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Obesity is a health concern for domestic cats. Obesity and severe energy restriction predispose cats to feline hepatic lipidosis. As choline is linked to lipid metabolism, we hypothesized that dietary choline supplementation would assist in reducing hepatic fat through increased lipoprotein transport and fatty acid oxidation. Twelve obese cats (body condition score [BCS] ≥ 8/9) were split into two groups. Cats were fed a control (n = 6, 4587 mg choline/kg dry matter [DM]) or a high choline diet (n = 6, 18,957 mg choline/kg DM) for 5 weeks, for adult maintenance. On days 0 and 35, fasted blood was collected, and the body composition was assessed. Serum lipoprotein and biochemistry profiles, plasma amino acids and plasma acylcarnitines were analyzed. The body weight, BCS and body composition were unaffected (p &gt, 0.05). Choline increased the serum cholesterol, triacylglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol and plasma methionine (p &lt, 0.05) and decreased the serum blood urea nitrogen and alkaline phosphatase (p &lt, 0.05). Choline also reduced the plasma acylcarnitine to free carnitine ratio (p = 0.006). Choline may assist in eliminating hepatic fat through increased fat mobilization and enhanced methionine recycling.

Objectives The aim of this study was to evaluate if de novo hepatic lipid synthesis contributes to fatty acid overload in the liver of cats with feline hepatic lipidosis (FHL). Methods Lipogenic gene expression of peroxisome proliferator-activated receptor-alpha ( PPAR-α), peroxisome proliferator-activated receptor-gamma ( PPAR-γ), fatty acid synthase ( FASN) and sterol regulatory element-binding factor ( SREBF1) were evaluated using quantitative RT-PCR in liver tissue of six cats with FHL and compared with the liver tissue of eight healthy cats. Results In liver tissue, PPAR-α, PPAR-γ and FASN mRNA expression levels were not significantly different ( P >0.12, P >0.89 and P >0.5, respectively) in the FHL group compared with the control group. SREBF1 gene expression was downregulated around 10-fold in the FHL group vs the control group ( P = 0.039). Conclusions and relevance The downregulation of SREBF1 in the liver tissue of cats with FHL does not support the hypothesis that de novo lipogenesis in the liver is an important pathway of fatty acid accumulation in FHL.

Feline hepatic lipidosis (HL), the most common hepatobiliary disease in cats, is characterized by the accumulation of excessive triglycerides (TGs) in more than 80% of hepatocytes. Forced oral feeding is recommended as the only therapy for this disease but the prognosis is often poor. As human placenta extract (Laennec) has been used to improve hepatic metabolism, we investigated the efficacy of this drug for the treatment of cats with HL. Ten cats diagnosed with HL in this study were treated with Laennec as a therapeutic drug. An immediate improvement in clinical symptoms was observed in all 10 cases. A statistical analysis indicated that the blood level of ALT (P = 0.029), AST (P = 0.029), ALP (P = 0.005), and T-Bil (P = 0.012) decreased significantly after treatment. All 7 hospitalized cases were eventually discharged from the hospital with a mean hospitalization duration of 4.8 days. The results of this study suggest that Laennec preparation has potential as an effective medicine for feline HL.

Summary Hepatic steatosis is a highly prevalent liver disease, yet research is hampered by the lack of tractable cellular and animal models. Steatosis also occurs in cats, where it can cause severe hepatic failure. Previous studies demonstrate the potential of liver organoids for modeling genetic diseases. To examine the possibility of using organoids to model steatosis, we established a long-term feline liver organoid culture with adult liver stem cell characteristics and differentiation potential toward hepatocyte-like cells. Next, organoids from mouse, human, dog, and cat liver were provided with fatty acids. Lipid accumulation was observed in all organoids and interestingly, feline liver organoids accumulated more lipid droplets than human organoids. Finally, we demonstrate effects of interference with β-oxidation on lipid accumulation in feline liver organoids. In conclusion, feline liver organoids can be successfully cultured and display a predisposition for lipid accumulation, making them an interesting model in hepatic steatosis research., Highlights • Feline organoids can be cultured from fresh and frozen liver and from needle biopsy • A feline-specific liver culture medium allows organoid expansion up to 32 passages • When fed fatty acids, feline liver organoids store more lipids than human organoids • Feline liver organoids can be used to model hepatic steatosis, In this study Kruitwagen and colleagues establish and characterize a feline liver organoid culture, which has adult stem cell properties and can be differentiated toward hepatocyte-like cells. They propose liver organoids as a tool to model hepatic steatosis and show that feline liver organoids accumulate more lipids than human organoids when provided with excess fatty acids.

