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.

Sodium in feline nutrition.

High sodium levels in cat food have been controversial for a long time. Nonetheless, high sodium levels are used to enhance water intake and urine volume, with the main objective of reducing the risk of urolithiasis. This article is a review of current evidence of the putative risks and benefits of high dietary sodium levels. Its secondary aim is to report a possible safe upper limit (SUL) for sodium intake. The first part of the manuscript is dedicated to sodium physiology, with a focus on the mechanisms of sodium homeostasis. In this respect, there is only few information regarding possible interactions with other minerals. Next, the authors address how sodium intake affects sodium balance; knowledge of these effects is critical to establish recommendations for sodium feed content. The authors then review the consequences of changes in sodium intake on feline health, including urolithiasis, blood pressure changes, cardiovascular alterations and kidney disease. According to recent, long-term studies, there is no evidence of any deleterious effect of dietary sodium levels as high as 740 mg/MJ metabolizable energy, which can therefore be considered the SUL based on current knowledge.

Nanoparticle Tracking Analysis for the Enumeration and Characterization of Mineralo-Organic Nanoparticles in Feline Urine.

Urinary stone disease, particularly calcium oxalate, is common in both humans and cats. Calcifying nanoparticles (CNP) are spherical nanocrystallite material, and are composed of proteins (fetuin, albumin) and inorganic minerals. CNP are suggested to play a role in a wide array of pathologic mineralization syndromes including urolithiasis. We documented the development of a clinically relevant protocol to assess urinary CNP in 9 healthy cats consuming the same diet in a controlled environment using Nanoparticle Tracking Analysis (NTA®). NTA® is a novel method that allows for characterization of the CNP in an efficient, accurate method that can differentiate these particles from other urinary submicron particulates. The predominant nanoscale particles in feline urine are characteristic of CNP in terms of their size, their ability to spontaneously form under suitable conditions, and the presence of an outer layer that is rich in calcium and capable of binding to hydroxyapatite binders such as alendronate and osteopontin. The expansion of this particle population can be suppressed by the addition of citrate to urine samples. Further, compounds targeting exosomal surfaces do not label these particulates. As CNP have been associated with a number of significant urologic maladies, the method described herein may prove to be a useful adjunct in evaluating lithogenesis risk in mammals.

Short term effects of increasing dietary salt concentrations on urine composition in healthy cats.

High dietary salt (NaCl) concentrations are assumed to be beneficial in preventing the formation of calcium oxalate (CaOx) uroliths in cats, since increased water intake and urine volume have been observed subsequent to intake. In human beings, dietary NaCl restriction is recommended for the prevention of CaOx urolith formation, since high NaCl intake is associated with increased urinary Ca excretion. The aim of the present study was to clarify the role of dietary NaCl in the formation of CaOx uroliths in cats. Eight cats received four diets that differed in Na and Cl concentrations (0.38-1.43% Na and 0.56-2.52% Cl dry matter, DM). Each feeding period consisted of a 21 day adaptation period, followed by a 7 day sampling period for urine collection. Higher dietary NaCl concentrations were associated with increased urine volume and renal Na excretion. Urinary Ca concentration was constant, but renal Ca excretion increased from 0.62 to 1.05 mg/kg bodyweight (BW)/day with higher dietary NaCl concentrations (P ≤ 0.05). Urinary oxalate (Ox), citrate, P and K concentrations decreased when NaCl intake was high (P ≤ 0.05), and urinary pH was low in all groups (6.33-6.45; P > 0.05). Relative supersaturation of CaOx in the urine was unaffected by dietary NaCl concentrations. In conclusion, the present study demonstrated several beneficial effects of high dietary NaCl intake over a relatively short time period. In particular, urinary Ca concentration remained unchanged because of increased urine volume. Decreased urinary Ox concentrations might help to prevent the formation of CaOx uroliths, but this should be verified in future studies in diseased or predisposed cats.