HYPERLIPIDEMIA AND XANTHOMATOSIS IN YELLOW-FOOTED ROCK WALLABIES (PETROGALE XANTHOPUS) UNDER MANAGED CARE.

Xanthomas are localized lipid deposits in organs with associated granulomatous inflammation. Xanthomatosis is a rare condition in both human and veterinary medicine and is often linked to inherited or acquired dyslipidemias. Three female yellow-footed rock wallabies (Petrogale xanthopus) at a single institution were diagnosed via biopsy with cutaneous xanthomas secondary to hypertriglyceridemia and hypercholesterolemia, and an additional two female yellow-footed rock wallabies were diagnosed with xanthomas at a second institution. All cases presented with cutaneous masses at the haired skin and paw pad junctions of the extremities, and/or mucocutaneous junctions of the face or urogenital tract. The clinically affected individuals were overconditioned or obese, had lipemic serum, and had elevations in blood cholesterol and triglyceride levels. When full lipid panels were performed, inverse high- and low-density lipoprotein fractions were observed. Six other individuals at the first institution had identical husbandry but were of more appropriate body condition, were normolipidemic, and had no xanthomas. One of the affected animals was also concurrently diagnosed with hepatic lipidosis via liver biopsy. Pedigree review and evaluation for underlying endocrine diseases such as hypothyroidism were performed. Because all affected animals were found to be related, a genetic predisposition is possible but requires further investigation. Consideration for the predisposition of some individuals for obesity, hyperlipidemia, and subsequent xanthoma formation should be factored in the husbandry and medical management of this species.

Emergency Management for Donkeys and Mules.

This article provides an overview of initial assessment and management of common emergency presentations in donkeys and mules. The principles are similar to those in horses (and ponies), but clinicians must be aware of differences in recognition of signs of pain/disease, approach to handling, pharmacology of some drugs, and subtle differences in the physiology and local anatomy in donkeys and mules. The epidemiology of common disease presentations will vary between pet/companion or working/farmed donkeys and mules. Regular dental checks, deworming, vaccination, and monitoring of behavior and quality of life are important aspects of preventive care.

Starch sources influence lipidaemia of diabetic dogs.

BACKGROUND: Hyperlipidaemia is considered a cause of other diseases that are clinically important and potentially life threatening. Combination of pea and barley as exclusive starch sources is known to interfere with glycemic control in diabetic dogs, but their effect on lipid profile of hiperlipidaemic dogs is yet to be evaluated. Twelve adult diabetic dogs were fed three dry extruded diets with different starch sources and different fat levels: peas and barley (PB), maize (Mi), and peas, barley and rice (Ba) with 15.7, 15.6 and 9.0% of their dry matter as fat, respectively. Plasmatic cholesterol and triglycerides concentration curves over 10 h were obtained after 60 days on each diet and with the same NPH insulin dose. ANOVA test or Friedman test were used to compare the dietary effects on triglycerides and cholesterol variables among the diets. RESULTS: Dogs presented lower mean (p = 0.05), fasting (p = 0.03), and time 8-h postprandial (p = 0.05) triglyceridemia after PB diet period than Ba diet period and time 4-h postprandial (p = 0.02) lower after PB than Mi diet. Cholesterolemia mean, minimum, maximum, area under the cholesterol curve and times points: 2, 4, 6, 8 and 10-h postprandial, had lower values after PB ingestion in comparison to Mi, without difference to Ba diet. CONCLUSION: Inclusion of pea and barley, as exclusive starch sources, in therapeutic diets for diabetic dogs can minimize plasmatic triglycerides and cholesterol concentration at fasting and at different postprandial time, compared to the maize diet or diet with lesser fat content.

Evaluating acute inflammation's effects on hepatic triglyceride content in experimentally induced hyperlipidemic dairy cows in late lactation.

