitney U-Test
(26) was used to compare the distributions of 2 independent
samples, so as to obtain a 95% confidence interval level.
Pearson’s correlation (26) was used to investigate the association
between the blood values for pH and BHBA in the 25 PT does.
Results
The ages, body condition scores, and body weights for all
3 groups of experimental does are summarized in Table 1. In
addition, the following information was collected and recorded
for only 1 or 2 of the 3 8-doe GTT groups: i) days in milk
(in HL does only); ii) daily milk production (in HL does only);
and iii) number of kids carried/delivered (in PT and HP does
only).
Blood chemistry results for PT, HP, and HL does are sum-
marized in Table 2 (27,28). Blood values were significantly lower
in PT does than in HP does for K1, pH, HCO3
2, base excess,
pCO2 (P , 0.001) and glucose (P , 0.005). Blood values were
significantly higher in PT does than in HP does for anion gap
(P , 0.005), and BHBA (P , 0.001).
Blood values were significantly lower in PT does than in HL
does for K1 (P , 0.005), and for glucose, pH, HCO3
2, base
excess, and pCO2 (P , 0.001). Blood values were significantly
higher in PT does than in HL does for Cl2 (P , 0.05), anion
gap and BHBA (P , 0.001).
When the blood values of the HP and HL groups were com-
pared, Na1 and Cl2 were significantly higher in the HP group
(P , 0.05) and urea nitrogen was significantly higher in the
HL group (P , 0.05).
The results of glucose tolerance tests are shown (Figure 1).
Blood glucose values were significantly lower in the PT group
than in the HP and HL groups, before glucose infusion was
begun (P , 0.01). Compared with pre-infusion values, at 30 min
post-infusion, blood glucose values were significantly higher in
all 3 groups (P , 0.05), but glucose values were not significantly
different between the 3 groups. At 90 min post-infusion, the
Table 1. Ages, body condition scores (BCS), body weights, and
days in milk (DIM), daily milk production, and number of fetuses in
pregnancy toxemia (PT) does, healthy pregnant non-lactating (HP)
does and healthy lactating non-pregnant (HL) does
8 PT Does 8 HP Does 8 HL Does
median median median
Parameter (range) (range) (range)
Age (years) 5.5 4.0 5.0
(2 to 8) (2 to 6) (2 to 6)
BCS 3.0 3.5 3.3
(3.0 to 3.5) (2.5 to 5) (2 to 4)
Body weight (kg) 68.5 64.5 60.0
(51 to 77) (55 to 70) (51 to 71)
DIM NA NA 132
(109 to 144)
Milk production (L) NA NA 2.1
(1.7 to 2.7)
Number of fetuses 2.5 2.0 NA
(2 to 3) (1 to 3)
BCS — body condition score; NA — not applicable; DIM — days in milk.
638 CVJ / VOL 57 / JUNE 2016
ARTICLE
blood glucose values in the HP and HL groups were significantly
lower than in the PT group (P , 0.001 and P , 0.05, respec-
tively) and blood glucose values in the HL group were similar
to pre-infusion levels. In contrast, values in both the PT group
and the HP group were significantly higher than pre-infusion
levels (P , 0.05). At 180 min post-infusion, the blood glucose
values were not significantly different between the PT and HP
groups, but PT group blood glucose values were still significantly
higher than the pre-infusion values (P , 0.05), which was clearly
indicative of glucose intolerance.
Blood pH values were compared with the blood BHBA values
in 25 does with clinical signs of pregnancy toxemia (Figure 2).
The Pearson’s correlation between these 2 variables was not sta-
tistically significant (P = 0.161). The blood BHBA values from
all 25 individual PT cases ranged between 2.9 to 8.0 mmol/L
(Figure 2).
Discussion
Glucose tolerance tests evaluate the body’s ability to normalize a
glucose load, whether administered by the IV or oral route (5,6).
The results of this study indicate that PT does do not respond
well to a glucose challenge, even though their pre-infusion blood
values were lower than those of the HP (P , 0.005) or HL does
(P , 0.001). The response of the HP does to the glucose chal-
lenge was intermediate between the PT and HL groups.
