Renal disease has a high incidence in cats, and some evidence implicates dietary P as well. To investigate this further, two studies in healthy adult cats were conducted. Study 1 (36 weeks) included forty-eight cats, stratified to control or test diets providing 1·2 or 4·8 g/1000 kcal (4184 kJ) P (0 or approximately 3·6 g/1000 kcal (4184 kJ) inorganic P, Ca:P 1·2, 0·6). Study 2 (29 weeks) included fifty cats, stratified to control or test diets, providing 1·3 or 3·6 g/1000 kcal (4184 kJ) P (0 or approximately 1·5 g/1000 kcal (4184 kJ) inorganic P, Ca:P 1·2, 0·9). Health markers, glomerular filtration rate (GFR) and mineral balance were measured regularly, with abdominal ultrasound. Study 1 was halted after 4 weeks as the test group GFR reduced by 0·4 (95 % CI 0·3, 0·5) ml/min per kg, and ultrasound revealed changes in renal echogenicity. In study 2, at week 28, no change in mean GFR was observed (P >0·05); however, altered renal echogenicity was detected in 36 % of test cats. In agreement with previous studies, feeding a diet with Ca:P <1·0, a high total and inorganic P inclusion resulted in loss of renal function and changes in echogenicity suggestive of renal pathology. Feeding a diet containing lower total and inorganic P with Ca:P close to 1·0 led to more subtle structural changes in a third of test cats; however, nephrolithiasis occurred in both diet groups, complicating data interpretation. We conclude that the no observed adverse effects level for total dietary P in adult cats is lower than 3·6 g/1000 kcal (4184 kJ), however the effect of inorganic P sources and Ca:P require further investigation.

Phosphorus is present in diets as naturally occurring P from raw materials or added as an inorganic salt. However, little is known about postprandial kinetics of P absorption in cats. Here, we describe several studies quantifying postprandial kinetics following the ingestion of diets of varying composition. Briefly, cats were fed a meal consisting of 50 % of their metabolic energy requirement in a randomised crossover design. A pre-meal baseline blood sample was taken via cephalic catheter and repeated measurements taken regularly up to 6 h post-meal to assess the whole blood ionised Ca, plasma P and parathyroid hormone concentrations. A diet containing 4·8 g total P/4184 kJ (1000 kcal), 3·5 g P from sodium dihydrogen phosphate (NaH2PO4)/4184 kJ (1000 kcal) and Ca:P 0·6 caused a marked increase in plasma P from baseline to a peak of 1·976 (95% CI 1·724, 2·266) mmol/l (P <0·001), whereas a diet containing 3·38 g total P/4184 kJ (1000 kcal), no added inorganic P and Ca:P 1·55 resulted in a postprandial decrease in plasma P (P = 0·008). Subsequent data indicate that added inorganic P salts in the diet above 0·5 g P/4184 kJ (1000 kcal) cause an increase in plasma P in cats, while diets below this do not. The data presented here demonstrate that sources of added inorganic P salts cause a temporary postprandial increase in plasma P in a dose-dependent manner, prolonged in diets with Ca:P <1·0. Dietary P derived from natural food ingredients (e.g. meat or vegetable matter) does not appear to have any effect on postprandial plasma P.

