More than one-third of humans and companion dogs in Western societies are overweight or obese. In people, vitamin D deficiency is widespread and associated with obesity, a now recognised inflammatory state. Low vitamin D status occurs in dogs with inflammatory conditions, but its relationship with obesity has not been investigated. In otherwise healthy privately owned adult dogs of ideal body condition (control, n 7) and dogs with overweight to obese body condition (treatment, n 8), serum 25-hydroxyvitamin D (25(OH)D) concentration and body composition as inferred from 2H-labelled water dilution space were evaluated. Subsequently, the dogs were transitioned to a commercial canine therapeutic weight-loss diet; control dogs were fed to maintain body weight and treatment dogs were energy-restricted to achieve a safe weight-loss rate. Thereafter, serum 25(OH)D concentration was re-evaluated 8 weeks after diet transition, and at the study end, which was 6 months or when ideal body condition was achieved. At study end, body composition analysis was repeated. Initial body condition scores and percentage body fat were positively correlated (ρ = 0·891; P < 0·001). However, percentage body fat and serum 25(OH)D concentration were not significantly correlated. Final serum 25(OH)D concentrations were greater (P < 0·05) than initial concentrations for control and treatment groups, indicating a diet but not weight-loss effect on vitamin D status. These findings suggest that vitamin D status of dogs is not affected by obesity or loss of body fat with therapeutic weight reduction.

For purely hypertrophic muscle it is postulated that the growth rate in number of nuclei is proportional to the cytoplasmic mass per nucleus multiplied by a growth constraining supplementary function. Growth constraint depends on the distance from any one of the limit number of nuclei, the limit muscle mass or the limit cytoplasmic mass per nucleus. Furthermore, theory and evidence are presented for a power (allometric) relationship between total number of nuclei (n) and muscle mass (m) given by the equation n = gmh. Evidence points to two clusters of values for h, one in the vicinity of h = 2/3 and the other h = 1/2. Both may depend on a linear relationship between number of nuclei inside muscle fibre and fibre cross-sectional area. The difference between the two situations can be derived from basic assumptions on either local or systemic diffusion mediated control of the number or division of satellite cell nuclei, leading directly to values of h either equal to 2/3 or V2. For likely values of h and suitable choices of growth constraints, almost all well known growth functions in the literature are derived as potentially applicable to total number of nuclei, or muscle mass or their ratio. Muscle mass growth will show a sigmoidal form for h = 1. This explains sigmoidal growth in body mass as it is mostly dominated by muscle mass. A possible linear growth phase before maturity is explicable from the cessation of either length (h = 1) or nuclear (h = 0) growth in muscle fibres, while cytoplasmic growth continues to maturity. Furthermore, two rat examples indicate that whole body protein growth can be described by the equations derived for muscle mass growth.

The effect of energy supply on physical composition of body weight gain between 45 and 100 kg was studied in Large White castrated males (cLW), crossbred Pietrain × Large White castrated males (cPPX) and boars (bPPX). The pigs were either given food ad libitum and kept in individual pens in experiment 1, or allocated to four energy levels (0·70, 0·80, 0·90, and 1·00 ad libitum) and kept in metabolism cages in experiment 2. Daily protein supplies were calculated to be the same at the four energy levels within each type of pig and non-limiting for growth. Five additional animals for each type of pig were slaughtered at 45 kg. Daily tissue gain was measured according to the comparative slaughter technique. The daily lean gain increased with metabolizable energy (ME) intake according to a linear-plateau relationship whereas the daily fat gain increased linearly. The type of pig significantly affected the slope of the relationship between lean gain and ME intake (from 15 to 22 g per extra MJ ME) but not the slope of the relationship between fat gain and ME intake (10 g per extra MJ ME on average). Increased energy intake was associated with increased fatness of body-weight gain, which was higher in cLW and cPP× than in bPP×.

The performance of 273 Hereford calves from lines previously selected for lean growth rate (LGR) or lean food conversion efficiency (LFCR), on a concentrate diet, was evaluated on a grassland diet over a period of 3 years. Both bull and heifer calves were tested, and each year the performance test ran from the 1st week of May (average age of 233 days) until the 1st week of October. Carcass lean content was predicted from body weight and ultrasonic backfat depth, and lean gain was calculated from the product of live-weight gain and predicted carcass lean content. The LGR line was superior to the control (C) line for live-weight gain on test, lean gain on test and lean gain from birth until the end of test. The LFCR line performed similarly to the C line for live-weight gain on test and lean gain on test, but was inferior for total lean gain. For lean gain on test, the proportional differences between the lines were similar to those predicted from parental breeding values for LGR, but they were smaller for total lean gain. The lines did not differ significantly for either fat depth or predicted carcass lean content.

