Associations between birth weight and CVD in adult life are supported by experiments showing that undernutrition in fetal life programmes blood pressure. In rats, the feeding of a maternal low-protein (MLP) diet during gestation programmes hypertension. The present study aimed to assess the potential for a nutritional insult to impact across several generations. Pregnant female Wistar (F 0 ) rats were fed a control (CON; n 10) or MLP (n 10) diet throughout gestation. At delivery all animals were fed a standard laboratory chow diet. At 10 weeks of age, F 1 generation offspring were mated to produce a second generation (F 2 ) without any further dietary change. The same procedure produced an F 3 generation. Blood pressure in all generations was determined at 4, 6 and 8 weeks of age and nephron number was determined at 10 weeks of age. F 1 generation MLP-exposed offspring exhibited raised (P,0·001) systolic blood pressure (male 143 (SEM 4) mmHg; female 141 (SEM 4) mmHg) compared with CON animals (male 132 (SEM 3) mmHg; female 134 (SEM 4) mmHg). Raised blood pressure and reduced nephron number was also noted in the F 2 generation (P, 0·001) and this intergenerational transmission occurred via both the maternal and paternal lines, as all three possible offspring crosses (MLP £ CON, CON £ MLP and MLP £ MLP) were hypertensive (132 (SEM 3) mmHg) compared with CON animals (CON £ CON; 123 (SEM 2) mmHg). No effect was noted in the F 3 generation. It is concluded that fetal protein restriction may play a critical role in determining blood pressure and overall disease risk in a subsequent generation.

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A second examination by retroflexion in the proximal colon did not increase the calculated miss rate relative to that performed by a forward view examination. These results do not support the addition of routine right colon retroflexion to colonoscopy.

Methionine, an essential sulphur-containing amino acid (SAA), plays an integral role in many metabolic processes. Evidence for the methionine requirements of adult dogs is limited, and we employed the indicator amino acid oxidation (IAAO) method to estimate dietary methionine requirements in Labrador retrievers (n 21). Using semi-purified diets, the mean requirement was 0·55 (95 % CI 0·41, 0·71) g/4184 kJ. In a subsequent parallel design study, three groups of adult Labrador retrievers (n 52) were fed semi-purified diets with 0·55 g/4184 kJ (test diet 1), 0·71 g/4184 kJ (test diet 2) or 1·37 g/4184 kJ (control diet) of methionine for 32 weeks to assess the long-term consequences of feeding. The total SAA content (2·68 g/4184 kJ) was maintained through dietary supplementation of cystine. Plasma methionine did not decrease in test group and increased significantly on test diet 1 in weeks 8 and 16 compared with control. Reducing dietary methionine did not have a significant effect on whole blood, plasma or urinary taurine or plasma N-terminal pro B-type natriuretic peptide. Significant effects in both test diets were observed for cholesterol, betaine and dimethylglycine. In conclusion, feeding methionine at the IAAO-estimated mean was sufficient to maintain plasma methionine over 32 weeks when total SAA was maintained. However, choline oxidation may have increased to support plasma methionine and have additional consequences for lipid metabolism. While the IAAO can be employed to assess essential amino acid requirements, such as methionine in the dog using semi-purified diets, further work is required to establish safe levels for commercial diet formats.