Inflammation appears to be a predisposing factor and key component of hepatic steatosis in a variety of species. Objectives were to evaluate effects of inflammation [induced via intravenous lipopolysaccharide (LPS) infusion] on metabolism and liver lipid content in experimentally induced hyperlipidemic lactating cows. Cows (765 ± 32 kg of body weight; 273 ± 35 d in milk) were enrolled in 2 experimental periods (P); during P1 (5 d), baseline data were obtained. At the start of P2 (2 d), cows were assigned to 1 of 2 treatments: (1) intralipid plus control (IL-CON; 3 mL of saline; n = 5) or (2) intralipid plus LPS (IL-LPS; 0.375 µg of LPS/kg of body weight; n = 5). Directly following intravenous bolus (saline or LPS) administration, intralipid (20% fat emulsion) was intravenously infused continuously (200 mL/h) for 16 h to induce hyperlipidemia during which feed was removed. Blood samples were collected at -0.5, 0, 4, 8, 12, 16, 24, and 48 h relative to bolus administration, and liver biopsies were obtained on d 1 of P1 and at 16 and 48 h after the bolus. By experimental design (feed was removed during the first 16 h of d 1), dry matter intake decreased in both treatments on d 1 of P2, but the magnitude of reduction was greater in LPS cows. Dry matter intake of IL-LPS remained decreased on d 2 of P2, whereas IL-CON cows returned to baseline. Milk yield decreased in both treatments during P2, but the extent and duration was longer in LPS-infused cows. Administering LPS increased circulating LPS-binding protein (2-fold) at 8 h after bolus, after which it markedly decreased (84%) below baseline for the remainder of P2. Serum amyloid A concentrations progressively increased throughout P2 in IL-LPS cows (3-fold, relative to controls). Lipid infusion gradually increased nonesterified fatty acids and triglycerides in both treatments relative to baseline (3- and 2.5-fold, respectively). Interestingly, LPS infusion blunted the peak in nonesterified fatty acids, such that concentrations peaked (43%) higher in IL-CON compared with IL-LPS cows and heightened the increase in serum triglycerides (1.5-fold greater relative to controls). Liver fat content remained similar in IL-LPS relative to P1 at 16 h; however, hyperlipidemia alone (IL-CON) increased liver fat (36% relative to P1). No treatment differences in liver fat were observed at 48 h. In IL-LPS cows, circulating insulin increased markedly at 4 h after bolus (2-fold relative to IL-CON), and then gradually decreased during the 16 h of lipid infusion. Inducing inflammation with simultaneous hyperlipidemia altered the characteristic patterns of insulin and LPS-binding protein but did not cause fatty liver.

Primary hyperlipidemia with associated ischemic strokes in a West Highland white terrier dog.

A 3-year-old spayed female, West Highland white terrier dog was evaluated because of a 4-month history of recurrent brain clinical signs. Magnetic resonance imaging (MRI) revealed multifocal brain lesions consistent with ischemic injuries. Blood analysis was unremarkable aside from severe hypertriglyceridemia and hypercholesterolemia with no underlying cause, suggesting primary hyperlipidemia. The patient was treated for hyperlipidemia and started on a low-fat diet and omega-3 supplementation. Clinical signs resolved over the following 12 months along with improvement in lipidemia. This represents the first reported case of MRI findings suggestive of multiple cerebrovascular injuries associated with primary hyperlipidemia in a dog, and the first primary hyperlipidemia reported in a West Highland white terrier dog.

Hyperlipidémie primaire associée à des accidents vasculaires cérébraux ischémiques chez un chien terrier West Highland white. Une femelle stérilisée West Highland white âgée de 3 ans fut évaluée à cause d'une histoire de signes cliniques cérébraux récurrents d'une durée de 4 mois. Une imagerie par résonnance magnétique (RMI) révéla des lésions cérébrales multifocales compatibles avec des blessures ischémiques. Une analyse sanguine s'avéra peu concluante sauf pour une hypertriglycéridémie et une hypercholestérolémie sévère sans cause sous-jacente, suggérant une hyperlipidémie primaire. Le patient fut traité pour l'hyperlipidémie et débuta une diète faible en gras et une supplémentation en oméga-3. Les signes cliniques se sont résolus dans les 12 mois suivants avec une amélioration de la lipidémie. Ceci représente le premier cas rapporté de trouvailles par MRI suggestives de lésions cérébro-vasculaires multiples associées avec une hyperlipidémie primaire chez un chien, et le premier cas d'hyperlipidémie primaire rapporté chez un terrier West Highland white.(Traduit par Dr Serge Messier).

