Hypertriglyceridemia in camelids is a challenging condition to manage and understand. When the serum of affected camelids becomes grossly lipemic, the condition is generally believed to be severe with a poor prognosis, but scientific reports1–4 of hypertriglyceridemia in camelids are rare. In a report of a case-series study1 of camelids with hepatic lipidosis, 5 of 7 camelids for which serum triglycerides concentrations had been measured were reportedly hypertriglyceridemic, but the degree of hypertriglyceridemia was not stated; only 2 had grossly lipemic serum. In other studies,2–4 hypertriglyceridemia was detected in camelids in conjunction with or independent of hepatic lipidosis. In general, the findings of those reports suggest that hypertriglyceridemia may co-exist with hepatic lipidosis and anorexia. Camelids in late gestation may be predisposed to development of hypertriglyceridemia, but other camelids are also susceptible.1 Insulin treatment combined with partial parenteral nutrition may help resolve the condition.2–4
Theories on the pathogenesis of hypertriglyceridemia in camelids are mainly extrapolated from theories on the pathogenesis of the condition in other large animal species. The manner in which animals physiologically respond to excess fat mobilization and the clinical abnormalities that can result from that mobilization vary by species. In Miniature Horses and ponies, as the capacity of the liver to process lipids via oxidative pathways is exceeded, concentrations of triglycerides in blood often rise.5,6 When excess fat is mobilized, lipoprotein A activity increases to meet metabolic demand,6 but increases in concentrations of ketones are small or occur infrequently.5,6 On the other hand, high triglycerides concentrations in the blood of cattle are rare.7,8 As fat is mobilized in cattle, the capacity of the liver to produce lipoproteins becomes overwhelmed, which results in the accumulation of fat within the liver or the shunting of fatty acids into the production of ketones and, in some situations, triglycerides.7,8 Development of hepatic lipidosis or restriction of feed intake in camelids causes increases in concentrations of circulating ketones and triglycerides,1,9,10 but the magnitude of the increase in ketone concentrations is smaller than that detected in cattle. Therefore, camelids with hypertriglyceridemia seem to be less similar to cattle and more similar to equids.
Although experimental hepatic lipidosis has been induced most frequently in lactating camelids,10 the naturally occurring condition has been reported in camelids of various signalments.1–4 Some potential causes of fat mobilization or impaired lipoprotein clearance have been investigated. In camelids, epinephrine induces the release of glucose, triglycerides, NEFA, and BHB into the bloodstream,11 whereas cortisol induces the release of glucose only.12 This suggests that catecholamine release may contribute to hypertriglyceridemia. The release of insulin causes an opposite effect, whereby serum or plasma concentrations of the aforementioned substrates decrease.11 Basal and stimulated production of insulin in camelids are low, and partial insulin resistance is rare, compared with findings in horses and cattle.13–15 With-holding of feed also results in low concentrations of circulating insulin.16 Camelids that develop hepatic lipidosis have lower insulin-to-cortisol ratios than those that do not.10,11
The insensitivity of peripheral tissues to insulin also affects the clearance of triglycerides from the blood of various species.5–8 The effect of insulin administration on blood glucose concentrations in camelids can be interpreted as indicating that tissues are partially resistant to insulin,14,15,17 but the impact of insulin resistance on fat metabolism in camelids has not been evaluated. Because of the multiple roles that insulin plays in the regulation of fat mobilization, ketone production, and peripheral triglyceride utilization, camelids with poor insulin production or decreased sensitivity to insulin in peripheral tissues could be at risk for hypertriglyceridemia. Additionally, treatment of camelids with insulin may increase the clearance of triglycerides from blood. Insulin administration has been reported11 to decrease blood triglycerides concentrations in camelids and has been used to treat camelids with hypertriglyceridemia.1,2,4 The purpose of the study reported here was to evaluate camelids with hypertriglyceridemia with regard to signalment, clinical features of disease, and response to treatment with insulin.
