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Biomedical subjects

A A Jackson

Publications and source records attributed to A A Jackson.

At least 145 records · Page 8Linked to original sources
PubMed1990

The interaction of vitamin A deficiency and rotavirus infection in the mouse.

Weanling mice were fed on a control diet ad lib., a vitamin A-deficient diet ad lib. or pair-fed to the intake of the vitamin A-deficient group. Vitamin A deficiency was induced by 63-70 d of age. On day 77 mice were given 30 microliters rotavirus/mouse orally and examined histologically 1 week later. There were no changes in relative liver weight in any of the groups, but following infection animals deficient in vitamin A showed a significant increase in spleen weight compared with the other groups. The relative weight of the thymus was reduced by vitamin A deficiency, in both non-infected and infected animals. The histology of the spleen, thymus and small intestine was similar in all three dietary groups before infection. The number of goblet cells per duodenal villus in vitamin A-deficient animals was significantly lower than that of control and pair-fed animals. In the small intestine of vitamin A-deficient animals, rotavirus infection caused dramatic changes to the mucosa, with almost complete destruction of the tips of the villi, but control and pair-fed animals had normal villi. It is concluded that although rotavirus infection and vitamin A-deficiency cause few changes alone, in their action together there is significant destruction of the mucosal barrier of the small intestine.

Animals↗
PubMed1990

Protein turnover and thermogenesis in response to high-protein and high-carbohydrate feeding in men.

The rates of energy expenditure and wholebody protein turnover were determined during a 9-h period in a group of seven men while they received hourly isocaloric meals of high-protein (HP) or high-carbohydrate (HC) content. Their responses to feeding were compared with those to a short period of fasting (15-24 h). The 9-h thermic response to the repeated feeding of HP meals was found to be greater than that to the HC meals (9.6 +/- 0.6% vs 5.7 +/- 0.4% of the energy intake, respectively, means +/- SEM, p less than 0.01). The rate of whole-body nitrogen turnover over 9 h increased from 17.6 +/- 2.2 g on the fasting day to 27.4 +/- 1.4 g during HC feeding (NS) and there was a further increase to 58.2 +/- 5.3 g resulting from HP feeding (p less than 0.001). By using theoretical estimates (based upon ATP requirements) of the metabolic cost of protein synthesis, 36 +/- 9% of the thermic response to HC feeding and 68 +/- 3% of the response to HP feeding could be accounted for by the increases in protein synthesis compared with the fasting state.

Adult↗
PubMed1990

Excessive faecal losses of vitamin A (retinol) in cystic fibrosis.

Vitamin A (retinol) deficiency is a recognised complication of cystic fibrosis and is presumed to be a consequence of an impairment in the digestion and absorption of dietary fats. The dietary intake of fat and retinol was assessed from a seven day weighed food intake in 11 subjects with cystic fibrosis and 12 matched controls. Faecal excretion of retinol and fat were measured from three day stool collections. There was little difference between the two groups in the intake of fat or retinol equivalents. When studied the subjects with cystic fibrosis were clinically stable and the apparent absorption of fat was not significantly different to that in the controls. There was a significant increase in the faecal losses of retinol in cystic fibrosis, which was unrelated to the degree of fat in the stool. In cystic fibrosis the median retinol recovered in the stool was 40% of the intake, compared with 1.8% in the controls. It is concluded that there is a specific defect in the handling of retinol by the gastrointestinal tract in cystic fibrosis, which may be unrelated to the digestion and absorption of dietary fat.

Adolescent↗
PubMed1990

15N-urea metabolism in the functioning human colon: luminal hydrolysis and mucosal permeability.

The biopsy channel of the colonoscope was used in a novel approach to the study of in vivo colonic nitrogen metabolism in 12 subjects. A tracer dose of 15N15N-urea was placed in the caecum in six and distal to the splenic flexure in six. The urine and stool were collected for 72 hours and isotopic enrichment was measured in a mass spectrometer. A similar proportion of the dose was recovered in the urine as 15N15N-urea from the right colon, 6%, as was recovered from the left, 4%, showing that the urea was absorbed intact. Urinary 15N14N-urea from the right colon was 18% of the dose compared to 13% from the left colon. This represents urea that has been hydrolysed and absorbed as ammonia. Less than 4% of the dose was recovered in the stool. The greatest proportion of the label, 74% from the right and 82% from the left, could not be accounted for in the urine or the stool and is presumed to have entered the metabolic pool of nitrogen. We conclude that; the colon is permeable to urea, intraluminal hydrolysis occurs and that urea nitrogen enters the metabolic pool of nitrogen in functionally significant quantities.

Adult↗
PubMed1990

Effect of undernutrition on the immune response to rotavirus infection in mice.