Lipemic uveitis and its etiologies in dogs: 75 cases.

OBJECTIVE: To describe clinical features of dogs with lipemic uveitis (LU). ANIMALS STUDIED: Seventy-five dogs (114 eyes) with LU. PROCEDURES: Medical records of dogs examined by the Cornell University ophthalmology service with a clinical diagnosis of LU between 2008 and 2017 were analyzed. Signalment and clinical case aspects, including concurrent ocular disease, systemic disease, and previous ophthalmic surgery, were recorded. RESULTS: Lipemic uveitis was diagnosed in 114 eyes of 75 dogs. The mean (±standard deviation) age of dogs was 9.0 years (±2.7 years). Miniature Schnauzers and Yorkshire Terriers were statistically overrepresented compared to the ophthalmology canine referral population. Lipemic flare varied in severity with loss of menace response due to markedly opaque flare seen in 15/114 eyes (13%). Two dogs developed LU after dietary indiscretion. Forty-nine eyes (43%) had concurrent ocular disease, most commonly keratoconjunctivitis sicca, ulcerative keratitis, and cataracts. Pseudophakia was present in 75/114 eyes (66%) and LU developed within 30 days of an intraocular surgical procedure in 63/114 eyes (55%). Hypertriglyceridemia was noted in 52 dogs of the 55 dogs tested (95%). Systemic disease affected 54/75 dogs (72%), of which diabetes mellitus, hyperadrenocorticism, and hypothyroidism were overrepresented compared to the referral population. Primary hyperlipidemia was identified in 12 dogs. Lipemic uveitis resolved at first reevaluation in 92/110 eyes (84%) and recurred in 6/114 eyes (5%) after complete resolution. CONCLUSIONS: Development of lipemic uveitis in dogs appears to require the combination of hyperlipidemia and uveitis. Systemic disease is commonly associated with LU in dogs.

Atypical Antipsychotic Drug Olanzapine Deregulates Hepatic Lipid Metabolism and Aortic Inflammation and Aggravates Atherosclerosis.

BACKGROUND/AIMS: Olanzapine, an atypical antipsychotic drug, has therapeutic effects for schizophrenia. However, clinical reports indicate that patients taking atypical antipsychotic drugs are at high risk of metabolic syndrome with unclear mechanisms. We investigated the effect of olanzapine on atherosclerosis and the mechanisms in apolipoprotein E-null (apoE-/-) mice. METHODS: ApoE-/- mice were used as in vivo models. Western blot analysis was used to evaluate protein expression. Conventional assay kits were applied to assess the levels of cholesterol, triglycerides, free cholesterol, cholesteryl ester, fatty acids, glycerol, and cytokines. RESULTS: Daily treatment with olanzapine (3 mg/kg body weight) for four weeks increased mean arterial blood pressure and the whitening of brown adipose tissue in mice. In addition, olanzapine impaired aortic cholesterol homeostasis and exacerbated hyperlipidemia and aortic inflammation, which accelerated atherosclerosis in mice. Moreover, lipid accumulation in liver, particularly total cholesterol, free cholesterol, fatty acids, and glycerol, was increased with olanzapine treatment in apoE-/- mice by upregulating the expression of de novo lipid synthesis-related proteins and downregulating that of cholesterol clearance- or very low-density lipoprotein secretion-related proteins. CONCLUSION: Olanzapine may exacerbate atherosclerosis by deregulating hepatic lipid metabolism and worsening hyperlipidemia and aortic inflammation.

Studies on the lipid-regulating mechanism of alisol-based compounds on lipoprotein lipase.