Materials and Methods
Case selection—Medical records of all alpacas and llamas treated at the Oregon State University Veterinary Teaching Hospital from 1995 through 2005 were reviewed to identify camelids with serum or plasma triglycerides concentrations > 60 mg/dL (hypertriglyceridemia).
Medical records review—Information obtained from each medical record included signalment, reproductive status, clinical features of disease, concomitant diseases, results of serum or plasma biochemical analyses, treatment, and outcome. Recorded biochemical valuesa included serum or plasma concentrations of NEFA, triglycerides, cholesterol, BHB, glucose, BUN, creatinine, albumin, and bilirubin as well as serum or plasma activities of AST, GGT, SDH, and CK. If a camelid died or was euthanatized during hospitalization, a necropsy and, in some situations, histologic evaluation of grossly abnormal tissues were performed. During hospitalization, histologic examination of a biopsy specimen of hepatic tissue was performed for 1 camelid. These data were used to investigate factors potentially associated with hypertriglyceridemia in camelids.
Medical records of hypertriglyceridemic camelids for which serum or plasma triglycerides concentrations had been recorded at multiple points during hospitalization were classified into 1 of 3 categories. Camelids with initial triglycerides concentrations that did not exceed 500 mg/dL were classified as HT-N or HT-I, depending on whether they had been treated with insulin. Camelids with triglycerides concentrations > 500 mg/dL and that were treated with insulin were classified as LIP-I. No comparison group was available for LIP-I camelids because all lipemic camelids had been treated with insulin. For camelids that were not treated with insulin, the first serum or plasma triglycerides concentration on record was considered the initial concentration and the second concentration on record was treated as the subsequent value for the purposes of comparison. For camelids that were treated with insulin, pretreatment concentration of triglycerides in serum or plasma was defined as the initial concentration on record and posttreatment concentration was defined as the first concentration of triglycerides measured after insulin had been administered. Once classified as HT-N, HT-I, or LIP-I, camelids were not reclassified, regardless of subsequent values of serum or plasma triglycerides concentrations. Data from the records of hypertriglyceridemic camelids for which only 1 triglycerides measurement was available were combined with those of other hypertriglyceridemic camelids for the purposes of characterization of signalment, serum or biochemical abnormalities, identification of disease states potentially related to hypertriglyceridemia, and comparison between camelids with a triglycerides concentration > 500 mg/dL and those with a triglycerides concentration < 500 mg/dL. In most circumstances in which only 1 triglycerides concentration was available, these values were obtained at admission and the associated camelids did not survive until another blood sample could be collected. Data from the records of other camelids treated for reasons other than hypertriglyceridemia at the hospital from 1995 to 2005 were used for comparisons.
Statistical analysis—To characterize the population of camelids with hypertriglyceridemia, distributions of sex and age among affected camelids were compared with respective distributions among the total population of nonhypertriglyceridemic camelids by use of a χ2 test. Age was classified into categories for analysis (neonates, ≤ 7 days; juveniles, 8 days to 2 years; breeding age adults, 3 to 9 years; and geriatrics, ≥ 10 years). Data regarding signalment at admission were available from 2002 through 2005, so only hypertriglyceridemic camelids admitted during that period (n = 26) were included in the analysis. Results of serum or plasma biochemical analyses among the different classifications of camelids with hypertriglyceridemia were compared by use of a statistical test appropriate for the distribution of the data. Normality of distribution was evaluated by use of a Kolmogorov-Smirnov test.