Heritabilities were high for all growth traits, e.g. 0·52 (s.e. 0·17), 0·54 (s.e. 0·17) and 0·59 (s.e. 0·17) for live-weight gain on test, lean gain on test and total lean gain, but lower for fat depth and carcass lean content, 0·25 (s.e. 0·17) and 0·14 (s.e. 0·16), respectively. Genetic correlations with LGR, measured on a concentrate diet, were 0·57 for lean gain on test and 0·56 for total lean gain. If only males were considered, these correlations rose to 0·80 and 0·70, respectively. Coheritabilities between the two environments for lean growth were close to 0·3. It is concluded that although there is some evidence for genotype × environment and genotype × sex interactions, selection for lean growth on a concentrate regimen will still be effective in improving grassland performance.

The performance of Hereford × Friesian calves sired by Hereford bulls selected for either lean growth rate (LGR) or lean food conversion ratio (LFCR), or by unselected Hereford bulls, was evaluated on 327 calves on three farms over 2 years. Animals started test at 130 days of age on average and remained on test for approximately 300 days, whereupon all animals were slaughtered and carcass dissections were undertaken. Individual food intake was measured on tioo of the farms (189 animals), but only intake per pen of animals was measured on the third farm and individual food intake had to be estimated. LGR, LFCR and other traits describing performance were calculated from the growth, food intake and carcass composition data.

If no breed or environment interactions exist it is expected that proportionately 0-5 of the genetic differences between selected and control line bulls would be transmitted to their offspring. For the LGR and LFCR line bulls these values were 0·38 and 0·44, respectively, however the LGR value had a much smaller confidence interval. Genetic correlations derived from regressing breeding values predicted from offspring performance on breeding values predicted from the bulk's own performance in the selection experiment were 0·62 (s.e. 0·28) and 0·96 (s.e. 0·28) for LGR and LFCR, respectively. Heritabilities were: live-weight gain on test, 0·27; daily gain, 0·48; food intake, 0·06; food conversion ratio, 0·46; predicted carcass lean content, 0·10; killing-out proportion, 0·10; LGR, 0·36 and LFCR, 0·48.

Correlated responses in two lines of Hereford cattle selected for lean growth rate (LGR) from birth to 400 days of age and lean food conversion ratio (LFCR) from 200 to 400 days of age for a period of 8 years were evaluated. Correlated changes were estimated by two methods: deviation of selected lines from a control line and restricted maximum likelihood. Generally, estimates from the two methods were similar but tended to be more precise for the latter. Statistically significant correlated responses occurred in growth rate in the LGR line and in lean proportion and food conversion ratio in both selected lines. Selection for LGR was accompanied by increases in body weight at various ages in both male and female progeny. In the LFCR line there were little or no changes in body weight for male calves but some increases at certain ages for female progeny. There were no adverse correlated responses detected in reproductive traits such as calving difficulty and calving and pre-weaning mortality.

Selection of bulls for rate and efficiency of lean gain was studied in a herd of Hereford cattle. There were two selection lines, one selected for lean growth rate (LGR) from birth to 400 days and the other for lean food conversion ratio (LFCR) from 200 to 400 days of age, for a period of 8 years. A control line bred by frozen semen from foundation bulls was also maintained. Generation interval was about 2·4 years and average male selection differentials, per generation were 1·2 and — 1·1 phenotypic standard deviation units for LGR and LFCR respectively.

Genetic parameters and responses to selection were estimated from the deviation of the selected lines from a control line and by restricted maximum likelihood (REML) techniques on the same material. Realized heritabilities were 0·40 (s.e. 0·12) for LGR and 0·40 (s.e. 0·13) for LFCR using the control line. Corresponding estimates from REML were 0·42 (s.e. 0·10) and 0·37 (s.e. 0·14). The estimate of the genetic correlation between LGR and LFCR was about — 0·69 (s.e. 0·12) using REML.

The estimates of direct annual genetic change using deviations from the control were 3·6 (s.e. 1·3) g/day for LGR and — 0·14 (s.e. 0·07) kg food per kg lean gain for LFCR. Corrsponding estimates from REML were similar but more precisely estimated. The correlated responses for LFCR in the LGR line was higher than the direct response for LFCR.