Objectives The aim of this study was to describe the cellular and stromal components of the hepatic progenitor cell niche in feline hepatic lipidosis (FHL). Methods Immunohistochemical staining for the progenitor/bile duct marker (K19), activated Kupffer cells (MAC387), myofibroblasts (alpha-smooth muscle actin [α-SMA]) and the extracellular matrix component laminin were used on seven liver biopsies of cats with FHL and three healthy cats. Double immunofluorescence stainings were performed to investigate co-localisation of different cell types in the hepatic progenitor cell (HPC) niche. Results HPCs, Kupffer cells, myofibroblasts and laminin deposition were observed in the liver samples of FHL, although with variability in the expression and positivity of the different immunostainings between different samples. When compared with the unaffected cats where K19 positivity and minimal α-SMA and laminin positivity were seen mainly in the portal area, in the majority of FHL samples K19 and α-SMA-positive cells and laminin positivity were seen also in the periportal and parenchymatous area. MAC387-positive cells were present throughout the parenchyma. Conclusions and relevance This is a preliminary morphological study to describe the activation and co-localisation of components of the HPC niche in FHL. Although the HPC niche in FHL resembles that described in hepatopathies in dogs and in feline lymphocytic cholangitis, the expression of K19, α-SMA, MAC387 and lamin is more variable in FHL, and a common pattern of activation could not be established. Nevertheless, when HPCs were activated, a spatial association between HPCs and their niche could be demonstrated.