Serum or plasma biochemical values for camelids that did or did not survive to discharge from the hospital and for camelids that had initial triglycerides concentrations of > 60 to ≤ 500 mg/dL or > 500 mg/dL were compared by use of a Mann-Whitney U test. Camelids with 1 or multiple triglycerides measurements were included in these analyses. When multiple measurements were available, initial and subsequent serum or plasma biochemical values of HT-N camelids were compared with pretreatment and posttreatment values of HT-I camelids by use of a Mann-Whitney U test. Initial and subsequent biochemical values within the HT-N category and pretreatment and posttreatment values within the HT-I category were compared by use of a Wilcoxon signed rank test. For LIP-I camelids, pretreatment and posttreatment serum or plasma biochemical values were compared by use of paired t tests. The intervals between measurement of initial and subsequent values in all 3 groups were compared by use of a Kruskal-Wallis 1-way ANOVA. A value of P < 0.05 was considered significant for all comparisons; statistical softwareb was used for all analyses.
Results
From 1995 through 2005, 550 camelids were admitted to the hospital, of which 31 (6%) were identified as hypertriglyceridemic via examination of all hematologic analyses performed on camelids during this period. Clinically normal camelids that did not require hematologic analysis and camelids with triglycerides concentrations < 60 mg/dL were considered nonhypertriglyceridemic. Results of multiple assessments of serum or plasma triglycerides concentrations were available for 20 camelids; the result of 1 assessment was available for each of 11 others, none of which had been treated with insulin.
Twenty camelids of various signalments were classified as HT-N, HT-I, or LIP-I (Table 1). Each classification included pregnant or lactating females and camelids of various ages. Compared with other camelids admitted to the hospital, hypertriglyceridemic camelids were not significantly different with respect to sex (P = 0.279) or age (P = 0.416). The interval between the 2 assessments of triglycerides concentrations used in the data analyses varied from 1 to 6 days and was not significantly different among the camelid classifications (median for HT-N camelids, 2 days [IQR, 1 to 2 days]; median for HT-I camelids, 1 day [IQR, 1 to 2 days]; and median for LIP-I camelids, 1 day [IQR, 1 to 2 days]).
Characteristics of 31 hypertriglyceridemic* alpacas and llamas that were treated with or without insulin at a referral hospita from 1995 through 2005, and for which results of 1 or multiple assessments of serum or plasma triglycerides concentrations were available. Camelids with multiple recorded assessments were classifed as HT-N, HT-I, or LIP-I camelids. The number of camelids that did not survive to discharge from the hospital is indicated in parentheses.
| Factor | No. of camelids with 1 assessment (n = 11) | Multiple assessments | ||
|---|---|---|---|---|
| No. of HT-N camelids (n = 6) | No. of HT-I camelids (n = 6) | No. of LIP-I camelids (n = 8) | ||
| Species | ||||
| Alpaca | 6 | 6 | 4 | 7 |
| Llama | 5 | 0 | 2 | 1 |
| Sex | ||||
| Female (not pregnant or lactating) | 5 | 3 | 3 | 4 |
| Female (pregnant or lactating) | 2 | 2 | 1 | 2 |
| Male | 4 | 1 | 2 | 2 |
| Disease | ||||
| Endoparasitism or diarrhea | 1 | 1 | 2 | 1 |
| Hepatic lipidosis | 2 (2) | — | — | 2 (1) |
| Spinal ataxia or other neurologic abnormalities | 2 (1) | 1 | 1 (1) | — |
| Neonatal sepsis | 1 | 1 | — | 1 (1) |
| Enteritis or hepatic necrosis | 1 (1) | 1 (1) | 1 | — |
| Colic | 1 | — | 1 | — |
| Mycoplasma haemolama infection | 2 (2) | — | — | — |
| Other diseases (noninfectious) | 1 | — | 1 (1) | 3 (2) |
| Other diseases (infectious) | — | 2 (1) | — | 1 |
| Age | ||||
| Neonate (1–7 d) | 2 | 1 | 0 | 2 |
| Juvenile (8 d–2 y) | 2 | 1 | 2 | 3 |
| Adult (3–9 y) | 7 | 4 | 3 | 3 |
| Geriatric (≥ 10 y) | 0 | 0 | 1 | 0 |
Hypertriglyceridemia was defined as serum or plasma triglycerides concentration > 60 mg/dL. 60 mg/dL. None of the camelids for which only 1 serum or plasma triglycerides concentration was available were treated with insulin. In HT-I and HT-N camelids, initial serum or plasma triglycerides concentration was > 60 to ≤ 500 mg/dL. In LIP-I camelids, initial serum or plasma triglycerides concentration was > 500 mg/dL. — = Not applicable.
