Diet is a modifiable risk factor for chronic disease and a potential modulator of telomere length (TL). The study aim was to investigate associations between diet quality and TL in Australian adults after a 12-week dietary intervention with an almond-enriched diet (AED). Participants (overweight/obese, 50–80 years) were randomised to an AED (n 62) or isoenergetic nut-free diet (NFD, n 62) for 12 weeks. Diet quality was assessed using a Dietary Guideline Index (DGI), applied to weighed food records, that consists of ten components reflecting adequacy, variety and quality of core food components and discretionary choices within the diet. TL was measured by quantitative PCR in samples of lymphocytes, neutrophils, and whole blood. There were no significant associations between DGI scores and TL at baseline. Diet quality improved with AED and decreased with NFD after 12 weeks (change from baseline AED + 9·8 %, NFD − 14·3 %; P < 0·001). TL increased in neutrophils (+9·6 bp, P = 0·009) and decreased in whole blood, to a trivial extent (–12·1 bp, P = 0·001), and was unchanged in lymphocytes. Changes did not differ between intervention groups. There were no significant relationships between changes in diet quality scores and changes in lymphocyte, neutrophil or whole blood TL. The inclusion of almonds in the diet improved diet quality scores but had no impact on TL mid-age to older Australian adults. Future studies should investigate the impact of more substantial dietary changes over longer periods of time.

The effect of body fat content on the protein metabolism of energy-restricted sheep has been studied in two experiments. In the first experiment, six Suffolk-cross wether sheep, three weighing about 39 kg and three of about 61 kg, were given progressively increasing amounts of casein-N from 0 to 3000 mg N/kg metabolic body weight (W0·75) daily with constant energy, 91 kJ/kg W0·75 daily, from a high-propionic acid mixture of volatile fatty acids (VFA). In the second experiment, two lean and two fat sheep of similar body weights were given progressively increasing amounts of casein with the same VFA mixture. All the animals attained a positive N balance when they were in negative energy balance. N balance was not affected by body fatness of the magnitude studied, although lean animals utilized increasing levels of standard VFA (acetate-propionate-butyrate 65:25:10, molar proportions) infusion for N accretion more efficiently than fat animals. Endogenous energy was utilized for protein accretion with an efficiency of 0·56. Supply of glucogenic VFA equivalent to 28 mmol glucose/kg W0·75 reduced fasting N excretion by 39%. Fasting heat production decreased from 335 to 300 kJ/kg W0·75 with the infusion of casein and glucogenic VFA. It is argued that fasting induces additional heat losses due to raised protein metabolism and is unsuited as a baseline for dietary assessment.

Dietary cholesterol induces hepatic inflammation and fibrosis in animals. We aimed to determine whether dietary cholesterol affects liver-related mortality in hepatitis C virus (HCV)-infected patients. We performed a retrospective cohort study using extended follow-up data from the Hepatitis C Antiviral Long-Term Treatment Against Cirrhosis Trial. The study included HCV patients with advanced fibrosis and compensated cirrhosis. The analysis included 657 patients who completed two FFQ. We assessed whether cholesterol intake, measured in mg/4184 kJ (mg/1000 kcal) of energy intake, was associated with liver-related death or transplantation. In 4·7 (sd 1·6) years, the incidence of liver-related death (n 46) or transplantation (n 52) was 31·8/1000 person-years. The relationship between cholesterol intake and liver-related death or transplantation was significantly different between men and women (test for interaction, P value=0·01). Each higher quartile of cholesterol intake was associated with an increased risk for liver-related death or transplantation in women (adjusted hazard ratio (AHR) 1·83; 95 % CI 1·12, 2·99; Ptrend=0·02), but not in men (AHR 0·96; 95 % CI 0·76, 1·22; Ptrend=0·73). Compared with women whose cholesterol intake was within the recommended guidelines (300 mg/d with a 8368 kJ (2000 kcal) diet), women who consumed more cholesterol had significantly increased risk for liver-related death or transplantation (AHR 4·04; 95 % CI 1·42, 11·5). High dietary cholesterol was associated with an increased risk for liver-related death and transplantation in HCV-infected women with advanced fibrosis or compensated cirrhosis. Future studies should assess whether reducing cholesterol intake, among women who consume an excessive amount, can decrease HCV-related mortality.

The ADP:O values in both cardiac and hepatic mitochondria have significantly decreased with an increase in protein level after 7, 14 and 21 d of feeding (Toyomizu et al. 1992). The present studies were undertaken to clarify tissue-specific effects of dietary protein levels on oxidative phosphorylation in the liver, kidney, skeletal muscles and small intestine and to characterize oxidative metabolism with diverse substrates in the liver. Chicks were fed on semi-purified diets of different protein levels (7, 25, 43 and 61% of metabolizable energy content) for 21 d. The responses of protein levels to oxidative phosphorylation showed tissue-dependency; although liver mitochondria of chickens fed on higher- protein diets exhibited reduced ADP:O values and state 3, neither changes in ADP:O value nor state 3 and state 4 rates were observed in the isolated mitochondria from kidney and skeletal muscles. Small intestinal mucosal mitochondria from chickens fed on a high (61%)-protein-energy diet showed significantly reduced ADP:O value and respiratory control ratio when compared with medium-protein- energy diets (25 and 43%). In liver mitochondria showing the most sensitive dependency to the levels of dietary protein, the ADP:O value decreased with increasing protein levels when pyruvate + malate- or glutamate-requiring complexes I, III and IV of the electron transport chain were used as substrates, but it did not change when succinate-requiring complexes II, III and IV or ascorbate + tetramethyl-p- phenylenediamine requiring complex IV was used. These results imply that impaired oxidative phosphorylation capacities with increasing dietary protein levels may be associated with functional damage to the respiratory chain for electron flow from NAD-linked substrates to the ubiquinone pool.