Healthy pregnant ruminants are insulin resistant at the end
of gestation and in early lactation (6,29,30). These homeorhetic
adaptations are necessary to ensure an adequate supply of
glucose for the gravid uterus and lactating mammary gland,
in support of the growing offspring, both prenatally and post-
natally (6,29). Reduced insulin sensitivity of peripheral tis-
sues during late gestation assures adequate transfer of glucose
from dam to fetus. If insulin-stimulated glucose utilization by
insulin-sensitive tissues is not limited, the fetus might not sur-
vive due to fetal hypoglycemia (30). A decline in blood insulin
concentration occurs in ewes in the early stages of pregnancy
and it has been suggested that this represents a homeorhetic
control mechanism for sparing glucose for the fetal brains and
fetoplacental units of the dams (31). Insulin concentrations in
maternal blood decrease considerably as the number of fetuses
increases (31). Increases in plasma concentrations of BHBA and
non-esterified fatty acids were observed in normal ewes, as the
number of fetuses increased, and also as lambing approached
(31). In female goats in early lactation, glucose utilization
Table 2. Blood chemistry values from 8 pregnancy toxemia (PT) does, healthy
pregnant non-lactating (HP) does and healthy lactating, non-pregnant (HL) does
8 PT Does 8 HP Does 8 HL Does
median median median Reference
Parameter (range) (range) (range) range
Na1 (mmol/L) 141.5a,b 143.0a 138.5b 142 to 155*
(129 to144) (139 to 147) (132 to 143)
K1 (mmol/L) 3.0a 3.9b 3.7b 3.5 to 6.7*
(2.1 to 3.7) (3.7 to 4.3) (3.4 to 4.2)
Cl2 (mmol/L) 111.5a,b 109.5b 103.5a 99 to 110*
(100 to 121) (100 to 112) (100 to 108)
Glucose (mmol/L) 1.6a 2.8b 2.8b 50 to 75*
(1.1 to 2.7) (2.0 to 3.6) (2.3 to 3.3)
pH 7.18a 7.40b 7.39b 7.32 to 7.5*
(6.95 to 7.33) (7.36 to 7.53) (7.36 to 7.42)
HCO3
2 (mmol/L) 9.0a 23.7b 24.2b 20 to 29**
(4 to 15) (20 to 30) (20 to 29)
Base excess (mmol/L) 219.5a 20.6b 0b 25 to 14**
(228 to 211) (26 to 15) (25 to 15)
Anion gap (mmol/L) 21.5a 14.5b 13.5 6 2.3b 12 to 24**
(17 to 26) (13 to 19) (11 to 17)
pCO2 (mmHg) 23.5a 36.7b 41.7b 38 to 45*
(17 to 29) (28 to 52) (33 to 45)
BUN (mmol/L) 5.2a,b 5.3a 7.9b 10 to 20*
(3.6 to 8.7) (3.2 to 7.1) (6.1 to 10.4)
BHBA (mmol/L) 6.8a 0.3b 0.4b , 1*
(4.3 to 8.0) (0.1 to 0.7) (0.2 to 0.5)
* Christian and Pugh (27).
** Stevens et al (28).
a,b Within a row, values with different superscript letters are significantly different among groups.
PT ≠ HL, P , 0.001 (Glucose, pH, HCO3
2, pCO2, BE, Anion gap, BHBA), P , 0.005 (K1),
P , 0. 05 (Cl2).
PT ≠ HP, P , 0.001 (K1, pH, HCO3
2, pCO2, BE, BHBA), P , 0.005 (Glucose, Anion gap).
HP ≠ HL, P , 0.05 (BUN, Na1 and Cl2).
BUN — blood urea nitrogen; BHBA — beta hydroxybutyric acid.
CVJ / VOL 57 / JUNE 2016 639
ARTICLE
appears to become less responsive to administration of insulin
(and, presumably, to the effects of endogenously produced
insulin). These adaptations to the usual effects of insulin dur-
ing early lactation were not maintained during mid-lactation
(32). Some factors associated with insulin resistance in human
females may mirror some of those involved in the development
of ruminant hepatic lipidosis and ketosis. These factors include
advancing pregnancy, obesity, hyperinsulinemia, fat feeding,
hyperlipidemia, malnutrition, and other hormones (growth
hormone and thyroxine) (30).
To our knowledge there is no prior study showing that obese
goats with PT have reduced tolerance to administered glucose.
