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1. The kinetics of glucose metabolism were evaluated in rats deprived of food 15-21 h after the administration of hypoglycaemic doses of hypoglycin (100 mg/kg body wt.) by following changes in the specific radioactivities of 14C and 3H in blood glucose after an intravenous dose of [U-14C,2-3H]glucose [Katz, Rostami & Dunn (1974) Biochem. J. 142, 161-170]. 2. During this time, recycling of glucose through the Cori cycle was virtually abolished, the rate of irreversible disposal of glucose and its total body mass were both decreased by about 70%, whereas there was little effect on the mean transit time for glucose. 3. It was concluded that hypoglycaemia is due to inhibition of gluconeogenesis.

The view that genetic selection for carcass yield has limited the size of the gastrointestinal tract (GIT) of modern broilers has sparked concerns that their capacity to cope with energy dilution or bulk is also limited. We investigated the capacity of male Ross 308 broilers to deal with increasing levels of bulk and aimed to identify a feed bulk dimension responsible for limiting feed intake (FI). About 528 day-old broilers were allocated to 48 pens and offered a common starter feed until day 8, and 1 of 7 feeds from day 8 to 36 of age: a basal control (B), which was diluted to 3 levels (15, 30, or 45%) with either oat hulls (OH) or sugar beet pulp (SBP). Feed intake was measured daily and birds were dissected for GIT measurements at day 15, 22, and 36. Feed intake increased in birds offered OH15 (135 g/d), OH30 (140 g/d), and SBP15 (138 g/d) compared with birds offered the B feed (106 g/d; SEM 2.4). By increasing FI, birds were able to compensate for the lower energy content of their feeds. The greatest increase in FI was seen on OH30: its energy content (2,273 kcal/kg) was 26% lower than the B feed (3,081 kcal/kg). There was evidence of adaptation on the bulky feeds, as during the last week only birds on SBP45 were limited in FI and performance. The relative weights of the GIT were greater in the SBP than OH series, suggesting that the former needed to accommodate a higher bulk intake. For the OH series the increase in the relative GIT weights was confined to the gizzard and small intestine; whereas for the SBP series, the increase was extended to proventriculus and large intestine. Because only SBP45 was limiting FI, we were unable to identify a bulk dimension to be used to predict FI. Our data reject the suggestion that modern broilers have a reduced ability to cope with reductions in feed energy content.

In 2 experiments, we investigated whether diet composition plays a role in pathogen-induced anorexia, the voluntary reduction in ADFI during infection in broilers. We hypothesized that either energy or CP dietary content could influence the extent of anorexia in Ross 308 broilers and infection outcomes with Eimeria maxima . From d 13 of age, half of the birds were infected, and half were uninfected. ADFI was measured daily, and BW every 3 d until d 29. Oocyst excretion was measured daily from d 17 to 23. The impact of parasitism on the small intestine was assessed on d 19 and 25. In Experiment 1, 336 birds were offered diets progressively diluted with lignocellulose, starting from a diet with 3,105 (kcal ME/kg) and 20% CP. There was a significant interaction between infection and diet on ADFI during the acute stage of infection (d 17 to 21): for control birds diet dilution decreased ADFI and consequently reduced energy and CP intake. For infected birds, diet dilution increased ADFI, leading to the same energy and CP intake across diets. Oocyst excretion and villi length to crypt depth ratio ( VCR ) were constant across infected treatments. In Experiment 2, 432 birds were offered diets with constant ME (3,105 kcal/kg), but different CP contents (24, 20, 26, and 12%). Infection significantly reduced ADFI. Although there was no interaction between infection and diet on ADFI, there was an interaction on CP intake during the acute stage of infection. Infected birds on the 20% CP diet achieved the same CP intake as uninfected birds. There were no differences in the VCR and ADG of the infected birds on 24, 20 and 16% CP treatments, but birds on 12% had the lowest ADG and excreted more oocysts. We suggest that during infection, birds target a nutrient resource intake, which appears to be beneficial for infection outcomes, while at the same time they avoid excess protein intake. We conclude that different mechanisms regulate ADFI in infected and uninfected birds.

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Holland et al. (1973) reported that diphenyleneiodonium causes hypoglycaemia in rats by impairing gluconeogenesis secondarily to inhibition of NADH oxidation in liver mitochondria, rather than as a consequence of its ability to catalyse an exchange of C1