Abstract:Cats can lose 25 to 30% of their obese body weight over 7 to 9 weeks without developing overt clinical signs of HL, provided that weight-reduction diets are highly palatable, contain a high quality protein, have a source of LCEFA, and are fortified with vitamins and microminerals. However, rapid weight loss may increase risk factors associated with development of diabetes mellitus.
“…In the current study, food-restricted glucose concentrations increased from week 0 to 24, suggesting decreased insulin sensitivity with weight gain; however, food-restricted blood insulin concentrations did not change over time. Szabo et al (2000) reported increased blood glucose concentrations in cats following ovariohysterectomy (and weight gain) with no increases in insulin concentration. Glucose concentrations reported by Szabo et al (2000) were similar to those measured in the current study.…”
Section: High-protein Diet Following Ovariohysterectomymentioning
confidence: 98%
“…Szabo et al (2000) reported increased blood glucose concentrations in cats following ovariohysterectomy (and weight gain) with no increases in insulin concentration. Glucose concentrations reported by Szabo et al (2000) were similar to those measured in the current study. Kanchuk et al (2003) reported increased insulin concentrations of neutered male v. intact male cats; however, changes over time within the neutered males were not statistically analyzed.…”
Section: High-protein Diet Following Ovariohysterectomymentioning
The objective of this study was to measure changes in body composition, physical activity and adipose and skeletal muscle gene expression of cats fed a high-protein (HP) diet or moderate-protein (MP) diet, following ovariohysterectomy. Eight cats were randomized onto HP or MP diets and were fed those diets for several months prior to baseline. All cats underwent an ovariohysterectomy at baseline (week 0) and were allowed ad libitum access to dietary treatments for 24 weeks. Food intake was measured daily, and BW and body condition score were measured weekly. Blood, adipose and skeletal muscle tissue samples were collected, physical activity was measured, and body composition was determined using DEXA (dual-energy X-ray absorptiometry) at weeks 0, 12 and 24. Caloric intake increased soon after ovariohysterectomy, resulting in increased ( P , 0.05) BW at weeks 12 and 24 compared to week 0. Body condition score and body fat percentage increased ( P , 0.05) over time. Blood glucose increased ( P , 0.05) linearly over time. Non-esterified fatty acids were decreased ( P , 0.05) at weeks 12 and 24 compared to week 0. Blood leptin increased ( P , 0.05) over time. Total physical activity decreased ( P , 0.05) from week 0 to weeks 12 and 24 in all cats. Adipose tissue mRNA abundance of adiponectin, hormone sensitive lipase, toll-like receptor-4, uncoupling protein-2 (UCP2) and vascular endothelial growth factor decreased ( P , 0.05) linearly over time, regardless of diet. Skeletal muscle mRNA abundance for glucose transporter-1, hormone sensitive lipase and UCP2 were decreased ( P , 0.05), regardless of dietary treatment. Our research noted metabolic changes following ovariohysterectomy that are in agreement with gene expression changes pertaining to lipid metabolism. Feeding cats ad libitum after ovariohysterectomy is inadvisable.
“…In the current study, food-restricted glucose concentrations increased from week 0 to 24, suggesting decreased insulin sensitivity with weight gain; however, food-restricted blood insulin concentrations did not change over time. Szabo et al (2000) reported increased blood glucose concentrations in cats following ovariohysterectomy (and weight gain) with no increases in insulin concentration. Glucose concentrations reported by Szabo et al (2000) were similar to those measured in the current study.…”
Section: High-protein Diet Following Ovariohysterectomymentioning
confidence: 98%
“…Szabo et al (2000) reported increased blood glucose concentrations in cats following ovariohysterectomy (and weight gain) with no increases in insulin concentration. Glucose concentrations reported by Szabo et al (2000) were similar to those measured in the current study. Kanchuk et al (2003) reported increased insulin concentrations of neutered male v. intact male cats; however, changes over time within the neutered males were not statistically analyzed.…”
Section: High-protein Diet Following Ovariohysterectomymentioning
The objective of this study was to measure changes in body composition, physical activity and adipose and skeletal muscle gene expression of cats fed a high-protein (HP) diet or moderate-protein (MP) diet, following ovariohysterectomy. Eight cats were randomized onto HP or MP diets and were fed those diets for several months prior to baseline. All cats underwent an ovariohysterectomy at baseline (week 0) and were allowed ad libitum access to dietary treatments for 24 weeks. Food intake was measured daily, and BW and body condition score were measured weekly. Blood, adipose and skeletal muscle tissue samples were collected, physical activity was measured, and body composition was determined using DEXA (dual-energy X-ray absorptiometry) at weeks 0, 12 and 24. Caloric intake increased soon after ovariohysterectomy, resulting in increased ( P , 0.05) BW at weeks 12 and 24 compared to week 0. Body condition score and body fat percentage increased ( P , 0.05) over time. Blood glucose increased ( P , 0.05) linearly over time. Non-esterified fatty acids were decreased ( P , 0.05) at weeks 12 and 24 compared to week 0. Blood leptin increased ( P , 0.05) over time. Total physical activity decreased ( P , 0.05) from week 0 to weeks 12 and 24 in all cats. Adipose tissue mRNA abundance of adiponectin, hormone sensitive lipase, toll-like receptor-4, uncoupling protein-2 (UCP2) and vascular endothelial growth factor decreased ( P , 0.05) linearly over time, regardless of diet. Skeletal muscle mRNA abundance for glucose transporter-1, hormone sensitive lipase and UCP2 were decreased ( P , 0.05), regardless of dietary treatment. Our research noted metabolic changes following ovariohysterectomy that are in agreement with gene expression changes pertaining to lipid metabolism. Feeding cats ad libitum after ovariohysterectomy is inadvisable.