Studies on the lipid-regulating effects of alisol compounds are reported that include alisol B, alisol A 24-acetate (24A), alisol A and an alisol B - 24A - alisol A mixture (content ratio = 1:1:1). The effects on the activity of lipoprotein lipase (LPL), a key lipid-modulating enzyme, were studied to investigate the molecular mechanism of lipid-regulating activity of alisols. The effects of alisols on regulating blood lipids and the activities of LPL were determined using a reagent kit method. The structure of LPL was obtained by homology modeling and the interactive mechanism of alisol monomers and the mixture with LPL was investigated by molecular simulation. The alisol monomer and mixture were shown to regulate blood lipids, suggesting that alisols may decrease the level of triglyceride (TG) by improving the activity of LPL. The order of intensity was: mixture > alisol A > alisol B > 24A, indicating that alisols of alismatis rhizoma feature a synergistic effect on LPL. The N- and C-terminus of LPL both represented the catalytic active domains of this lipid-regulating effect. Cys306, Gln129 and Ser166 were the key amino acid residues resulting in the lipid-regulating effect of the alisol monomer while Ser166 and Arg18 were found to be responsible for the lipid-regulating effect of the mixture. The C-terminus of LPL was indirectly involved in the enzymatic process. A folded side chain of alisols or the parent ring was found to bind somewhat weaker to LPL than an open side chain or parent ring. The hydroxyl groups on the C14-, C22-, C28-, C30- and C31-terminus in the side chain, the ring ether structure in C23-position, and the acetyl group in C29-position represented the key sites for the lipid-regulating action of alisols. Meanwhile, the C30-site hydroxyl group played an important role in the synergistic effect of the alisol mixture.

Role of miR29c in goose fatty liver is mediated by its target genes that are involved in energy homeostasis and cell growth.

BACKGROUND: A short period of overfeeding can lead to severe hepatic steatosis in the goose, which is physiological, suggesting that geese, as a descendent of a migrating ancestor, may have evolutionally developed a unique mechanism that operates in contrast to the mechanism underlying pathological fatty liver in humans or other mammals. In this study, we report that suppression of miR29c and upregulation of its target genes in goose fatty liver vs. normal liver could be part of a unique mechanism that contributes to the regulation of energy homeostasis and cell growth. RESULTS: Our data showed that miR29c expression was comprehensively inhibited in energy homeostasis-related tissues (the liver, fat and muscle) of overfed vs. normally fed geese, which is different from miR29c induction that occurs in tissues of the diabetic rat. To address the function of miR29c, three predicted target genes (i.e., Insig1, Sgk1 and Col3a1) that participate in energy homeostasis or cell growth were validated by a dual-fluorescence reporter system and other in vitro assays. Importantly, expression of Insig1, Sgk1 and Col3a1 was upregulated in goose fatty liver. In line with these observations, treatment of goose hepatocytes with high glucose or palmitate suppressed the expression of miR29c but induced the expression of the target genes, suggesting that hyperglycemia and hyperlipidemia, at least partially, contribute to the suppression of miR29c and induction of the target genes in goose fatty liver. In addition, pharmacological assays indicated that RFX1 was a transcription factor involved in the expression of miR29c. CONCLUSIONS: This study suggests that miR29c may play a role in the regulation of energy homeostasis and tissue growth via its target genes, contributing to the tolerance of the goose to severe hepatic steatosis.

Impact of hyperlipidaemia on intermediary metabolism, faecal microbial metabolites and urinary characteristics of lipoprotein lipase deficient vs. normal cats.

Findings in humans and rats indicate that hyperlipidaemia may be associated with enhanced endogenous oxalate (Ox) synthesis, which may be relevant for calcium oxalate (CaOx) urolith formation. Moreover, changes in lipid metabolism are proposed to negatively affect gut microbiota. This study aimed to investigate those potential interactions in hyperlipidaemic cats. Therefore, 10 normal control cats and seven lipoprotein lipase (LPL)-deficient cats were fed a low-fat diet for seven weeks. During the last week of the study, cats were housed in metabolic cages to collect urine and faeces. Blood was taken on the last day of the study. The LPL-deficient cats had significantly higher serum triglyceride concentrations than normal cats, while lactate dehydrogenase (LDH) activity was not different. Urinary relative supersaturation with CaOx, urinary Ox, calcium, and citrate excretions, and urine pH did not differ between groups. Lower faecal acetic, propionic and total short-chain fatty acid concentrations were observed in the LPL-deficient cats. In conclusion, hyperlipidaemia does not appear to be a specific risk factor for CaOx urolith formation in cats. In contrast to results in rats, hyperlipidaemia was not accompanied by elevated serum LDH activity. As LDH can synthesise Ox from glycolate or other precursors, this might be one possible explanation for the similar urinary parameters in the LPL-deficient and normal cats. Non-diet-induced hyperlipidaemia was not associated with marked changes in faecal microbial metabolites, suggesting no differences in the composition of the intestinal microbiota.

