Lipid and metabolic profiles in female dogs with mammary carcinoma receiving dietary fish oil supplementation

Costa-Santos, Keidylania; Damasceno, Karine Araújo; Portela, Ricardo Wagner; Santos, Ferlando Lima; Araújo, Genira Carneiro de; Martins-Filho, Emanoel Ferreira; Silva, Laís Pereira; Barral, Thiago Doria; Santos, Stefanie Alvarenga; Estrela‐Lima, Alessandra

doi:10.1186/s12917-019-2151-y

Cited by 14 publications

(10 citation statements)

References 60 publications

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“…Acute respiratory failure was identified as the cause of death. Considering the cause of death and the presence of late metastases, similar results were described by Costa-Santos et al [ 25 ]. In the current study, the histological analyses of the affected organs confirmed the presence of metastases.…”

Section: Discussionsupporting

confidence: 83%

Pharmacokinetics of Carboplatin in Combination with Low-Dose Cyclophosphamide in Female Dogs with Mammary Carcinoma

Machado¹,

Yamamoto

Pippa

et al. 2022

Animals

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This prospective study aimed to evaluate the effect of metronomic cyclophosphamide on carboplatin’s tolerability, efficacy, and pharmacokinetics in dogs with mammary carcinoma. Sixteen female dogs with mammary carcinoma were divided into groups: 300 mg/m2 intravenous (i.v.) carboplatin therapy (G1 = 8) or 300 mg/m2 i.v. carboplatin which was associated with 12.5 mg/m2 oral cyclophosphamide in a metronomic regimen (G2 = 8). The investigated animals underwent a clinical evaluation, a mastectomy, a carboplatin chemotherapy, and serial blood sampling for the pharmacokinetic analysis. The adverse events and survival rates were monitored. A non-compartmental analysis was applied to calculate the pharmacokinetic parameters of carboplatin in the 2nd and 4th chemotherapy cycles. Carboplatin PK showed high interindividual variability with a 10-fold variation in the area under the plasma concentration–time curve (AUC) in G1. The systemic plasma exposure to carboplatin was equivalent in both of the treatments considering the AUC and maximum plasma concentration (Cmax) values. Although the red blood cells (p < 0.0001), platelets (p = 0.0005), total leukocytes (p = 0.0002), and segmented neutrophils (p = 0.0007) were reduced in G2, the survival rate increased (p = 0.0044) when it was compared to G1. In conclusion, adding low daily doses of cyclophosphamide to a carboplatin therapy showed promising outcomes in female dogs with mammary tumors.

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Section: Discussionsupporting

confidence: 83%

Pharmacokinetics of Carboplatin in Combination with Low-Dose Cyclophosphamide in Female Dogs with Mammary Carcinoma

Machado¹,

Yamamoto

Pippa

et al. 2022

Animals

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“…An estimated 34–59% of pet dogs in developed countries are overweight or obese [ 3 , 9 , 101 , 102 , 103 , 104 ]. Multiple comorbidities are associated with canine obesity, most notably: orthopaedic disease, exacerbation of breathing difficulties, and urinary incontinence, along with significantly decreased life expectancy [ 105 , 106 , 107 , 108 ]. Canine obesity is associated with increased blood pressure, dyslipidaemia, and insulin resistance, and this has been characterised as “obesity-related metabolic dysfunction” [ 109 , 110 ].…”

Section: Canine Obesity Geneticsmentioning

confidence: 99%

The Genetic Basis of Obesity and Related Metabolic Diseases in Humans and Companion Animals

Wallis

Raffan

2020

Genes

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Obesity is one of the most prevalent health conditions in humans and companion animals globally. It is associated with premature mortality, metabolic dysfunction, and multiple health conditions across species. Obesity is, therefore, of importance in the fields of medicine and veterinary medicine. The regulation of adiposity is a homeostatic process vulnerable to disruption by a multitude of genetic and environmental factors. It is well established that the heritability of obesity is high in humans and laboratory animals, with ample evidence that the same is true in companion animals. In this review, we provide an overview of how genes link to obesity in humans, drawing on a wealth of information from laboratory animal models, and summarise the mechanisms by which obesity causes related disease. Throughout, we focus on how large-scale human studies and niche investigations of rare mutations in severely affected patients have improved our understanding of obesity biology and can inform our ability to interpret results of animal studies. For dogs, cats, and horses, we compare the similarities in obesity pathophysiology to humans and review the genetic studies that have been previously reported in those species. Finally, we discuss how veterinary genetics may learn from humans about studying precise, nuanced phenotypes and implementing large-scale studies, but also how veterinary studies may be able to look past clinical findings to mechanistic ones and demonstrate translational benefits to human research.

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“…An estimated 34-59% of pet dogs in developed countries are overweight or obese [3,8,[88][89][90][91]. Multiple comorbidities are associated with canine obesity, most notably orthopaedic disease, exacerbation of breathing difficulties and urinary incontinence, along with significantly decreased life expectancy [92][93][94][95]. Canine obesity is associated with increased blood pressure, dyslipidaemia and insulin resistance and this has been characterised as 'obesity-related metabolic dysfunction'.…”

Section: Canine Obesity Geneticsmentioning

confidence: 99%

The Genetic Basis of Obesity and Related Metabolic Diseases in Humans and Companion Animals

Wallis

Raffan

2020

Preprint

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Obesity is one of the most prevalent health conditions in humans and companion animals across the world. Obesity is associated with multiple health conditions across species including premature mortality. It is therefore of importance across the fields of medicine and veterinary medicine. The regulation of body weight is a homeostatic process vulnerable to disruption by genetic and environmental factors. It is well established that the heritability of obesity is high in humans and laboratory animals, with ample evidence that the same is true in companion animals. In this review, we provide an overview of how genes link to obesity in humans, drawing on a wealth of information from laboratory animal models, and summarising the mechanisms by which obesity causes related disease. Throughout, we focus on how large-scale human studies and niche investigations of rare mutations in severely affected patients have improved our understanding of obesity biology and can inform our ability to interpret results of animal studies. For dogs, cats and horses, we review the similarities in obesity pathophysiology to humans and review those genetic studies that have been done to investigate them. Finally, we discuss how veterinary genetics may learn from humans about studying precise, nuanced phenotypes and implementing large-scale studies, but also how veterinary studies may be able to look past clinical findings to mechanistic ones and demonstrate translational benefits to human research.

show abstract

Lipid and metabolic profiles in female dogs with mammary carcinoma receiving dietary fish oil supplementation

Cited by 14 publications

References 60 publications

Pharmacokinetics of Carboplatin in Combination with Low-Dose Cyclophosphamide in Female Dogs with Mammary Carcinoma

Pharmacokinetics of Carboplatin in Combination with Low-Dose Cyclophosphamide in Female Dogs with Mammary Carcinoma

The Genetic Basis of Obesity and Related Metabolic Diseases in Humans and Companion Animals

The Genetic Basis of Obesity and Related Metabolic Diseases in Humans and Companion Animals

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