Dissertação de Mestrado Integrado em Medicina Veterinária Nesta dissertação pretendeu-se relacionar a lipidose hepática felina e a colangite neutrofílica, considerando a hipótese de que a primeira pudesse predispor ou conduzir ao desenvolvimento da segunda. Com base em 9 casos clínicos realizou-se também a caracterização e a comparação dos achados clínicos, dos parâmetros analíticos, da ecografia abdominal, da citologia hepática e da microbiológia de bílis, entre animais com suspeita de uma destas afeções ou ambas. Os critérios de inclusão abrangeram felinos, independentemente do sexo ou idade, que apresentassem alterações ecográficas e/ou ao exame citológico compatíveis com lipidose hepática felina e/ou colangite, e aos quais tivesse sido realizada cultura microbiológica de bílis. A citologia hepática foi realizada em 67% destes animais e permitiu a sua separação em grupos e subgrupos. No grupo A incluiram-se os animais com evidências de lipidose hepática felina confirmada citologicamente - casos 1,2,4,7,8, (56%) e no grupo B os animais com suspeita desta doença, mas sem evidências da mesma ao exame citológico - caso 5 (11%). No grupo C incluiram-se os animais com suspeita clínica, analítica e imagiológica destas doenças, mas sem registo de citologia hepática - casos 3, 6 e 9 (33%). O grupo A foi ainda subdividido em A1 e A2, tendo por base a suspeita de colangite concomitante ou não, respetivamente. Todos os animais motraram alterações da ecotextura hepática - 89% exibiram hiperecogenecidade hepática e apenas 11% (grupo B) hipoecogenecidade. Deste modo conclui-se que a presença concomitante de lipidose hepática felina pode ser a razão do aumento da ecogenecidade hepática muitas vezes descrito nos animais com colangite. Dos animais submetidos a exame citológico, 83% identificou-se a presença de alterações compatíveis com a presença de lipidose hepática felina. Nos animais suspeitos de terem colangite, apenas foi possível observar presença de conteúdo inflamatório como no caso 5 (grupo B). Este resultado mostra que, na presença das duas doenças em concomitância, a citologia hepática preveligia o diagnostico de lipidose hepática felina, o que conduz a um diagnostico plausível, mas inapropriado desta afeção. Nestas situações recomenda- se a realização de histopatologia. Na cultura microbiológica de bílis mostrou-se negativa em 88% da amostra. Relativamente ao grupo com suspeita de colangite, a taxa de positividade foi de 14% (1 caso positivo). A cultura foi positiva ao crescimento de Staphylococcus epidermidis. A taxa de culturas positivas foi baixa e o microorganismo em questão pode ter sido isolado devido a contaminação cutânea da amostra ou pelos hábitos felinos de grooming. As maiores limitações do presente estudo passam pela baixa amostragem e pelo fato de não terem sido realizadas histopatologias hepáticas. Por esta última razão não foi possível fazer o diagnóstico definitivo de uma das afeções em estudo (colangite) e não foram observadas alterações do parênquima hepático que permitissem estabelecer a relação pretendida entre as duas doenças. ABSTRACT - In this dissertation, it was intended to relate feline hepatic lipidosis and neutrophilic cholangitis, considering the hypothesis that the first could predispose or lead to the development of the second. In addition, the characterization and comparison of clinical findings, analytical parameters, abdominal ultrasonography, hepatic cytology and bile microbiology was made within group of 9 animals suspected of having one or both of these affections. The Inclusion criteria were felines, regardless of sex or age, with echographic and/or cytological abnormalities compatible with feline hepatic lipidosis and/or cholangitis, and that had a microbiological culture of bile. Hepatic cytology was performed in 67% of the total sample and allowed separation of the animals into groups and subgroups. In group A, were included the animals with suspicion of feline hepatic lipidosis confirmed by hepatic cytological examination - cases 1,2,4,7,8, (56%), and in group B were the animals with suspicion of feline hepatic lipidosis but with no evidence of this affection on cytological examination - case 5 (11%). Group C included the animals with clinical, analytic, and ultrasonografic suspicion of this affection but without record of hepatic cytological examination - cases 3, 6 and 9 (33%). Group A was further subdivided into A1 and A2, based on the suspicion of cholangitis concomitant or not, respectively. All animals presented hepatic echotexture abnormalities - 89% had hepatic hyperechogenicity and only 11% (group B) hypoechogenicity. Thus, it is concluded that the concomitant presence of feline hepatic lipidosis may be the reason for the increase in liver echogenicity often described in animals with cholangitis. Of the animals submitted to cytological examination, 83% showed the presence of alterations compatible with the presence of feline hepatic lipidosis. In the cases that were suspected of cholangitis, it was only possible to observe the presence of inflammatory contents in case 5 (group B). This result shows that, in the presence of both diseases, liver cytology confirms only the diagnosis of feline hepatic lipidosis, without confirmation of cholangitis. In these situations it is recommended to perform histopathology. Bile microbiological culture was negative in 88% of the animals. Regarding the cases with suspected cholangitis, the positivity rate was 14% (1 positive case). The culture was positive for Staphylococcus epidermidis. The rate of positive cultures was low and the microorganism in question may have been isolated due to skin contamination of the sample or due to the feline grooming habits. The major limitations of the present study were the low casuistic and the fact that hepatic histopathology was not performed. For this last reason, it was not possible to diagnose one of the affections under study (cholangitis). It was also not possible to observe alterations of the liver parenchyma and there to establish the desired relationship between the two diseases. N/A

Feline hepatic lipidosis was detected in two adult male cheetahs after a prolonged state of anorexia at Kuwait zoo. Blood and tissue samples collected for bacteriological and virological examination produced negative results. Biochemical analysis was carried out on the serum extracted from the rest of the blood samples which indicated a state of hypoglycemia in animal #1 (51.2 mg/dl) and a high level of liver enzymes (T.billi 1.7, 0.9 mg/dl, ALP 65.4, 69.2 IU/L, AST 40, 49.4 IU/L, ALT 54.3, 53.2 IU/L), TP 11.2, 9.5 g/dl and BUN 35.2, 32.7 mg/dl in cheetah #1 and # 2, respectively. The blood values for CRE (0.3, 1.3 mg/dl) were below normal standard values for both animals. Animal #1 died shortly during the course of investigation and by examination of the liver it was enlarged with diffuse icteric surface and greasy texture on cut surface. There was excessive infiltration of lipid cells into hepatocytes detected by histological examination suggesting a case of hepatic lipidosis. Correction of feeding protocol for captive cheetahs by the provision of varied prey items to meet their nutritional requirements is necessary.