Three days after insulin treatment was discontinued, serum or plasma triglycerides concentrations increased to levels detected before insulin treatment (200 to 400 mg/dL) in 2 of the HT-I camelids; both were treated with insulin for a second time. Two HT-N camelids that were not originally treated with insulin were treated when the results of serum or plasma biochemical analysis indicated that triglycerides concentrations exceeded 300 mg/dL and the camelids were failing to improve clinically (ie, continued inappetence and passive demeanor).
Various primary diseases were diagnosed in camelids with hypertriglyceridemia (Table 1); treatments varied in accordance with the diagnosis. Medications given to the 31 camelids included anti-inflammatory drugs (flunixin meglumine, aspirin, ketoprofen, and dimethyl sulfoxide), antimicrobials (potassium penicillin, gentamicin, amikacin, ceftiofur, ampicillin, oxytetracycline, and metronidazole), gastroprotectants (sucralfate), glucocorticoids (dexamethasone), diuretics (furosemide and mannitol), analgesics (butorphanol, ketamine, lidocaine, and fentanyl), prokinetic drugs (metoclopramide and lidocaine), and antiparasitic drugs (amprolium, sulfadimethoxine, and fenbendazole). Twenty-eight camelids received > 1 medication.
All camelids that received insulin were also treated with constant rate infusions of glucose (1% to 5%), most often as a component of a parenterally administered solution for partial nutritional support. The type of insulin administered varied throughout the study period on the basis of availability and clinician preference. For initial treatment of camelids with severe lipemia or those in an unresponsive state for which an immediate effect was desired, regular insulinc (0.2 U/kg [0.09 U/lb], IV) was administered (most commonly q 6 h; maximum frequency, q 1 h). Regular insulin was usually discontinued within 24 hours of response to treatment. Among all other hypertriglyceridemic camelids, ultralente insulind (0.4 U/kg [0.18 U/lb], SC, q 24 h) was the more common treatment.17 For all camelids treated with insulin, blood glucose concentrations were measured every 3 to 12 hours; the frequency of measurements varied with the severity of disease.
Eight of 20 camelids did not survive to discharge from the hospital; 2 were classified as HT-N camelids, 2 were classified as HT-I camelids, and 4 were classified as LIP-I camelids (Table 1). Triglycerides concentrations in the serum or plasma of all nonsurviving HT-I camelids were within the reference range (44 to 60 mg/dL) at the time of death or euthanasia, whereas those of nonsurviving HT-N camelids were never < 200 mg/dL and progressively increased to 300 to 400 mg/dL 2 to 6 days after initial evaluations. For nonsurviving LIP-I camelids, serum or plasma triglycerides concentrations at the time of death or euthanasia were less than half of initial concentrations. Among the 11 camelids for which serum or plasma triglycerides concentration was measured only once, 6 did not survive to discharge from the hospital; hepatic lipidosis was diagnosed in 2 of the nonsurvivors at necropsy. When results of serum or plasma biochemical analyses for survivors and nonsurvivors were compared, only SDH activity was significantly (P = 0.005) higher among camelids that did not survive. Almost all nonsurvivors that had been treated with insulin were euthanatized in response to untreatable primary diseases and not to treatment failure specifically.
Serum or plasma concentrations of NEFA, BHB, cholesterol, glucose, and albumin were significantly different in camelids with triglycerides concentrations > 500 mg/dL, compared with findings in hypertriglyceridemic camelids with triglycerides concentrations ≤ 500 mg/dL. For any analyte, initial and pretreatment values in HT-N and HT-I camelids did not differ significantly (Table 2). After HT-I camelids were treated with insulin, the triglycerides concentration was significantly (P = 0.031) lower than the pretreatment value and significantly (P = 0.015) lower than the subsequent concentration in HT-N camelids. Values of all other analytes were not significantly different after insulin treatment in HT-I camelids. In HT-N camelids, no significant differences between initial and subsequent values of any analyte were detected.