The effect of moderate and severe undernutrition on the immune response to EDIM rotavirus was studied in mice. A moderate state of undernutrition was produced by feeding weanling mice either 15 or 30% less diet than the control group had eaten on the previous day, for 7 weeks. After 6 weeks, mice were given 30 microliters/mouse of EDIM rotavirus orally and the antibody production was measured 1 week later. The delayed-type hypersensitivity (DTH) response to picryl chloride (PC) was measured as an index of cell-mediated immunity. For severe undernutrition, weanling mice were fed either 30 or 50% less diet than the control group had eaten on the previous day, for 12 weeks. After 11 weeks of feeding, animals were given 30 microliters/mouse of EDIM rotavirus either orally or intramuscularly and the antibody production was measured 1 week later. In moderate undernutrition, the serum antibody levels specific to rotavirus and the DTH response to PC were normal in all dietary groups compared with the control group. In severe undernutrition, the antibody levels following oral challenge of rotavirus were similar in all dietary groups. There was a significant impairment of serum antibody levels following intramuscular challenge in the group fed 50% less than the control group. It is concluded (1) that a balanced reduction in food intake does not impair the immune response, unless severe restriction is maintained for a long period of time, and (2) that the antibody response varies with the route of immunization.

Animals↗
PubMed1990

Excessive excretion of 5-oxoproline and decreased levels of blood glutathione in type II diabetes mellitus.

Levels of blood glutathione (GSH) were measured in 26 type II diabetes mellitus patients compared to 36 controls. Total blood GSH did not differ significantly between the two groups (mean +/- s.d., 8.0 +/- 1.5 vs. 7.7 +/- 1.3 mmol/g Hb, respectively); however reduced GSH was lowered in diabetes mellitus (5.0 +/- 1.0 vs. 5.8 +/- 1.0 mmol/gHb; P = 0.01), whereas oxidized GSH was increased (0.4 +/- 0.2 vs. 0.2 +/- 0.1 mmol/gHb; P = 0.001). Urinary excretion of 5-oxoproline was excessive in the diabetic patients (14.5 +/- 9.9 vs. 3.8 +/- 1.4 mmol/24 h; P = 0.004), and was positively correlated with levels of glycosylated haemoglobin (r = 0.69; P less than 0.01).

Adult↗
PubMed1989

Whole body protein turnover and resting metabolic rate in homozygous sickle cell disease.

1. Whole body protein turnover and resting metabolic rate were measured in six adults with homozygous sickle cell disease (genotype HbSS) and in six normal adults (genotype HbAA) of similar age. 2. Turnover was measured with prime/intermittent oral doses of [15N]glycine over 18 h and resting energy expenditure was measured by indirect calorimetry. 3. In HbSS, nitrogen flux (0.9 +/- 0.08 g day-1), protein synthesis (6.0 +/- 0.5 g day-1 kg-1) and protein degradation (5.6 +/- 0.5 g day-1 kg-1) were significantly increased compared with HbAA nitrogen (flux 0.5 +/- 0.02 g day-1 kg-1, protein synthesis 3.2 +/- 0.2 g day-1 kg-1 and protein degradation 2.8 +/- 0.2 g day-1 kg-1). 4. Resting energy expenditure was significantly higher in HbSS compared with HbAA when expressed per unit of body weight (115 +/- 3 and 94 +/- 4 kJ day-1 kg-1, respectively) or weight 0.75(317 +/- 6 and 269 +/- 8 kJ day-1 kg-0.75, respectively). 5. The increase in protein turnover and energy expenditure suggest that patients with HbSS exist in a hypermetabolic state that requires greater dietary energy compared with HbAA.

Adult↗
PubMed1989

The excretion of 5-oxoproline in urine, as an index of glycine status, during normal pregnancy.

The urinary excretion of 5-oxoproline, which may be used as an index of glycine status, was investigated in 30 normal pregnant women during different stages of pregnancy and in 18 non-pregnant female volunteers. During an 18-h study there was little variation in the 5-oxoproline/creatinine index, and a single sample gave a representative value. The excretion of 5-oxoproline/creatinine (mumol/mmol) rose progressively as pregnancy advanced (non-pregnant mean 10, SD 5, first trimester mean 46, SD 12, second trimester mean 150, SD 180, and third trimester mean 280, SD 320) and by the third trimester was over 20 times greater than in non-pregnant women. The data suggest that as pregnancy advances the endogenous production of glycine may be insufficient to satisfy the increasing demands.

Female↗
PubMed1988

In vivo metabolism of nitrogen precursors for urea synthesis in the postprandial rat.