A charge made against feeding dry foods to cats is that the high carbohydrate (i.e. starch) content results in high blood glucose levels which over time may have detrimental health effects. The present study determined the post-meal concentrations of plasma glucose and insulin in adult cats (seven males and four females) and dogs (Labrador retrievers; four males and five females) fed dry diets with low-starch (LS), moderate-starch (MS) or high-starch (HS) levels. In a cross-over design with at least 7 d between the test meals, plasma glucose and insulin concentrations were measured following a single meal of a LS, MS and HS diet (209 kJ/kg bodyweight). Only the HS diet resulted in significant post-meal increases in plasma glucose concentration in cats and dogs although the time-course profiles were different between the species. In cats, plasma glucose concentration was significantly increased above the pre-meal concentration from 11 h until 19 h after the meal, while in dogs, a significant increase above baseline was seen only at the 7 h time point. Plasma insulin was significantly elevated in dogs 4 -8 h following the MS diet and 2-8 h after the HS diet. In cats, plasma insulin was significantly greater than baseline from 3-7 and 11-17 h after the HS diet. The time lag (approximately 11 h) between eating the HS diet and the subsequent prolonged elevation of plasma glucose concentration seen in cats may reflect metabolic adaptations that result in a slower digestive and absorptive capacity for complex carbohydrate.Key words: Feline: Canine: Glycaemia: Insulinaemia: CarbohydrateHaving evolved as a carnivore consuming a diet naturally high in animal protein and low in carbohydrate has contributed to the belief that feeding carbohydrates to cats (particularly through dry commercial pet foods in which the carbohydrate source is predominantly starch) is detrimental to the cat's health and may play a role in the pathogenesis of a number of feline disorders, most notably type 2 diabetes mellitus (DM). The mechanisms suggested to underlie the development of DM in cats fed high-carbohydrate diets include direct 'glucotoxic' effects (e.g. apoptosis of pancreatic b-cells) and gradual 'burnout' of pancreatic b-cells due to prolonged stimulation and insulin secretion in response to elevated plasma glucose concentration (1) .The carbohydrate content of manufactured dry cat foods varies widely, typically contributing between 25 and 50 % of the metabolisable energy of the diet, although, recently, dry diets with a carbohydrate content of 10 -15 % metabolisable energy have appeared on the market. The aim of the present study was to determine the post-meal profiles of plasma glucose and insulin concentrations in cats following a meal of a low-starch (LS) diet, a moderate-starch (MS) diet and a high-starch (HS) diet. A secondary aim was to carry out a species comparison of the glucose and insulin response to the same diets in dogs. Dogs also belong to the mammalian order Carnivora (but are not obligate carnivores like the...

Data from intravenous (i.v.) glucose tolerance tests suggest that glucose clearance from the blood is slower in cats than in dogs. Since different physiological pathways are activated following oral administration compared with i.v. administration, we investigated the profiles of plasma glucose and insulin in cats and dogs following ingestion of a test meal with or without glucose. Adult male and female cats and dogs were fed either a high-protein (HP) test meal (15 g/kg body weight; ten cats and eleven dogs) or a HP þ glucose test meal (13 g/kg body-weight HP diet þ 2 g/kg body-weight D-glucose; seven cats and thirteen dogs) following a 24 h fast. Marked differences in plasma glucose and insulin profiles were observed in cats and dogs following ingestion of the glucose-loaded meal. In cats, mean plasma glucose concentration reached a peak at 120 min (10·2, 95 % CI 9·7, 10·8 mmol/l) and returned to baseline by 240 min, but no statistically significant change in plasma insulin concentration was observed. In dogs, mean plasma glucose concentration reached a peak at 60 min (6·3, 95 % CI 5·9, 6·7 mmol/l) and returned to baseline by 90 min, while plasma insulin concentration was significantly higher than pre-meal values from 30 to 120 min following the glucose-loaded meal. These results indicate that cats are not as efficient as dogs at rapidly decreasing high blood glucose levels and are consistent with a known metabolic adaptation of cats, namely a lack of glucokinase, which is important for both insulin secretion and glucose uptake from the blood.

Although the implications of long-term high Ca intakes have been well documented in growing dogs, the health consequences of Ca excess in adult dogs remain to be established. To evaluate the impact of feeding a diet containing 7·1 g/4184 kJ (1000 kcal) Ca for 40 weeks on Ca balance and health parameters in adult dogs, eighteen neutered adult Labrador Retrievers, (nine males and nine females) aged 2·5-7·4 years were randomised to one of two customised diets for 40 weeks. The diets were manufactured according to similar nutritional specifications, with the exception of Ca and P levels. The diets provided 1·7 and 7·1 g/4184 kJ (1000 kcal) (200(SD26) and 881(SD145) mg/kg body weight0·75 per d, respectively) Ca, respectively, with a Ca:P ratio of 1·6. Clinical examinations, ultrasound scans, radiographs, health parameters, metabolic effects and mineral balance were recorded at baseline and at 8-week intervals throughout the study. Dogs in both groups were healthy throughout the trial without evidence of urinary, renal or orthopaedic disease. In addition, there were no clinically relevant changes in any of the measures made in either group (all P>0·05). The high-Ca diet resulted in a 3·3-fold increase in faecal Ca excretion (P0·05). Ca intakes of up to 7·1 g/4184 kJ (1000 kcal) are well tolerated over a period of 40 weeks, with no adverse effects that could be attributed to the diet or to a high mineral intake.