Median (IQR) values of initial and subsequent or pretreatment and posttreatment serum or plasma biochemical analytes in camelids with hypertriglyceridemia (triglycerides concentration > 60 to ≤ 500 mg/dL) that were (HT-I; n = 6) or were not (HT-N; 6) treated with insulin.
| Analyte | Reference range | HT-N | HT-I | ||
|---|---|---|---|---|---|
| Initial | Subsequent | Pretreatment | Posttreatment | ||
| Triglycerides (mg/dL) | 44.0–60.0 | 92.5 (67.0–135) | 156 (123–476)* | 175 (113–456) | 60.5 (30.0–107)* |
| NEFA (mEq/L) | < 0.24 | 0.65 (0.56–1.35) | 0.73 (0.45–1.04) | 0.89 (0.59–1.18) | 0.33 (0.32–0.60) |
| BHB (mg/dL) | 0.12–0.75 | 3.27 (0.28–9.30) | 3.69 (0.70–12.4) | 2.70 (1.79–4.30) | 0.94 (0.80–2.12) |
| Cholesterol (mg/dL) | 12.0–68.0 | 35.0 (29.0–72.0) | 46.0 (34.0–62.0) | 56.0 (47.0–93.0) | 31.0 (22.3–55.8) |
| Glucose (mg/dL) | 88.0–151 | 173 (154–340) | 212 (139–387) | 153 (116–247) | 182 (122–277) |
| BUN (mg/dL) | 13.0–28.0 | 19.0 (17.0–26.0) | 12.0 (10.0–14.0) | 48.0 (22.0–80.0) | 36.0 (17.5–53.0) |
| Creatinine (mg/dL) | 0.90–1.70 | 1.80 (1.30–2.10) | 1.10 (0.90–2.10) | 2.80 (1.20–5.20) | 2.20 (1.58–3.05) |
| Albumin (g/dL) | 3.50–4.90 | 2.90 (2.40–3.30) | 2.85 (2.20–3.40) | 2.95 (2.40–3.70) | 2.40 (1.88–2.98) |
| Total bilirubin (mg/dL) | < 0.40 | 0.15 (0.10–0.30) | 0.25 (0.10–0.50) | 0.20 0.20–0.20) | 0.20 (0.18–0.25) |
| CK (U/L) | 43.0–750 | 270 (54.0–976) | 560 (44.0–1380) | 150 (70.0–330) | 106 (90.3–210) |
| GGT (U/L) | 10.0–37.0 | 34.0 (30.0–36.0) | 43.0 (27.0–100) | 40.5 29.0–43.0) | 30.0 (12.5–75.8) |
| AST (U/L) | 127–298 | 384 (182–475) | 750 (146–886) | 320 (233–548) | 530 (318–1390) |
| SDH (U/L) | 1.50–15.7 | 9.80 (4.00–11.5) | 8.75 (6.20–9.20) | 6.05 (2.90–18.1) | 7.20 (2.00–15.6) |
In HT-N camelids, subsequent values were those determined second in chronologic sequence after initial values were obtained.
Value is signifcantly (P < 0.05) lower than the HT-I camelid pretreatment value and the HT-N camelid subsequent value.
Significant decreases in serum or plasma concentrations of triglycerides, NEFA, cholesterol, or albumin were detected in LIP-I camelids after treatment (Table 3). Serum or plasma activity of SDH also decreased, albeit not significantly, in these camelids after treatment.
