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S J Kay

Publications and source records attributed to S J Kay.

8 recordsLinked to original sources
PubMed2006

The influence of physical activity on abdominal fat: a systematic review of the literature.

UNLABELLED: The relationship between excess abdominal adipose tissue, metabolic and cardiovascular health risk has stimulated interest in the efficacy of physical activity in specifically perturbing this adipose depot. The evolution of imaging techniques has enabled more direct measurement of changes in abdominal and visceral fat. The purpose of this summary was to systematically review the relationship between physical activity and abdominal fat. METHODS: Database searches were performed on MEDLINE, CINAHL, SPORT DISCUS and PUBMED, from 1985 to 2005 with keywords "exercise", "abdominal fat" and "visceral fat". RESULTS: Nineteen randomized controlled trials (RCTs) and eight non-randomized controlled trials were selected. In RCTs using imaging techniques to measure change in abdominal fat in overweight or obese subjects, seven out of 10 studies (including three trials with type 2 diabetics) reported significant reductions compared with controls. Reductions in visceral and total abdominal fat may occur in the absence of changes in body mass and waist circumference. Waist-to-hip ratio is not a sensitive measure of change in regional adiposity in exercise studies. No studies fulfil the Consolidated Standards of Reporting Trials (CONSORT) statement's criteria for the highest quality of randomized trial; however, many studies were in progress or published before the opportunity to comply with these recommendations. Therefore, limited evidence from a number of studies suggests a beneficial influence of physical activity on reduction in abdominal and visceral fat in overweight and obese subjects when imaging techniques are used to quantify changes in abdominal adiposity. More rigorous studies are needed to confirm these observations.

Abdominal Fat↗
PubMed1995

Low rates of proviral integration in SWR/J-RF/J hybrid mice.

A high frequency of proviral acquisition has previously been reported in the offspring of SWR/J-RF/J hybrid mice. In the present study, it was investigated whether this proviral acquisition would be useful for large-scale insertional mutagenesis studies. A population of SWR/J-RF/J hybrid mice with a predominantly SWR/J background was created. Lines of mice with such a background and partially congenic for two active proviruses from the RF/J strain were generated (the insert lines). Control lines were derived from mice which had no proviral loci but had an otherwise similar genetic background. DNA samples of mice in the insert lines were screened for the appearance of new proviral loci by Southern hybridization. The rate of proviral acquisition, calculated from the observed number of new proviral loci was 0.023 new proviruses per mouse. This rate is lower than found in previous studies and too low for large-scale insertional mutagenesis studies. A sensitivity experiment indicated that there was adequate detection of new proviral loci. The number of segregating proviruses was consistent with the number of newly acquired proviruses actually detected. Two additional crosses between mice in the insert lines and SWR/J mice were performed. The rate of proviral acquisition was greatly increased when SWR/J females were initially mated to insert mice, but remained unchanged when SWR/J males were used. This suggested that mice in the insert lines had acquired a maternally transmitted factor, which was suppressing viral expression and thus reducing the rate of proviral acquisition.

Animals↗
PubMed1987

Pleiotropic effect of the gene hairless on hepatotoxicity of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin in mice.

Treatment of mice of the A2G-hr/+ congenic line with 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) resulted in the development of hepatic porphyria over a period of 4 weeks. Female mice responded to a lesser extent than did males. The degree of porphyria in haired heterozygotes (hr/+) was less than in the corresponding hairless homozygotes (hr/hr) and the haired mice had lower resting metabolic rates than hairless mice. Adaptation of mice of either genotype to a 32-33 degrees C environment resulted in a decrease in resting metabolic rate and a reduction in hepatic porphyrin levels. Histologically-demonstrated necrotic changes in livers were accompanied by increased activity of alanine aminotransferase and sorbitol dehydrogenase in the plasma; however, there was no clear temporal trend in plasma enzyme levels. Elevated environmental temperature reduced the plasma alanine aminotransferase activity. The study provided evidence for a pleiotropic effect of variation at the hr locus being expressed in TCDD hepatotoxicity. Suggestions for mechanisms whereby the effect can be mediated through alterations in resting metabolic rate are made.

Alanine Transaminase↗
PubMed1986

Mechanistic studies of the inhibition of hepatic uroporphyrinogen decarboxylase in C57BL/10 mice by iron-hexachlorobenzene synergism.

Porphyria was induced in C57BL/10 mice with iron overload by a single oral dose (100 mg/kg) of hexachlorobenzene (HCB). Within 2 weeks hepatic uroporphyrinogen decarboxylase (EC 4.1.1.37) was inhibited, reaching a maximum (greater than 95%) at 6-8 weeks. There was no recovery by 14 weeks, despite a fall in liver HCB concentrations to only 6% of the day-3 value. The major rise in hepatic porphyrin levels occurred after 4 weeks and secondary inhibition of uroporphyrinogen synthase (EC 4.2.1.75) was inferred from the progressively greater proportion of uroporphyrin I present relative to the III isomer. Plasma alanine aminotransferase (EC 2.6.1.2) activity was also elevated. Although, in further studies, total microsomal cytochrome P-450 content and ethoxyphenoxazone de-ethylase activity reached a peak a few days after dosing and had declined significantly at the time of maximum inhibition of the decarboxylase, additional treatment of HCB-dosed mice with a cytochrome P1-450 inducer, beta-naphthoflavone, enhanced the inhibition, whereas piperonyl butoxide, an inhibitor of cytochrome P-450, partially protected. Uroporphyrinogen decarboxylase was not radiolabelled in vivo by [14C]HCB. There was no major difference in the ability to hydroxylate HCB between hepatic microsomes from induced C57BL/10 mice and those from the insensitive DBA/2 strain. By contrast, lipid peroxidation, in the presence of NADPH, was 8-fold greater in control C57BL/10 microsomes than in DBA/2 microsomes and was stimulated by iron treatment (although not by HCB). The results suggest that the inhibition of hepatic uroporphyrinogen decarboxylase is unlikely to be due to a direct effect of a metabolite of HCB but to another process requiring a specific cytochrome P-450 isoenzyme and an unknown iron species.

Alanine Transaminase↗
PubMed1984

Incomplete correlation of 2,3,7,8-tetrachlorodibenzo-p-dioxin hepatotoxicity with Ah phenotype in mice.

Pretreatment of male mice of the inbred strains A2G, BALB/c, C57BL/10, and AKR with iron dextran synergized the action of a single dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 75 micrograms/kg) in causing hepatic porphyria and necrosis 35 days later. There was no effect in DBA/2 mice. Increased porphyrin levels were associated with decreased hepatic activity of uroporphyrinogen decarboxylase. Iron alone had no effect on porphyrin levels or decarboxylase activity. In male BALB/c mice given TCDD alone there was a delay in the onset of porphyria. Female BALB/c, AKR, and AKR X DBA/2 F1 mice were more resistant to the porphyrinogenic effect of TCDD than males. Development of porphyria did not correlate with Ah phenotype of the mice. The inheritance of sensitivity to TCDD in crosses of the AKR and DBA/2 strains, both Ah nonresponsive, was studied by a biometrical genetic analysis. The inheritances of increased porphyrin levels and of increased plasma activity of enzymes indicative of hepatic necrosis were both complex. Segregation of alleles at more than one locus was required to explain the data. A lack of correlation of porphyrins with plasma enzyme levels in the F2 generation suggested that the expression of these traits was determined independently. Genes other than Ah influence the development of TCDD-induced hepatotoxicity in mice.

Animals↗