Cats play an important role as pets in the present society. Thus, the knowledge about their main diseases and causes of death is fundamental to prevent various pathologies. However, when dealing with domestic cats there are very few researches in Veterinary Medicine. The aim of this study is to identify the causes of death of cats through a retrospective study of necropsies in the Animal Pathology Laboratory in the Federal University of Uberlândia (Brazil), in a period of 36 years, in which 350 cat necropsies were conducted. The most frequent causes of death of these animals were digestive system diseases (48 cats – 13.71%), and among them, feline hepatic lipidosis was the most frequent etiology (18.75%). The second most affected system was the respiratory (10.86%) and acute pneumonia, pulmonary edema, and diaphragmatic hernia were the main diseases to cause death of cats with some kind of disorder in this system. Other decease causes were rabies, squamous cell carcinoma, fibrous osteodystrophy, fractures and traumatism, hypovolemic shock, and feline lower urinary tract disease. This type of analysis can provide basic information about the most common diseases in felines, contributing with veterinarians as they adopt control and prevention actions against diseases. Os gatos apresentam papel relevante como animal de estimação na sociedade atual. Neste sentido, o conhecimento das principais enfermidades e causas de morte desses animais é fundamental para prevenção de várias patologias. No entanto, quanto ao gato doméstico, essas pesquisas ainda são escassas na medicina veterinária. Assim, este trabalho realizou um estudo retrospectivo das causas de morte de gatos registradas das necropsias efetuadas pelo Laboratório de Patologia Animal da Universidade Federal de Uberlândia, em um período de 36 anos, no qual 350 gatos foram necropsiados. As doenças do sistema digestivo foram as mais frequentes (48 gatos – 13,71%) e destas, a lipidose hepática foi a etiologia de maior ocorrência (18,75%). O sistema respiratório foi o segundo mais afetado (10,86%), sendo pneumonia aguda, edema pulmonar e hérnia diafragmática as principais doenças deste sistema responsáveis pela morte de gatos. Outras causas de óbito importantes foram raiva, carcinoma de células escamosas, osteodistrofia fibrosa, fraturas e traumatismos, choque hipovolêmico e síndrome urológica felina. Este tipo de análise pode fornecer informações básicas sobre as enfermidades que mais acometem os felinos de uma determinada região, contribuindo para que os profissionais médicos veterinários passem a adotar as respectivas ações de prevenção e controle.

Feline hepatic lipidosis (FHL) is a common and potentially fatal liver disorder. Although the pathophysiologic mechanisms of FHL remain elusive, there is an imbalance between the influx of fatty acids from peripheral fat stores into the liver, de novo liposynthesis, and the rate of hepatic oxidation and dispersal of hepatic TAG via excretion of very-low density lipoproteins. The diagnosis of FHL is based on anamnestic, clinical, and clinicopathologic findings, associated with diagnostic imaging of the liver, and cytology, or histological examination of liver biopsies. Fluid therapy, electrolyte correction and adequate early nutrition are essential components of the therapy for FHL.

Research in various species has indicated that diets deficient in labile methyl groups (methionine, choline, betaine, folate) produce fatty liver and links to steatosis and metabolic syndrome, but also provides evidence of the importance of labile methyl group balance to maintain normal liver function. Cats, being obligate carnivores, rely on nutrients in animal tissues and have, due to evolutionary pressure, developed several physiological and metabolic adaptations, including a number of peculiarities in protein and fat metabolism. This has led to specific and unique nutritional requirements. Adult cats require more dietary protein than omnivorous species, maintain a consistently high rate of protein oxidation and gluconeogenesis and are unable to adapt to reduced protein intake. Furthermore, cats have a higher requirement for essential amino acids and essential fatty acids. Hastened use coupled with an inability to conserve certain amino acids, including methionine, cysteine, taurine and arginine, necessitates a higher dietary intake for cats compared to most other species. Cats also seemingly require higher amounts of several B-vitamins compared to other species and are predisposed to depletion during prolonged inappetance. This carnivorous uniqueness makes cats more susceptible to hepatic lipidosis.

Background Feline hepatic lipidosis (HL) is associated with alterations in lipid and carbohydrate metabolism. The adipokines, adiponectin, and leptin have lipid-lowering and insulin-sensitizing effects. Hypothesis Serum concentrations of adiponectin and leptin are altered in feline HL. Animals Client-owned cats: 55 healthy and 45 with liver disease. Methods Cats with liver disease were categorized as having HL (n = 20), HL and concurrent disease (n = 19), or other liver disease (n = 6), based on clinical signs, laboratory findings, abdominal ultrasound examination as well as liver cytopathology, histopathology, or both. Serum samples were collected and body condition score determined. Results Mean serum concentrations of adiponectin were higher in overweight cats with HL (4.5 μg/mL), HL and concurrent disease (4.4 μg/mL), or other liver disease (6.1 μg/mL), as compared with healthy cats (1.5 μg/mL; P