Mean ± SD values of serum or plasma biochemica analytes in 8 lipemic (triglycerides concentration > 500 mg/dL) camelids before and after treatment with insulin.
| Analyte | Pretreatment value | Posttreatment value | P value |
|---|---|---|---|
| Triglycerides (mg/dL) | 2,350 ± 2,080 | 1,050 ± 1,140 | 0.008 |
| NEFA (mEq/L) | 1.80 ± 1.10 | 0.90 ± 0.60 | 0.025 |
| BHB (mg/dL) | 8.80 ± 9.00 | 7.60 ± 7.10 | 0.547 |
| Cholesterol (mg/dL) | 226 ± 129 | 171 ± 98.8 | 0.035 |
| Glucose (mg/dL) | 451 ± 446 | 362 ± 260 | 0.333 |
| BUN (mg/dL) | 53.1 ± 39.2 | 51.0 ± 55.8 | 0.822 |
| Creatinine (mg/dL) | 2.60 ± 1.30 | 2.40 ± 1.60 | 0.612 |
| Albumin (g/dL) | 3.40 ± 0.40 | 2.80 ± 0.40 | 0.001 |
| Total bilirubin (mg/dL) | 0.40 ± 0.20 | 0.30 ± 0.10 | 0.239 |
| CK (U/L) | 245 ± 219 | 631 ± 1,240 | 0.374 |
| GGT (U/L) | 146 ± 283 | 114 ± 214 | 0.244 |
| AST (U/L) | 628 ± 817 | 579 ± 578 | 0.631 |
| SDH (U/L) | 22.4 ± 24.5 | 8.20 ± 7.30 | 0.058 |
A value of P < 0.05 was considered signifcant.
Serum or plasma triglycerides concentrations in 11 of 14 HT-I and LIP-I camelids decreased by approximately 50% or were within the reference range within 24 hours of treatment with insulin. Values for all 14 camelids decreased by approximately 50% within 6 days of hospitalization and were within the reference range at the time of discharge or euthanasia.
Discussion
High concentrations of triglycerides in serum or plasma were detected among camelids that were evaluated for disease at the referral hospital in our study; 6% of all admitted camelids were hypertriglyceridemic. Hypertriglyceridemia did not appear to be associated with sex, age, or reproductive status. The condition was detected in camelids that had a broad range of primary diseases and not just those with liver abnormalities. Hepatic lipidosis has also been reported1,2,10 in camelids of various signalments, suggesting that disorders of fat metabolism in camelids cannot be solely attributed to negative energy balance. This inference is supported by the lack of an increase in serum or plasma triglycerides concentration in camelids for which feed intake was restricted to 0.25% of body wt/d.10 Other factors that may contribute to increased concentrations of triglycerides in the serum or plasma of camelids include shunting of intrahepatic fat into lipoprotein production or inhibition of uptake by peripheral tissues. Catecholamines may stimulate fat mobilization in camelids11; therefore, hypertriglyceridemia may develop in any camelid with increased catecholamine release.
In the study reported here, high concentrations of triglycerides in serum or plasma appeared to be associated with more severe systemic disease. Camelids with mild to moderate hypertriglyceridemia (61 to 500 mg/dL) had serum or plasma concentrations of other lipids that were comparable to the high concentrations reported in camelids fed a restricted amount of feed,9,10,16 but had few other severe serum or plasma biochemical abnormalities. In contrast, many camelids with severe hypertriglyceridemia in our study were ketotic and had a high serum or plasma NEFA concentration, which is compatible with the biochemical abnormalities reported in camelids with hepatic lipidosis.9,10,16 Several HT-I and LIP-I camelids were azotemic; the degree of azotemia was less severe among HT-N camelids. Interestingly, azotemia can inhibit the clearance of triglycerides from blood in humans.18 The effect of azotemia on the clearance of triglycerides from blood in camelids is unclear.