(1) Adult postprandial rats were given a continuous, intravenous infusion of 15N-labelled glutamate, alanine, ammonium chloride and glutamine amide for 6 h. The enrichment in the free hepatic pool was measured for ammonia, glutamine amide, urea, aspartate, glutamate and alanine. (2) Glutamine and glutamate supplied significantly more nitrogen to urea than ammonium chloride or alanine. (3) Glutamate was not a significant source of hepatic ammonia, hence in this situation it is not necessary to impute a major role to glutamate dehydrogenase in hepatic ammoniagenesis for urea synthesis. (4) Glutamine and ammonia, mostly of intestinal origin in the postprandial state, were major precursors of hepatic ammonia. (5) The nitrogen of glutamate and alanine moved to urea primarily through aspartic acid.

Alanine↗
PubMed1988

Urea kinetics in adults with homozygous sickle cell disease.

The kinetics of urea metabolism were measured in four adults with homozygous sickle cell disease (HbSS). On a dietary intake of 1.2 to 2.7 g protein/kg/d the rate of urea production was 188 to 277 mg nitrogen/kg/d. A relatively small proportion of the urea was excreted in the urine (40 per cent), with a high fixed rate of hydrolysis in the bowel, 145 mg nitrogen/kg/d. Although 50 per cent of the nitrogen from hydrolysed urea was resynthesized to urea, and a further 10 per cent may have been lost in the stool, it is estimated that 58 mg nitrogen/kg/d was available for synthetic metabolic activity. Urea kinetics in sickle cell disease subjects are markedly different from normals, and this may be a reflection of the metabolic demands for increased red cell synthesis.

Adult↗
PubMed1987

Urinary excretion of 5-oxoproline (pyroglutamic aciduria) as an index of glycine insufficiency in normal man.

1. The evidence is accumulating to suggest that glycine, the simplest amino acid, is conditionally essential in man. Benzoic acid, by conjugation with glycine to form hippuric acid, is known to deplete the free glycine pool of the body. Glycine is one substrate for the enzyme glutathione synthase (EC 6.3.2.3) and in the inborn error of metabolism in which glutathione synthase function is defective, increased quantities of 5-oxoproline are excreted in the urine. 2. An oral dose of 4-10 g sodium benzoate was given to six normal adults to deplete the metabolic pool of glycine, and the urinary excretion of 5-oxoproline was followed for 6 h. In five of the six, a significant increase in the urinary 5-oxoproline was seen within 3 h. 3. These findings show that 5-oxoprolinuria can result from limited glycine availability, and may provide a useful test for assessing glycine sufficiency in a range of physiological and pathological states.

Adult↗
PubMed1987

Whole-body protein turnover in man determined in three hours with oral or intravenous 15N-glycine and enrichment in urinary ammonia.

Studies were carried out in eight normal adults to simplify the continuous infusion-end product method for measuring whole-body protein turnover using 15N-glycine. When a priming dose of label suitable for the urea pool was followed by intermittent oral doses of label, plateau enrichment was maintained in urinary urea and ammonia from 9 to 18 h, giving values for nitrogen flux (18 h) of 0.69 +/- 0.05 g N/kg/d with urea and 0.46 +/- 0.01 g N/kg/d with ammonia. With a priming dose appropriate for the ammonia pool, plateau was reached in urinary ammonia in less than 120 min and maintained for up to 6 h. Nitrogen flux (3 h) with oral 15N-glycine was 0.96 +/- 0.12 g N/kg/d, and with intravenous label was 0.61 +/- 0.13 g N/kg/d. There was a significant linear relationship between flux measured with oral and intravenous isotope. It is suggested that different components of protein turnover are measured with the different approaches, and that the short method in particular measures rapidly turning over proteins associated with the gastrointestinal tract.

Adult↗
PubMed1986

Blood glutathione in severe malnutrition in childhood.

The blood glutathione (GSH) concentration was measured in 25 severely malnourished children and compared with a group of normal adults. In children with marasmus GSH (3.3 +/- 0.7 mg/gHb) was not different from normal (2.9 +/- 0.4 mg/gHb). However there was a highly significant decrease in all forms of oedematous malnutrition, kwashiorkor (1.5 +/- 0.4 mg/gHb) and marasmic kwashiorkor (1.7 +/- 0.7 mg/gHb). There was no relationship between wasting or stunting and blood GSH.

Child, Preschool↗
PubMed1986

Severe undernutrition in Jamaica. Kwashiorkor and marasmus: the disease of the weanling.

The syndromes of severe undernutrition, marasmus and kwashiorkor, have causes related to the interplay of social and medical considerations in the society. Kwashiorkor supervenes when the individual is exposed to a level of stress that exceeds the body's ability to cope. One final common pathway, through which a variety of environmental factors exert an effect, may be associated with oxidant damage to cells. In kwashiorkor there is a severe decrease in the level of both oxidised and reduced glutathione in the red cell. This could be caused by a decreased production, increased consumption or a combination of the two. This is discussed with specific reference to the metabolism of glycine and the possible causal relationship to the pathophysiology of the disease process.

Developing Countries↗