Two 4-year-old spayed female Siamese cats were seized by the British Columbia Society for the Prevention of Cruelty to Animals after confinement to an abandoned housing unit without food for 9 weeks. One cat was found dead, and the second was euthanized within 24 hours due to neurologic deterioration despite therapy. Polioencephalomalacia of the caudal colliculus, hepatic lipidosis, cachexia, and congestive heart failure with cardiomyocyte atrophy were identified in both cats through postmortem examination and attributed to a prolonged period of starvation. Brain lesions were likely the result of thiamine deficiency (Chastek paralysis), which can be associated with both malnutrition and liver disease. This case highlights the importance of thiamine supplementation during realimentation of cats with hepatic lipidosis. Heart failure resulting from cachexia may have contributed to the death of the first cat and the morbidity of the second cat.

BACKGROUND: Feline hepatic lipidosis (FHL) is a common cholestatic disease affecting cats of any breed, age and sex. Both choline deficiency and low hepatic phosphatidylethanolamine N-methyltransferase (PEMT) activity are associated with hepatic lipidosis (HL) in humans, mice and rats. The PEMT expression is known to be upregulated by oestrogens, protecting the females in these species from the development of HL when exposed to choline deficient diets. The aim of the present study was to evaluate the influence of sex hormones on choline synthesis via the PEMT pathway in healthy male and female cats before and after spaying/neutering, when fed a diet with recommended dietary choline content. RESULTS: From six female and six male cats PEMT activity was assayed directly in liver biopsies taken before and after spaying/neutering, and assessed indirectly by analyses of PEMT-specific hepatic phosphatidylcholine (PC) species and plasma choline levels. Hepatic PEMT activity did not differ between intact female and male cats and no changes upon spaying/neutering were observed. Likewise, no significant differences in liver PC content and PEMT-specific polyunsaturated PC species were found between the sexes and before or after spaying/neutering. CONCLUSION: These results suggest that choline synthesis in cats differs from what is observed in humans, mice and rats. The lack of evident influence of sex hormones on the PEMT pathway makes it unlikely that spaying/neutering predisposes cats for HL by causing PC deficiency as suggested in other species.

This study was designed to determine whether dietary carnitine supplement could protect cats from ketosis and improve carnitine and lipid metabolism in experimental feline hepatic lipidosis (FHL). Lean spayed queens received a diet containing 40 (CL group, n = 7) or 1000 (CH group, n = 4) mg/kg of L-carnitine during obesity development. Plasma fatty acid, beta-hydroxybutyrate and carnitine, and liver and muscle carnitine concentrations were measured during experimental induction of FHL and after treatment. In control cats (CL group), fasting and FHL increased the plasma concentrations of fatty acids two- to threefold (P0.0001) and beta-hydroxybutyrate10-fold (from a basal 0.22 +/- 0.03 to 1.70 +/- 0.73 after 3 wk fasting and 3.13 +/- 0.49 mmol/L during FHL). In carnitine-supplemented cats, these variables increased significantly (P0.0001) only during FHL (beta-hydroxybutyrate, 1.42 +/- 0.17 mmol/L). L-Carnitine supplementation significantly increased plasma, muscle and liver carnitine concentrations. Liver carnitine concentration increased dramatically from the obese state to FHL in nonsupplemented cats, but not in supplemented cats, which suggests de novo synthesis of carnitine from endogenous amino acids in control cats and reversible storage in supplemented cats. These results demonstrate the protective effect of a dietary L-carnitine supplement against fasting ketosis during obesity induction. Increasing the L-carnitine level of diets in cats with low energy requirements, such as after neutering, and a high risk of obesity could therefore be recommended.