Camelids that were classified as LIP-I in our study had higher pretreatment serum or plasma concentrations of NEFA and BHB and higher activities of AST and SDH, compared with HT-I and HT-N camelids. Although high values of these analytes are reportedly associated with hepatic lipidosis in camelids,1 hepatic lipidosis was diagnosed at necropsy or after histologic evaluation of a biopsy specimen obtained from the liver in only 4 camelids. Concentrations of NEFA in the serum or plasma of HT-N and HT-I camelids were lower than those in LIP-I camelids. That finding is more consistent with values reported for camelids from which feed has been withheld.9,10,16 A causal relationship between hypertriglyceridemia and hepatic lipidosis in camelids has not been established; however, on the basis of the findings of our study, we speculated that camelids with more severe hypertriglyceridemia may be at greater risk for developing hepatic lipidosis.
Nonsurvival was not associated with high concentrations of triglycerides or other lipids in serum or plasma at the time of admission, which suggested that hyperlipemia is a manageable condition. Often the cause of death was attributable to another disease state that was poorly responsive to treatment. Of all the serum or plasma analytes assessed in camelids that did or did not survive, only SDH activity was significantly higher among camelids that did not survive. The high activity of SDH in nonsurvivors may have been an indicator of severe pathologic changes in the liver, leading to or as a result of an inability of the body to respond appropriately to fat mobilization because of a primary disease state.
The results of the study reported here support the hypothesis that insulin administration aids in the clearance of triglycerides from and inhibition of the release of NEFA and BHB into the bloodstream. Healthy camelids are insulin deficient and insulin resistant, compared with some other species of domestic animals13; therefore, they may be less able physiologically to counteract factors that promote the mobilization of fat or impair the clearance of peripheral triglycerides. Some of the camelids in our study may have had a limited capacity to produce insulin or a high resistance to insulin, as suggested by the high prevalence of hyperglycemia in all groups (data not shown). Almost all nonsurvivors that had been treated with insulin were euthanatized in response to poorly responsive primary diseases and not to treatment failure specifically. Two LIP-I camelids and 2 camelids for which only 1 triglycerides concentration was recorded (and for which no treatment with insulin was administered) had hepatic lipidosis. One of the LIP-I camelids with hepatic lipidosis survived. In contrast, both nontreated camelids with hepatic lipidosis did not survive. Exogenous insulin may have prevented or reversed hepatic lipidosis in treated camelids11,14; however, that possibility was not investigated here.
Because all camelids that received insulin also received a constant rate infusion of dextrose, the effects of insulin cannot be separated from those of dextrose. Repeated administration of dextrose can reduce the secretion of insulin13 and may promote hyperglycemia and fat mobilization. This hypothesis has not been evaluated in camelids with hypertriglyceridemia.
In the study reported here, hypertriglyceridemia was detected in alpacas and llamas with a wide range of disease states. Whether the high concentrations of triglycerides in serum or plasma were a result of or contributed to those states is unknown. The relationships between hypertriglyceridemia and hepatic lipidosis, lactation, and pregnancy in camelids were less clear than those presumed in other species.7,8 Given the diversity of signalments and disease states among hypertriglyceridemic camelids in our study, we recommend including measurement of serum or plasma triglycerides concentrations in the routine diagnostic evaluation of sick alpacas and llamas.
ABBREVIATIONS
| NEFA | Nonesterified fatty acids |
| BHB | β-hydroxybutyrate |
| AST | Aspartate aminotransferase |
| GGT | γ–glutamyltransferase |
| SDH | Sorbitol dehydrogenase |
| CK | Creatine kinase |
| HT-N | Hypertriglyceridemic and not insulin-treated |
| HT-I | Hypertriglyceridemic and insulin-treated |
| LIP-I | Lipemic and insulin-treated |
| IQR | Interquartile range |
Hitachi 717 biochemical analyzer, Boehringer Mannheim Corp, Indianapolis, Ind.
SigmaStat, version 2.0, SPSS Inc, Chicago, Ill.
Humulin-R, Eli Lilly Co, Indianapolis, Ind.
Humulin-U, Eli Lilly Co, Indianapolis, Ind.
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