Clustering analysis of lipoprotein profiles to identify subtypes of hypertriglyceridemia in Miniature Schnauzers.

BACKGROUND: Hypertriglyceridemia (HTG) is prevalent in Miniature Schnauzers, predisposing them to life-threatening diseases. Varied responses to management strategies suggest the possibility of multiple subtypes. HYPOTHESIS/OBJECTIVE: To identify and characterize HTG subtypes in Miniature Schnauzers through cluster analysis of lipoprotein profiles. We hypothesize that multiple phenotypes of primary HTG exist in this breed. ANIMALS: Twenty Miniature Schnauzers with normal serum triglyceride concentration (NTG), 25 with primary HTG, and 5 with secondary HTG. METHODS: Cross-sectional study using archived samples. Lipoprotein profiles, generated using continuous lipoprotein density profiling, were clustered with hierarchical cluster analysis. Clinical data (age, sex, body condition score, and dietary fat content) was compared between clusters. RESULTS: Six clusters were identified. Dogs with primary HTG were dispersed among 4 clusters. One cluster showed the highest intensities for triglyceride-rich lipoprotein (TRL) and low-density lipoprotein (LDL) fractions and also included 4 dogs with secondary HTG. Two clusters had moderately high TRL fraction intensities and low-to-intermediate LDL intensities. The fourth cluster had high LDL but variable TRL fraction intensities with equal numbers of NTG and mild HTG dogs. The final 2 clusters comprised only NTG dogs with low TRL intensities and low-to-intermediate LDL intensities. The clusters did not appear to be driven by differences in the clinical data. CONCLUSIONS AND CLINICAL IMPORTANCE: The results of this study support a spectrum of lipoprotein phenotypes within Miniature Schnauzers that cannot be predicted by triglyceride concentration alone. Lipoprotein profiling might be useful to determine if subtypes have different origins, clinical consequences, and response to treatment.

Ponies, miniatures, and younger equids are at higher risk of fecalith obstruction compared to a general colic population.

OBJECTIVE: To determine breed, age, and sex predispositions for fecalith obstruction and to evaluate short-term survival and prognostic factors following surgical treatment of fecalith intestinal obstruction in equids. ANIMALS: 151 equids. METHODS: Medical records of equids undergoing surgery for fecalith obstruction from 2000 to 2020 were reviewed. Signalment, history, presenting clinicopathological data, surgical findings, complications, and short-term survival were recorded and compared between survivors and nonsurvivors. Signalment of the fecalith population was compared to a contemporaneous colic population. Clinical factors were assessed for association with outcome. RESULTS: 64 females, 53 castrated males, and 31 intact males were included. Three equids presented twice. Miniature horses, ponies, and miniature donkeys/mules represented 48% (71/148) of fecalith population and full-sized breeds represented 52% (77/148). Miniature horses and ponies were overrepresented and equids ≤ 1 year of age were overrepresented in the fecalith population compared to the colic population. One hundred thirty-nine equids (92%) survived to discharge, 6% (9/148) were euthanized intraoperatively, and 2% (3/148) were euthanized during hospitalization. Nonsurvivors showed more severe colic signs on admission, tachycardia on admission, and hyperlipemia. Equids with postoperative colic (P = .01) and complications (P = .002) were less likely to survive. CLINICAL RELEVANCE: Miniature horses and ponies were overrepresented compared to the colic population; however, full-sized breeds were also affected. Surgical treatment had an excellent short-term prognosis. Severe colic signs, tachycardia, hyperlipemia, postoperative colic, and surgical complications negatively affected short-term survival.

Novel lipoprotein density profiling in healthy dogs of various breeds, healthy Miniature Schnauzers, and Miniature Schnauzers with hyperlipidemia.