Feline hepatic lipidosis (HL) is a common, potentially life-threatening disease resulting from prolonged anorexia and increased catabolism. This retrospective study included cats diagnosed with HL based on liver cytology or histopathology (years 2004-2015), and aimed to identify clinical and laboratory parameters associated with mortality. The study included 71 cats (47 females and 24 males) and 85 control cats with non-HL diseases. Most HL cats (90 per cent) were mixed breed, neutered (70; 99 per cent), female (47; 66 per cent), indoor cats (56; 79 per cent), fed dry commercial diets (44 cats; 62 per cent), and with a median age of 7.5 years (range 1.5-16.0). Common primary conditions included gastrointestinal diseases, pancreatitis and cholangiohepatitis (31 cats; 44 per cent) and stressful events (14; 20 per cent). HL was idiopathic in 20 cats (28 per cent). The overall mortality was 38 per cent (27/71 cats). Older age, as well as dullness, weakness, ptyalism, hypoproteinaemia, hypoalbuminaemia, increased serum creatine kinase activity, hypocholesterolaemia and hepatic failure at presentation were significantly (P≤0.033) associated with mortality. The primary disease was unassociated with mortality. Worsening hypoalbuminaemia, hyperammonaemia, hyperbilirubinaemia, electrolyte disorders, and occurrence of cavitary effusions or hypotension during hospitalisation were significantly (P≤0.045) associated with mortality. A decrease of serum β-hydroxybutyrate during hospitalisation was significantly (P=0.01) associated with survival, likely reflecting improvement in the catabolic state. The identified risk factors may be therapeutic targets.

The effects of weight gain and subsequent weight loss on glucose tolerance and insulin response were evaluated in 12 healthy cats. Intravenous glucose tolerance tests (IVGTT) were performed at entry into the study, after a significant gain of body weight induced by feeding palatable commercial cat food ad libitum, after a significant loss of body weight induced by feeding a poorly palatable purified diet to discourage eating and promote fasting, and after recovery from fasting when body weight had returned to pre-study values and cats were eating commercial foods. A complete physical examination with measurement of body weight was performed weekly, a CBC and serum biochemistry panel were evaluated at the time of each IVGTT, and a liver biopsy specimen obtained 2 to 4 days after each IVGTT was evaluated histologically for each cat. Mean serum glucose and insulin concentrations after glucose infusion and total amount of insulin secreted during the second 60 minutes and entire 120 minutes after glucose infusion were significantly (P < .05) increased after weight gain, as compared with baseline. At the end of weight loss, cats had hepatic lipidosis and serum biochemical abnormalities consistent with feline hepatic lipidosis. There was a significant (P < .05) increase in mean serum glucose concentration and t1/2, and a significant (P < .05) decrease in mean serum insulin concentration and the glucose disappearance coefficient (K) after glucose infusion for measurements obtained after weight loss, compared with those obtained after weight gain and at baseline. Insulin peak response, insulinogenic index, and total amount of insulin secreted during the initial 10 minutes, 20 minutes, and 60 minutes after glucose infusion were decreased markedly (P < .05), compared with measurements obtained after weight gain and at baseline. In addition, the total amount of insulin secreted for 120 minutes after glucose infusion was decreased markedly (P < .05) in measurements obtained after weight loss, compared with those obtained after weight gain. At the end of recovery, all cats were voluntarily consuming food, serum biochemical abnormalities identified after weight loss had resolved, the number and size of lipid vacuoles in hepatocytes had decreased, and results of IVGTT were similar to those obtained at baseline. These findings confirmed the reversibility of obesity-induced insulin resistance in cats, and documented initial deterioration in glucose tolerance and insulin response to glucose infusion when weight loss was caused by severe restriction of caloric intake.

The usefulness of computed tomography (CT) for the diagnosis of feline hepatic lipidosis (FHL) was evaluated. Liver CT number was 54.7+/-5.6 HU (mean+/-SD) in 26 healthy cats. We fast 6 healthy cats for 72 hr to induced FHL experimentally and the cats were assessed by CT and serum biochemical analysis. Liver CT number of the six cats was 53.8+/-3.0 HU before fasting, 46.8+/-2.4 HU after fasting, and 50.2+/-3.6 HU two weeks after restarted feeding. The decreased CT number was associated with the elevation of serum non-esterified fatty acid (NEFA) and beta-hydroxybutyrate levels. These results indicate that measurement of CT number of the liver is an effective procedure for the diagnosis of FHL.

