Paßlack N. et al. 2016
Dietary calcium (Ca) concentrations might affect regulatory pathways within the Ca and vitamin D metabolism and consequently excretory mechanisms. Considering large variations in Ca concentrations of feline diets, this study is focused on the physiological impact on Ca homeostasis.
Calcium (Ca) homeostasis in cats is hormonally regulated by calcitriol, parathyroid hormone (PTH) and calcitonin. In addition to these hormones, fibroblast growth factor 23 (FGF23) has also been recognized to affect Ca and phosphorus (P) metabolism. FGF23 increases renal P excretion, decreases gastrointestinal P absorption, downregulates PTH and decreases plasma calcitriol concentrations. In this way, not only calcitriol, but also plasma P concentrations are reduced by FGF23. It has been demonstrated that FGF23 is elevated in cats with chronic kidney disease, and increases with disease progression. In particular, FGF23 plasma concentrations are elevated in cats with CKD and associated azotemia and hyperphosphatemia.
The recommended allowance for dietary Ca in healthy adult cats is indicated with 2.9 g/kg dry matter (DM), assuming an energy density of 16.7 MJ metabolizable energy (ME)/kg. However, large variations in feline Ca intake can be supposed. On the one hand, commercial diets might differ from the recommendations. The European Pet Food Industry Federation (FEDIAF) recommends a minimum dietary Ca concentration of 10.0 g/kg DM, and the Association of American Feed Control Officials (AAFCO) indicates an adult maintenance minimum of 6.0 g Ca/kg DM for cats. On the other hand, home-prepared diets for companion animals can show nutritional imbalances and variations in Ca concentration
Experimental design
Ten healthy adult cats (European Shorthair, 5 neutered males, 5 intact females, 47 ± 17 months) of the cat colony of the Institute of Animal Nutrition, Freie Universität Berlin, received 6 experimental diets in 6 feeding periods. All cats were fed the same diet at the same time. The diets were formulated to fulfil the recommendations for adult cats. The Ca levels of the 6 experimental diets were: 0.6%, 0.8%, 1.5%, 1.9%, 2.2%, 2.4% (DM). For all experimental diets, the same premix with trace elements and vitamins was used, ensuring similar concentrations of these nutrients among the diets. The premix contained vitamin D3 as source of vitamin D. Dicalcium phosphate (CaHPO4) was used as dietary Ca source.
Blood:
Vitamin D3 as well as the vitamin D metabolites 1α,25(OH)2D3 and 24,25(OH)2D3 were not affected by increasing dietary Ca levels. The concentrations of wPTH, iPTH and FGF23 in the serum of the cats were not affected by the varying Ca concentrations in the diets. The experimental diets did not affect the hematological parameters of the cats.
Urine:
The urine volume increased up to a dietary Ca concentration of 1.9% and subsequently decreased in the groups 2.2–2.4% Ca. The fasting and postprandial urinary pH decreased with increasing levels of Ca in the diets, reaching values from 7.09/6.91 to 6.02/6.01. However, the urinary pH marginally increased up to 6.22/6.19 after feeding the diet 2.4% Ca. The urinary Ca concentrations were not affected by varying Ca levels in the diets. The renal Ca excretion was small and decreased at low dietary Ca levels (0.6% Ca and 0.8% Ca; the urinary oxalate (Ox) concentrations decreased from 174 mg/l to 126 mg/l with increasing dietary Ca levels; he citrate concentrations first decreased from 133 mg/l (0.6% Ca) to 31.4 mg/l (1.9% Ca), but then increased up to 111 mg/l (2.4% Ca).
Faeces:
The faecal DM content increased from 35.0% (0.6–0.8% Ca) to 45.8% (2.2% Ca) and moderately decreased to 43.6% after feeding the diet 2.4% Ca. The daily amount of faeces showed an increase from 8.00 g DM to 12.9 g DM with the higher levels of Ca in the diets.
The results of the present study could not demonstrate a decrease of PTH with increasing levels of dietary Ca. This difference between the previous and the present study might be explained by the different sources of dietary Ca or by the observed individual variations in the serum PTH concentrations of the cats in the present study. It is also interesting to notice that iPTH concentrations were partly lower when compared to wPTH concentrations.
The unaffected serum Ca and phosphate concentrations might also explain why FGF23 serum concentrations remained unchanged by varying dietary Ca concentrations. It has been demonstrated that hypercalcemia and hyperphosphatemia increase plasma FGF23 concentrations in mice and cats.
The divergence between urinary P concentration and urinary Ca concentration in the current study is probably ultimately a direct result of the uncoupling between the intestinal absorption of the two ions and might be an explanation for the marked effects of the diets on the urinary pH of the cats.
Higher intestinal Ca concentrations could be interesting with regard to CaOx urolith prevention. Recent studies from humans and dogs indicate that high dietary Ca concentrations could be advantageous, because of an intestinal complexation between Ca and Ox, lowering their intestinal absorption and renal excretion and therefore reducing the risk for the development of CaOx or other Ca containing crystals and stones. In the present study, urinary Ox concentrations were comparable when the diets with the low and moderate Ca levels (0.6– 1.5% Ca) were fed but decreased when feeding the high-Ca diets (1.9–2.4% Ca). Thus, it can be assumed that the hypothesis of an intestinal complexation between Ca and Ox in the case of high Ca levels in a diet could also apply to cats. However, it should be considered that the amounts of Ox are normally low in cat food, limiting its complexation with Ca in the intestine. Moreover, the demonstrated decrease of the urinary Ox concentrations with increasing dietary Ca levels was only moderate, indicating only a small risk reduction for the formation of feline CaOx uroliths by higher dietary Ca levels.
Conclusions
The present study demonstrated that the Ca excretion of cats is mainly regulated by changes in intestinal absorption and not via adjustment of renal excretion. Although the PTH and FGF23 concentrations in the blood of the cats were unaffected by increasing levels of dietary Ca, the observed decrease of the calcitriol precursors 25(OH)D2 and 25(OH)D3 indicates diet dependent hormonal control mechanisms. High dietary dicalcium phosphate levels were associated with a low urine pH. Future studies should investigate the physiological relevance of the acidifying effect in the feline organism.