BACKGROUND: Despite the importance of abnormalities in lipoprotein metabolism in clinical canine medicine, the fact that most previously used methods for lipoprotein profiling are rather laborious and time-consuming has been a major obstacle to the wide clinical application and use of lipoprotein profiling in this species. The aim of the present study was to assess the feasibility of a continuous lipoprotein density profile (CLPDP) generated within a bismuth sodium ethylenediaminetetraacetic acid (NaBiEDTA) density gradient to characterize and compare the lipoprotein profiles of healthy dogs of various breeds, healthy Miniature Schnauzers, and Miniature Schnauzers with primary hypertriacylglycerolemia. A total of 35 healthy dogs of various breeds with serum triacylglycerol (TAG) and cholesterol concentrations within their respective reference intervals were selected for use as a reference population. Thirty-one Miniature Schnauzers with serum TAG and cholesterol concentrations within their respective reference intervals and 31 Miniature Schnauzers with hypertriacylglyceridemia were also included in the study. RESULTS: The results suggest that CLPDP using NaBiEDTA provides unique diagnostic information in addition to measurements of serum TAG and cholesterol concentrations and that it is a useful screening method for dogs with suspected lipoprotein metabolism disorders. Using the detailed and continuous density distribution information provided by the CLPDP, important differences in lipoprotein profiles can be detected even among dogs that have serum TAG and cholesterol concentrations within the reference interval. Miniature Schnauzers with serum TAG and cholesterol concentrations within the reference interval had significantly different lipoprotein profiles than dogs of various other breeds. In addition, it was further established that specific lipoprotein fractions are associated with hypertriacylglyceridemia in Miniature Schnauzers. CONCLUSIONS: The results of the present study suggest that density gradient ultracentrifugation using NaBiEDTA is a useful screening method for the study of lipoprotein profiles in dogs. Therefore, this method could potentially be used for diagnostic purposes for the separation of dogs suspected of having lipoprotein abnormalities from healthy dogs.

Hyperlipidaemia in trypanosomiasis of naturally infected horses: possible cachexia-anorexia syndrome?

Trypanosomiasis caused by Trypanosoma evansi commonly produces wasting disease with signs of emaciation and cachexia mainly at the end stage. The present study was conducted to explore the possible hyperlipaemia or hyperlipidaemia and its association with cachexia-anorexia in equine trypanosomiasis. Out of the fifteen confirmed animals, none of the plasma sample was opaque. There was a significant increase in plasma triglyceride, total cholesterol and blood urea nitrogen and a highly significant increase in low-density lipoprotein (LDL) levels. A mild increase in high-density lipoprotein (HDL) and very low-density lipoprotein levels were observed, while the relative percentage of HDL and LDL was altered with high significance. A moderate increase in triglyceride and highly significant increase in LDL might be the reasons for retention of appetite and lipolysis. Possible protein breakdown and presence of lipolysis might be the reasons for cachexia in equine trypanosomiasis.

Comparison of a commercially available veterinary digital refractometer to analogue refractometer and laboratory chemistry analyzer in the evaluation of canine serum total protein.

OBJECTIVE: To assess the agreement between measurements of total protein (TP) concentrations in canine serum samples between a commercially available veterinary digital refractometer (DR), an analog handheld refractometer (AR), and a laboratory-based chemistry analyzer (LAB). An additional objective was to assess the effects of various potential interferents (ie, hyperbilirubinemia, increased BUN, hyperglycemia, hemolysis, and lipemia) on DR measurements. SAMPLE: 108 canine serum samples. PROCEDURES: Serum samples were measured in duplicate on the DR, which reported TP concentration, assessed via optical reflectance and critical angle measurement. These serum samples were also assessed on the AR and LAB for comparison. Serum samples with grossly visible lipemia, hemolysis, and icterus were noted. Medical records were retrospectively assessed to determine concentrations of BUN, glucose, and bilirubin. RESULTS: Method comparisons among the various data generated by the analyzers were completed using linear regression, Bland Altman, and calculation of intraclass coefficients. Mean bias between DRTP and LABTP in samples without potential interferents was 0.54 g/dL with 95% limits of agreement of -0.17 to 1.27 g/dL. One-third of DRTP samples without potential interferents had > 10% difference from their LABTP comparison. Interferents, particularly marked hyperglycemia, can result in inaccurate measurements on the DR. CLINICAL RELEVANCE: There was a statistically significant difference between DRTP and LABTP measurements. TP measurements in samples with any potential interferent, particularly hyperglycemia, should be assessed cautiously on DR and AR.