1. Weanling rats, aged 21 d, given a 40 g casein/kg diet for 25 d were compared with ‘age-matched’ controls given a 200 g casein/kg diet and with ‘weight-matched’ weanling controls.

2. The protein-malnourished rats demonstrated failure of weight gain and linear growth, hypoproteinaemia, hypoalbuminaemia and fatty liver.

3. Autoradiography of the tibia was carried out 24 h after intraperitoneal injection of Na235SO4 (0.1, 1.0, 2.0, 5, 10 μCi/g body-weight). Sections of tibia, humerus and costochondral junction were stained by haematoxylin and eosin, resorcin-crystal violet and picro-fuchsin, Alcian Blue at pH 0.1 and pH 2.5, Alcian Blue at pH 5.7 with magnesium chloride (0.1, 0.7, 1.0 m), and by Alcian Blue after ovine testicular hyaluronidase (EC 3.2.1.35) digestion. The width of the upper tibial epiphysis was measured and the histological and histochemical features of the epiphyses studied.

4. The incorporation of 35SO4 into the epiphyses of the protein-malnourished animals was markedly reduced. The chondrocytes were small and flattened with frequent pyknotic nuclei. The staining characteristics of the cartilagenous matrix was qualitatively similar in all animals. The epiphyses in malnutrition were found to be thin, all zones being affected. The upper tibial epiphyses (mean±sd; μm) were 202 ±46 for the protein-malnourished animals, 367±52 for age-matched controls and 578±40 for weight-matched controls.

5. The changes found resemble those after hypophysectomy and the possible hormonal factors are discussed.

1. The dietary requirements for protein and amino acids of the growing gosling (0–7 weeks) were calculated according to body composition, maintenance needs and the absorption rate of amino acids from feeds.

2. The diets were formulated by least-cost linear programming, using the calculated requirements for amino acids, with or without minimal glycine + serine requirements. The diets formulated without minimal requirements of glycine + serine were supplemented with various amounts of glycine, and fed to growing goslings.

3. The calculated requirements for protein and essential amino acids were lower than those suggested for growing broilers and turkeys. The requirements (g/MJ metabolizable energy) at 0–2, 2–4 and 4–7 weeks of age respectively, were: lysine 0·88, 0·48, 0·43; methionine + cystine 0·48, 0·38, 0·29; protein 14·5, 9·3, 7·6.

4. The goslings did not respond to glycine supplementation of the diet.

1. The effect of riboflavine deficiency on in vivo incorporation of [2–14C]glycine into proteins of liver homogenates and its subcellular fractions has been studied on rats maintained on a 16 % protein diet.

2. Riboflavine deficiency did not seem to affect the in vivo incorporation of [2–14C]g1ycine into proteins of liver homogenates. But riboflavine deficiency caused increased and reduced invivo incorporation of [14C]amino acid into mitochondrial and microsomal proteins, respectively.There was no significant change in the in vivo incorporation of [14C]amino acid into proteins ofnuclear, ribosomal and soluble fractions in riboflavine deficiency.

3. Riboflavine deficiency caused enhanced and reduced proportions of liver mitochondrial and microsomal proteins, respectively.

4. The results are discussed as suggestive of enhanced and reduced protein synthesis in the mitochondrial and microsomal fractions, respectively, of riboflavine-deficient rats.

1. Q-strain mice selected for high-line (QLF) or low-line (QSC) body-weights at 6 weeks of age were culled to litters of two or eight (QLF-2, QLF-8, QSC-2, QSC-8) at birth andwere suckled in these groups until 19 d of age.

2. Body-weights were measured daily for all groups and body compositions compared at birth and 19 and 42 d of age. Food intakes and urinary and faecal nitrogen were measured during metabolism trials between 19 and 42 d.

3. QLF-2 and QSC-2 mice grew faster than the corresponding groups of eight until 19 d of age. They also deposited more fat as a percentage of total gain.

4. In the period 19–42 d the influence of genetic selection reappeared and was manifest in a slowing of growth rates of QLF-2 and QSC-2 animals so that by 42 d of age therewere no differences in body-weight between the groups within a line.

5. During the period 19–42 d the total food intakes of each group within a line did not differ although, on the basis of food intake per unit metabolic body-weight (g/kg body-weight0.75 per d) QLF-2 and QSC-2 ate less food than QLF-8 and QSC-8respectively.

6. The differences in body-weight at 19 d between groups were largely overcome by the increased contribution of protein and water to the weight gain of the groups of eight duringthe post-weaning period.

1. Parenchymal cells were isolated from the liver of rats that had been deprived of dietary protein for 3 weeks.

2. The cells were two-thirds the diameter of those derived from livers of normal animals and consumed oxygen at a rate of 16.2±2.7 μl/h per 106 viable cells, half the normal value.

3. Albumin and transferrin were synthesized at rates of 0.94±0.12 and 0.60±0.07 μg/h per 106 viable cells respectively and urea at a rate of 0.77±0.12 μg/h per 106 cells. This represents a 25-50% decrease in the rates of synthesis measured in cells isolated from normal livers.

4. The results are discussed in relation to the long-term effects of malnutrition on liver cell function.