Dissertação de Mestrado Integrado em Medicina Veterinária Inicialmente descrita como uma doença idiopática por Barsanti et al em 1977, a lipidose hepática felina (LHF) é caracterizada actualmente como uma patologia secundária a um processo primário em mais de 95% dos casos. Esta patologia é mais comum em gatos com condição corporal elevada sujeitos a um período prolongado de privação de alimento. Os gatos apresentam alguma predisposição para a acumulação de triglicéridos a nível hepático o que, em caso de doença, resulta em vacuolização gorda hepatocelular. Durante o período de anorexia ao qual estão sujeitos, vai ocorrer lipólise da gordura das reservas corporais. Apesar de os mecanismos fisiopatológicos que desencadeiam esta síndrome não serem completamente conhecidos, verifica-se um desequilíbrio na circulação de ácidos gordos entre o fígado e o tecido adiposo, resultando no comprometimento na capacidade de remoção dos ácidos gordos da corrente sanguínea por parte do fígado. O objectivo do estudo de casos consistiu na caracterização de uma amostra de sete gatos diagnosticados com lipidose hepática felina, atendendo à predisposição de género, idade e peso. Descreveram-se os sinais clínicos, físicos e laboratoriais de todos os pacientes. Os gatos analisados foram apresentados à consulta com história de anorexia (71%), perda de peso (57%), prostração (57%), obstipação (57%) e vómito, adipsia e anúria com menor incidência. O período de anorexia variou entre sete e quinze dias, tendo duração média de onze dias. ABSTRACT - Initially described as an idiopathic disease by Barsanti et al in 1977, feline hepatic lipidosis (FHL) is characterized as a current condition secondary to a primary process in over 95% of cases. This condition is more common in cats with high body condition subject to a prolonged period of food deprivation. The cats have a predisposition to the accumulation of triglycerides in the liver which, in case of disease, results in fat hepatocellular vacuolation. During the period of anorexia which they are subjected, lipolysis of fat from body stores will occur. Even though the physiopathological mechanisms that trigger this syndrome are not fully understood, there is an imbalance in the movement of fatty acids between the liver and adipose tissue, resulting in impairment of the ability to remove the fatty acids from the bloodstream by the liver. The aim of this study consisted in the characterization of a sample of seven cats diagnosed with feline hepatic lipidosis, given the predisposition of gender, age and weight. The clinical signs, physical and laboratory examinations were described for all patients. The cats were presented to consultation with a history of anorexia (71%), weight loss (57%), prostration (57%), constipation (57%) and vomiting, adipsia, and anuria with lower incidence. The period of anorexia was between seven to fifteen days, and the average was eleven days. Changes in the physical examination with the highest incidence were jaundice (71%), dehydration (71%), abdominal pain on palpation (43%) and dysphagia (14%). The complementary exams showed increased activity of liver enzymes and increased liver parenchyma hyperecogenecity was shown in the abdominal ultrasonography. The primary disease was diagnosed in five cases. The treatment was directed to the primary cause, in cases where it has been determined, and in other cases it directed the treatment for the disease likely. Of the seven cats in the study, treatment was successful in five cases and two cats were euthanized.

A 3-year-old Domestic Shorthair cat was presented with weight loss, anorexia and icterus. Feline hepatic lipidosis and gallbladder mucocoele were diagnosed; this is the first report of gallbladder mucocoele in the cat. The case was managed successfully with cholecystojejunostomy, gastrostomy tube placement and tube feeding for 3 months. The cat has survived over the long term with minimal complications.

Anorexia in obese cats may result in feline hepatic lipidosis (FHL). This study was designed to determine plasma lipids and lipoprotein profiles in queens at different stages during experimental induction of FHL (lean, obese, FHL), and after 10 weeks of treatment. Results were compared with those obtained from lean queens of same age fed the same diet but at a maintenance level, once a day. Hepatic lipidosis led to an increase in plasma triacylglycerol (TG), very low density lipoprotein (VLDL) and low density lipoprotein (LDL), and an enrichment of LDL with TG and of high density lipoprotein (HDL) with cholesterol, suggesting that VLDL secretion is enhanced, VLDL and LDL catabolism is lowered, and lipoprotein exchanges are impaired in FHL. This study also showed that cholesterolaemia is increased in cats fed at a dietary rhythm of one meal per day compared to ad libitum feeding.