Does postprandial lipemia interfere with blood gas analysis and assessment of acid-base status in dogs?

To evaluate the interference of postprandial lipemia on blood gas parameters and to assess the acid-base status by the quantitative approach of the strong ion model blood samples of 15 healthy dogs were collected during fasting (0 h) and at one (1 h), three (3 h) and five (5 h) hours after the induction of lipemia with a hypercaloric diet. Total cholesterol (TC) and triglyceride (TG) levels were used to assess lipemia and these were correlated with the parameters evaluated accordingly. Anion gap decreased at 5 h without correlation with TC and TG, whereas other parameters measured by the blood gasometer did not change. In the evaluation of the acid base state, the apparent strong ion difference (SIDa) and the strong ion gap (SIG) showed a decrease at 5 h without correlation with lipemia. Lipid levels correlated with the effective strong ion difference (SIDe), the concentration of total non-volatile weak acids (Atot), albumin, phosphate, and magnesium. The SIDe increased at 1 h and at 3 h; the Atot at 1 h, 3 h, and 5 h; albumin increased at 1 h and 3 h; phosphate increased at 1 h, 3 h and 5 h; and magnesium decreased at 5 h. Though postprandial lipemia does not interfere with blood gas analysis, it can cause errors in the variables used to assess the acid-base status, which are dependent on biochemical analytes. Therefore, caution is required when interpreting electrolyte disturbances that result from the postprandial state.

Evaluation of gallbladder motility assessed by ultrasonography in dogs with hyperlipidemia.

BACKGROUND: The pathogenesis of gallbladder (GB) mucoceles in dogs is unknown. It has been proposed that hyperlipidemia could impair GB motility and contribute to GB mucocele formation. HYPOTHESIS/OBJECTIVES: The objective of this study was to compare GB motility in dogs with hyperlipidemia to control dogs using ultrasonography. We hypothesized that hyperlipidemic dogs will have decreased GB motility compared with controls. ANIMALS: Twenty-six hyperlipidemic and 28 healthy, age-matched control dogs were prospectively enrolled. METHODS: Cholesterol and triglyceride concentrations were measured in all dogs. Hyperlipidemia was defined as hypercholesterolemia (>332 mg/dL) and/or hypertriglyceridemia (>143 mg/dL) using a biochemical analyzer. Ultrasound was performed before feeding, and 60 and 120 minutes after ingestion of a high fat diet. Gallbladder volumes (GBV) and ejection fractions (EF) were calculated. RESULTS: Hyperlipidemic dogs had significantly larger GBVs (ml/kg) before feeding and 60 minutes after feeding of 1.2 (0.4-7.5; P = .008) and 0.6 (0.1-7.2; P = .04) compared with controls 0.6 (0.2-2.6) and 0.4 (0.1-1.9), respectively. Severely hyperlipidemic dogs had significantly larger GBV at baseline, 60 minutes, and 120 minutes of 1.7 (0.6-7.5; P = .03), 1.3 (0.4-7.2; P = .02), and 1.3 (0.2-8.2; P = .04), respectively compared with mildly hyperlipidemic dogs. EFs at 60 and 120 minutes between controls, hyperlipidemic, and severely hyperlipidemic were all 0.3 at 60 minutes and 0.5, 0.3, and 0.3 at 120 minutes, respectively which were not statistically different. CONCLUSIONS AND CLINICAL IMPORTANCE: Hyperlipidemia leads to GB distention in dogs which could lead to retention of bile and gallbladder disease.

Successful multimodal treatment of extreme hypertriglyceridemia in a juvenile diabetic dog.