In fact, the IV infusion of glucose to ewes and does affected
with PT has been recommended as a therapeutic strategy by
several authors (1,2,18,33). Others, however, have questioned
its efficacy in both ewes and does with PT, because the survival
rate in both ewes (14) and does (3) with PT was independent
of the plasma concentration of glucose, and because the survival
rate was poor in PT does (3 of a total of 22 cases) even after
removal of the fetuses (by cesarian section or by pharmaceutical
induction of parturition) and treatment with several medical
regimens that provided supplemental glucose (3). Furthermore,
administration of glucose to PT ewes was followed by a decrease
in blood glucose values to below pre-treatment values by 6 h
post-treatment, which may have resulted from a depressing effect
of glucose infusion on hepatic glucose production and release
into the blood stream (14).
Because the rate of occurrence of PT was essentially the same
in Saanen and Alpine does in this herd, the age of the HL does
was given greater value in the selection process than was breed.
An effort was made to mirror the breeds represented in the
PT group, but not at the expense of BCS and age.
The present study suggests that failure of glucose therapy,
at least in obese PT does, might be related to the presence of
marked hepatic lipidosis in such cases, as has been shown in
humans (22) and dairy cows (9–13). The apparent inability of
the livers in such cases to process glucose and avoid prolonged
hyperglycemia might make the use of glucose therapy in such
cases unhelpful, or even detrimental.
Malnutrition and/or feed restriction reduces the gluco-
regulatory actions of insulin (30). In sheep, the effect of fasting
(12 and 24 h) on insulin response was more marked in obese
than in lean individuals (16), but in dairy cows, the magnitude
and duration of malnutrition required to develop lipid-related
metabolic disorders are largely unknown (30). We did not
attempt to determine the impact that decline in food intake by
the PT does in our study might have had on the response to
the IV glucose load, because the dry does were fed as a group,
and it was not possible to determine the feed consumption
of individual does. Obese pregnant does in the last month of
gestation and not eating would be at increased risk for develop-
ing hyperketonemia and hepatic lipidosis, because they would
be aggravating their energy deficit and mobilizing body fat
reserves (2).
Acidosis occurs frequently in ovine pregnancy toxemia (18).
According to Marteniuk and Herdt (18), ketone bodies are
metabolic acids, and the development of acidosis (ketoacidosis)
in association with hyperketonemia is common in most species.
However, in this study of 25 goats with pregnancy toxemia (all
having the characteristic clinical signs and blood BHBA values
$ 2.9 mmol/L) the Pearson’s correlation was non-significant,
which means that there are probably other factors contribut-
ing to the severity of the metabolic acidosis besides BHBA
(Figure 2). In humans, a moderate degree of lactic acidosis may
be seen in some patients with diabetic ketoacidosis (34). How
this occurs is not clear, although marked hypovolemia is likely
to play an important role (34). Further studies are necessary to
clarify this finding.
In summary, the results of this study clearly demonstrate
that PT goats are glucose intolerant. There was little correla-
tion between blood BHBA and pH. In our experience, blood
pH values are a fairly reliable indicator of which PT goats are
likely to survive and which are certain to die (3).
Acknowledgment
This study received financial support from the Faculdade de
Medicina Veterinária, Universidade de Lisboa, Portugal. CVJ
Figure 2. Blood pH and BHBA values in 25 does with clinical
signs of pregnancy toxemia (PT) and beta hydroxybutyric acid
(BHBA) values . 2.9 mmol/ L.
pH
BHBA mmol/L
7.6
7.5
7.4
7.3
7.2
7.1
7
6.9
6.8
2 3 4 5 6 7 8 9
R = 20.289
Figure 1. Blood glucose concentrations (mmol/L) in 8 does with
pregnancy toxemia (PT), 8 healthy pregnant non-lactating (HP)
does, and 8 healthy lactating non-pregnant (HL) does, before
and after IV administration of 0.5 L of a 5% glucose solution.
* Differences between groups P , 0.01 (0 min).
† Differences between groups P , 0.05 (90 min, PT versus HP),
P , 0.001 (90 min, PT versus HL).
‡ Differences within the groups compared with the baseline P , 0.05
(0 min).
Glucose mmol/L
Time (minutes)
12
10
8
6
4
2
0
0 30 90 180
PT
HP
HL
640 CVJ / VOL 57 / JUN E 2016
ARTICLE
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