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Biomedical subjects

D A York

Publications and source records attributed to D A York.

At least 109 records · Page 6Linked to original sources
PubMed1988

Cigarette smoking and the thermic responses to isocaloric meals of varying composition and palatability.

The 4-h thermic responses to glucose and a liquid formula meal (Study 1), and to a solid food 'breakfast' meal and the liquid formula meal (Study 2) were measured in a group of young weight-stable female subjects. The groups recruited for the two studies consisted of nine smokers and seven non-smokers (Study 1) and six smokers and eight non-smokers (Study 2). The habitual smokers presented after a 12-h abstention from cigarettes but were permitted to smoke following the meal; their thermic responses were thus due to the combined thermogenic effects of smoking and feeding. The mean thermic responses to all three types of meal were greater for the smokers than for the non-smokers, and the magnitude of this difference was similar irrespective of the type of meal given (range 52 kJ-70 kJ). The thermic responses to the liquid formula meal tended to be greater than those to an isocaloric glucose load for smokers and non-smokers (Study 1). In Study 2, the increase in energy expenditure occurring during the first hour following the 'breakfast' meal was consistently greater than the 1-h response to the liquid formula meal. The larger thermic response to feeding to all three meal-types observed in the groups of smokers when compared with non-smokers, is attributed to the actions of cigarettes smoked (mean 4.6) during the period of measurement. It is concluded that whilst the thermic response to feeding is augmented in cigarette smokers this increase is an additive effect and is independent of the size and nature of the thermic effect of the meal.

Adult↗
PubMed1987

Hypothalamic control of brown adipose tissue in Zucker lean and obese rats. Effect of electrical stimulation of the ventromedial nucleus and other hypothalamic centres.

Electrophysiological stimulation of the hypothalamic ventromedial nucleus (VMN) resulted in an increase in interscapular brown adipose tissue (BAT) temperature in both lean and obese (fa/fa) rats. Graded stimulations resulted in progressively larger temperature increases in both lean and obese (fa/fa) groups. Both intraperitoneal injection of propranolol and surgical denervation (but not sham denervation) abolished the increase in BAT temperature following VMN stimulation, in both lean and obese (fa/fa) groups. Electrical stimulation of the supraoptic region, and certain anterior hypothalamic regions also resulted in increases in BAT temperature of lean and obese (fa/fa) rats, but stimulation of the dorsomedial nucleus and regions of the lateral hypothalamus did not affect BAT temperature. All hypothalamic regions capable of activating BAT gave a similar maximum rise in temperature for a given stimulus in lean and obese (fa/fa) rats. These results suggest that the efferent sympathetic pathway from the VMN and other hypothalamic regions of BAT is normal in the obese (fa/fa) rat.

Adipose Tissue, Brown↗
PubMed1987

Normal levels of serum corticosterone and hepatic glucocorticoid receptors in obese (fa/fa) rats.

In an attempt to understand the hyper-responsiveness to glucocorticoids that is characteristic of genetically obese fa/fa rats, we have measured the levels of free corticosterone in serum from lean and obese rats as well as the number of "cytosolic" and "nuclear" binding sites in livers of these rats. Both the lean and obese rats had similar amounts of free corticosterone available for biological activity at 4 weeks and 10 weeks of age. Measurement of glucocorticoid binding to hepatic glucocorticoid receptors failed to show any differences between genotypes leading to the suggestion that the abnormal glucocorticoid response in obese rats may be due either to post-receptor defects or to a permissive action of the steroid in the expression of the fa/fa genotype.

Adrenalectomy↗
PubMed1987

Corticosterone inhibition of the intracerebroventricular effect of 2-deoxy-D-glucose on brown adipose tissue thermogenesis.

The effects on food intake, blood glucose and the binding of guanosine 5-diphosphate (GDP) to mitochondria from interscapular brown adipose tissue (IBAT) were examined following the injection of 2-deoxy-D-glucose (2-DOG) into the third ventricle of the brain. Microinjections of 2-DOG increased food intake and blood glucose within 30 to 60 min, but binding of GDP to mitochondria from IBAT, on the other hand, was reduced. The order of sensitivity to 2-DOG was IBAT--feeding--hyperglycemia. Implantation of a 50 mg pellet of corticosterone inhibited the stimulatory effect of 2-DOG on feeding and hyperglycemia and prevented the inhibition of GDP binding to mitochondria from IBAT. These data are consistent with the hypothesis that glucocorticoid may inhibit glucose metabolism at multiple sites in the hypothalamus.

Adipose Tissue, Brown↗
PubMed1987

Energetic efficiency and brown adipose tissue uncoupling protein of obese Zucker rats fed high-carbohydrate and high-fat diets: the effects of adrenalectomy.