OBJECTIVE: To describe the therapeutic protocol used to normalize severe hypertriglyceridemia in a dog. CASE SUMMARY: A 7-month-old, 1.2-kg female Pomeranian presented with acute polyuria, polydipsia, and ocular discoloration. Diagnoses included diabetic ketosis, severe hypertriglyceridemia (>225 mmol/L [>20,000 mg/dl]), lipemia retinalis, and bilateral uveitis. The triglyceride concentration was near normal within 2 days of initiating treatment with fenofibrate, regular insulin constant rate infusion (CRI), manual therapeutic plasma exchange (TPE), and a low-fat diet. All clinical signs resolved. The dog has had no relapse of hypertriglyceridemia at the time of writing the manuscript, 6 months later, with continued treatment of diabetes mellitus. NEW OR UNIQUE INFORMATION PROVIDED: This is the first case report documenting the combination of fenofibrate, insulin CRI, and manual TPE for treatment of severe hyperlipidemia in a dog. Detailed protocols for manual TPE and a novel insulin CRI are provided. A discussion of multiple spurious biochemical and hematologic errors associated with the severe hypertriglyceridemia is also provided.

Hypertriglyceridemia in equines with refractory hyperinsulinemia treated with SGLT2 inhibitors.

Background: Sodium-Glucose CoTransporter-2 (SGLT2) inhibitors, the -flozin group of drugs, which block glucose reuptake in the renal proximal tubule, are being increasingly used off-label to treat horses with refractory hyperinsulinemia. After 2 years of use by animals in our group, a horse on canagliflozin was incidentally noted to be hyperlipemic. Case Description: We have been following a cohort of equines (n = 20) treated with SGLT2 inhibitors due to refractory hyperinsulinemia. The animals are owned by members of the Equine Cushing's and Insulin Resistance Group and treated by their attending veterinarians. The index case was a 23 years old gelding with a 2 years history of recurring laminitis that began canagliflozin therapy to control hyperinsulinemia which was no longer responsive to metformin. Between 6 and 10 weeks post start of therapy, significant weight loss was noticed. Two days later he was hospitalized with colic symptoms and hyperlipemia but was bright, alert, and eating well throughout. Canagliflozin was discontinued and triglycerides returned to normal reference values within 10 days. A subsequent study of 19 other horses on SGLT2 inhibitors revealed varying degrees of hypertriglyceridemia, all asymptomatic. Conclusion: While this class of drugs holds great promise for cases of refractory hyperinsulinemia and laminitis that do not respond to diet or metformin therapy, hypertriglyceridemia is a potential side effect. In our experience, animals remained asymptomatic and eating well. Further study of hypertriglyceridemia in horses on SGLT2 inhibitors and the possible mitigating effect of diet is indicated. To our knowledge, this is the first report of hypertriglyceridemia with canagliflozin treatment in equines.

Identification and management of ocular lipid deposition in association with hyperlipidaemia in captive moray eels, Gymnothorax funebris Ranzani, Gymnothorax moringa (Cuvier) and Muraena retifera Goode and Bean.

Ocular lipid deposition and its surgical management and possible association with systemic hyperlipidaemia in captive moray eels are described. Ophthalmologic examinations, haematology and plasma biochemistry analyses were performed on an initial population of captive moray eels (n=10): green moray, Gymnothorax funebris Ranzani; spotted moray, Gymnothorax morninga (Cuvier) and reticulated moray, Muraena retifera Goode and Bean. Recently captured green moray eels comprised the control group (n=9). Clinical signs compatible with ocular lipid deposition were identified in six of ten captive eels (60%) vs. none of the controls. Green moray eels in the initial captive population (n=5) had significantly higher total protein, triglyceride, cholesterol and aspartate amino transferase values than the control eels. Dietary management was attempted in all captive eels, and surgical intervention was performed in three eels, including two from a separate population, with improved ocular clarity within 1month post-operatively. Histopathological evaluation of surgical specimens and two eyes from an additional affected eel that died suggested ocular lipid deposition. Eels in captivity have an apparent predisposition for hyperlipidaemia and ocular lipid deposition. Although limited in this study and complicated by exhibit restraints, dietary management was minimally effective, while surgery improved ocular clarity.