The purpose of this study was to characterize the lipid classes in hepatic and adipose tissues from cats with idiopathic hepatic lipidosis (IHL). Concentrations of triglyceride, phospholipid phosphorus, and free and total cholesterol were determined in lipid extracts of liver homogenates from 5 cats with IHL and 5 healthy control cats. Total fatty acid composition of liver and adipose tissue was also compared. Triglyceride accounted for 34% of liver by weight in cats with IHL (338 +/- 38 mg/g wet liver) versus 1% in control cats (9.9 +/- 1.0 mg/g wet liver, P < .001). The mass of cholesterol ester was significantly higher in triglyceride-free (TG-free) liver from cats with IHL (741 +/- 340 micrograms/g TG-free wet liver) compared to healthy cats (31 +/- 11 micrograms/g TG-free wet liver, P < .05). Total fatty acid composition of hepatic tissue in the 2 groups differed; palmitate was higher (19.5 +/- 1.1% of total fatty acids in cats with IHL versus 9.2 +/- 2.7% in controls, P < .05), stearate was lower (8.5 +/- 0.8% versus 16.8 +/- 1.1%, P < .05), oleate was higher (41.2 +/- 1.6% versus 31.1 +/- 1.8%, P < .05), and arachidonate was lower (1.2 +/- 0.2% versus 6.0 +/- 0.9%, P < .05). The total fatty acid composition of adipose tissue also differed between the 2 groups; palmitate was higher (26.2 +/- 1.2% in cats with IHL versus 21.3 +/- 0.6% in controls, P < .05), total monounsaturated fatty acids were higher (48.4 +/- 1.0% versus 45.0 +/- 0.8%, P < .05), linolenate was lower (13.3 +/- 1.6% versus 17.5 +/- 0.9%, P < .05), total (n-6) fatty acids were lower (13.8 +/- 1.38% versus 18.4 +/- 0.83%, P < .05), linolenate was lower (0.2 +/- 0.04% versus 0.7 +/- 0.06%, P < .06), and total (n-3) fatty acids were lower (0.3 +/- 0.02% versus 1.3 +/- 0.32%, P < .05). The fatty acid composition of both liver and adipose tissue was similar for stearate, oleate, linoleate, and linolenate in cats with IHL. These results support the hypothesis that the origin of hepatic triglyceride in cats with IHL is the mobilization of fatty acids from adipose tissue.

Hepatic lipidosis occurs when lipid mobilized to the liver exceeds lipid leaving the liver via formation of very-low-density lipoproteins or by oxidation. Hepatic lipidosis in cats is associated with overt liver dysfunction. In affected cats, excess lipid is mobilized to the liver because of starvation. Removal of hepatic lipid may be impaired because of protein malnutrition, a relative carnitine deficiency, or oxidative damage to peroxisomes and other hepatic organelles. Hepatic lipidosis occurs in adult cats, and is manifest by signs of weight loss, depression, vomiting, and icterus. Diagnosis is achieved by evaluating laboratory and diagnostic imaging data, in conjunction with a liver biopsy. Aggressive tube feeding is the treatment of choice. With this treatment, survival rates are 60% to 80%.

The physical, clinicopathologic, and survival rates of 77 cats with severe spontaneous hepatic lipidosis are detailed in this report. Cats were subdivided into groups designated as idiopathic lipidosis if no other disease process was recognized, or secondary lipidosis if another disease process was diagnosed. Cats were also subdivided into groups designated as survivors or nonsurvivors on the basis of successful recuperation at 4 months after initial diagnosis. Differences between disease and survival groups were evaluated for significance. Overall, more female cats and middle-aged cats were affected. Presenting complaints of vomiting, anorexia, weakness, and weight loss were common. Physical assessment of most cats showed obvious hepatomegaly, jaundice, dehydration, and a weight loss > or = 25% of usual body weight. Neurobehavioral signs indicative of hepatic encephalopathy, other than ptyalism and depression, were rare. Clinicopathologic features are characterized by hyperbilirubinemia and increased activities of serum ALT, AST, and ALP, with only small if any increase in gamma GT activity. Clinical features distinguishing cats with hepatic lipidosis from those with other serious cholestatic disorders include absence of hyperglobulinemia and low gamma GT activity relative to ALP activity. Although coagulation tests were abnormal in 45% of cats tested (n = 44), few cats showed clinical bleeding tendencies. Most cats received prophylactic vitamin K1 therapy. Forty two cats received aggressive nutritional and supportive care and of these 55% survived. Cats with idiopathic disease were significantly younger, had significantly higher ALP activity and bilirubin concentration, and had a slightly better survival rate than cats with secondary lipidosis. Low PCV, hypokalemia, and an older age were significantly related to nonsurvival. Because of the variety of diets and food supplements used in case management, the influence of nutritional factors on survival could not be evaluated.