“…No caso da LHF, grande parte dos gatos que a desenvolvem são obesos e, ao sofrerem um processo patológico causador de anorexia, mobilizam ácidos graxos das reservas adiposas através de lipólise (Ettinger and Feldman, 2004). Com efeito, o substrato energético utilizado deixa de ser a glucose e passa a ser os ácidos graxos e as cetonas (Szabo et al, 2000). A excessiva acumulação de triacilgliceróis nos hepatócitos afeta a função hepática e pode culminar em morte (Hall et al, 1997).…”
RESUMO.Este relato mostra o caso de um felino sem raça definida, de um ano e quatro meses de idade diagnosticado com lipidose hepática secundaria à colangiohepatite. Relata a importância dos exames complementares no diagnóstico da doença e o tratamento à base de suporte nutricional contendo alto teor proteico, que demonstrou ser essencial na recuperação do paciente.
Palavras chaves: disfunção hepática, hiperbilirrubinemia, icterícia
Hepatic lipidosis secondary to Cholangiohepatitis in domestic feline without definite breed -Case reportABSTRACT. This report shows a case of feline without definite breed, whit one-year and four-month-old diagnosed with hepatic lipidosis secondary to cholangiohepatitis. It reports the importance of complementary tests in the diagnosis of the disease and the treatment based on nutritional support containing high protein content, which has been shown to be essential for patient recovery.
Keywords: Hepatic dysfunction, hyperbilirubinemia, jaundiceLipidosis hepática secundaria a colangiohepatitis en felino mestizo: Reporte de un caso RESUMEN. El presente caso muestra un felino mestizo, de un año y cuatro meses de edad, con diagnóstico de lipidosis hepática secundaria a colangiohepatitis. Informa sobre la importancia de las pruebas complementarias en el diagnóstico de la enfermedad y el tratamiento de la base de apoyo nutricional que contiene un alto contenido de proteínas, que resultó ser esencial en la recuperación del paciente.
“…Em possa afetar gatos de qualquer idade, a doença surge mais comumente entre os quatro e os quinze anos. Existem vários mecanismos fisiopatológicos que estão na base do desenvolvimento da FHL: o aumento do fluxo de ácidos graxos livres para o fígado, o aumento da síntese hepática de ácidos graxos, as alterações na oxidação dos ácidos graxos no hepatócito e a diminuição do transporte pelas lipoproteínas de muito baixa densidade (Szabo et al, 2000). Brown et al (2000) propõem como causas o aumento da lipólise periférica secundária a uma deficiência absoluta ou relativa em insulina, o fígado gordo induzido por má nutrição proteicocalórica (similar ao kwashiorkor ou marasmus em humanos), a deficiência em aminoácidos essenciais (arginina e metionina) a que dá origem a uma incapacidade de sintetizar apoproteínas suficientes para mobilizar os lipídios hepáticos, a deficiência em compostos lipotróficos, a deficiência congénita ou adquirida da oxidação dos ácidos gordos e a lesão peroxissomal hepática devido a stress oxidativo.…”
*Autor para a correspondência RESUMO. A lipidose hepática felina é uma das hepatopatias mais comuns e potencialmente fatal que acomete gatos domésticos. Na maioria das vezes afeta gatos privados de alimento ou que passaram por períodos prolongados de anorexia. É um processo patológico que atinge gatos adultos, podendo estar associado a colangiohepatite, obstruções biliares ou neoplasia intra-hepática ou apresentar caráter idiopático. Normalmente, os ácidos graxos que circulam no fígado são captados e metabolizados para produzir energia ou se convertem em triglicérides e são segregados de novo para a circulação. A doença pode se apresentar como resultado de uma desordem na oxidação dos ácidos graxos pelos hepatócitos, ou da incapacidade do fígado para segregar as lipoproteínas encarregadas de transportar as triglicérides através da corrente sanguínea. A doença é bastante comum, e tende a afetar gatos obesos. A anorexia prolongada pode causar acúmulo significativo de gordura no fígado e o aparecimento das manifestações clínicas. Qualquer que seja a causa metabólica da lipidose hepática, a recuperação do animal requer diagnóstico precoce, início imediato da terapia sintomática e sonda de alimentação para suporte nutricional.
Palavras chaves: Anorexia, hepatócitos, triglicérides, obesidadeUltrasonographic and clinical parameters in the case of feline hepatic lipidosis: Case report ABSTRACT: Feline hepatic lipidosis is one of the most common and potentially fatal hepatopathies that affects domestic cats. Most of the time it affects cats deprived of food or who have gone through prolonged periods of anorexia. It is a pathological process that affects adult cats, and may be associated with cholangiohepatitis, biliary obstruction or intrahepatic neoplasia or idiopathic character. Normally, the fatty acids that circulate in the liver are picked up and metabolized to produce energy or converted to triglycerides and are segregated back into the circulation. The disease may occur as a result of a disorder in the fatty acid oxidation by hepatocytes, or the inability of the liver to secrete the lipoproteins in charge of transporting the triglycerides through the bloodstream. The disease is quite common, and tends to affect obese cats. Prolonged anorexia can cause significant accumulation of fat in the liver and the onset of clinical manifestations. Whatever the metabolic cause of hepatic lipidosis, recovery of the animal requires early diagnosis, immediate initiation of symptomatic therapy, and feeding probe for nutritional support.
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