The influence of diet on the response of lean and obese fa/fa rats to adrenalectomy has been studied. Adrenalectomized and sham-operated rats were fed either a semi-synthetic high-carbohydrate (HC) or high-fat (HF) diet for 13 days. Energetic efficiency, calculated for measurements of energy storage and energy intake, was increased in obese rats fed both HC and HF diets and reduced close to values of lean rats after adrenalectomy. Brown adipose tissue mitochondrial GDP binding and uncoupling protein concentration were reduced in control obese rats fed both HC and HF diets. After adrenalectomy the level of GDP binding and uncoupling protein concentration were increased to levels of lean rats. Molar ratios of GDP binding to uncoupling protein were similar in lean and obese rats, were unaffected by adrenalectomy, but were elevated in rats fed the HC diet (0.40 +/- 0.02 vs 0.28 +/- 0.03). The data suggests that diet, but not obese genotype, may influence the masking of mitochondrial uncoupling protein.

Adipose Tissue, Brown↗
PubMed1986

Thermogenesis and sympathetic activity in BAT of overfed rats after adrenalectomy.

Resting oxygen consumption was elevated by 30% in young rats fed a cafeteria diet compared with their chow-fed controls and by 22% in cafeteria-fed, adrenalectomized (ADX) rats compared with the ADX chow-fed group, but injection of propranolol reduced oxygen consumption in the cafeteria-fed animals and abolished these differences. Brown adipose tissue (BAT) mass was increased by cafeteria feeding, and the activity of the mitochondrial proton conductance pathway (assessed from purine nucleotide binding) was enhanced by adrenalectomy and by cafeteria feeding. Norepinephrine turnover in BAT (determined from the time-dependent loss of tissue [3H]norepinephrine specific activity) was increased by 105% in sham-operated, cafeteria-fed rats, by 142% in chow-fed ADX rats, and by 400% in cafeteria-fed ADX rats, compared with chow-fed controls. Cardiac norepinephrine turnover was elevated by 80% in sham-operated, cafeteria-fed rats, but unaffected by adrenalectomy. These data indicate that the enhanced thermogenesis and BAT activity induced by adrenalectomy in chow- or cafeteria-fed rats is due to increased sympathetic activity in the tissue.

Adipose Tissue, Brown↗
PubMed1986

Influence of propranolol on the acute thermic effect of feeding in man.

The influence of a beta-adrenergic blocker on the thermic effect of feeding (TEF) a meal was investigated in 7 healthy male volunteers. Metabolic rate (MR) was measured before and for 180 min after the consumption of 2.0 MJ 'Ensure' (Abbott Laboratories, Queensborough, Kent, UK); there were 14, 33 and 53% of energy from protein, fat and carbohydrate, respectively. On one occasion propranolol (ICI plc, Macclesfield, Ches., UK) was administered intravenously at 0.1 mg/kg body weight at meal feeding. On the second occasion a similar volume of saline was infused. Serial blood samples (10 ml) were collected before and at 30-min intervals for 180 min after meal feeding. Mean (+/- SD) resting MR was 104 (13) and 116 (11) kJ/kg and MR increased by 12.8% and 10.8% after the test meal with and without propranolol, respectively. These differences were not significant. The postprandial changes in serum glucose and triiodothyronine were similar in the two trials. The magnitude of the rise of serum insulin was similar in the two trials, but the pattern was not. beta-Adrenergenic blockade resulted in an early peak in insulin output at 30 min compared with 60 min for the control trial. We conclude that propranolol had no influence on TEF in this study.

Adult↗
PubMed1986

The effects of 2-deoxy-D-glucose on brown adipose tissue of lean and obese Zucker rats.

The response of brown adipose tissue (BAT) thermogenesis, as measured by mitochondrial GDP binding, of lean and obese Zucker fa/fa rats to 2-deoxy-D-glucose (2-DOG) has been investigated. 2-DOG reduced BAT mitochondrial GDP binding of lean rats but had no effect in obese rats. Adrenalectomy increased BAT GDP binding in obese rats and restored the 2-DOG inhibitory effect. Corticosterone inhibited GDP binding in lean rats and abolished the 2-DOG inhibitory effect. 2-DOG induced hyperphagia and hyperglycaemia in lean rats, but these effects were either absent or attenuated in the obese. The possibility that a glucocorticoid inhibition of glucose metabolism impairs sympathetic activity in the obese rats is discussed.

Adipose Tissue, Brown↗
PubMed1986

The effect of cigarette smoking on the thermic response to feeding.

Resting energy expenditures, the thermic responses to a standard meal (2.09 MJ 'Ensure') and energy intakes were measured in eight age/weight matched pairs of female smokers and non-smokers. The mean thermic response to the standard meal (including the thermic effects of smoking) was 35 percent greater for the smokers when compared with the mean thermic response to the standard meal alone shown by the non-smoker controls (P less than 0.05). There was a tendency for the smokers' energy intakes and resting metabolic rates to be higher then those of the non-smokers (5 percent and 9 percent respectively), but neither of these differences achieved statistical significance. Eleven smokers (three male and eight female) were studied after a 7-day period of abstention from smoking. Total energy expenditure following the meal did not change and the absence of a significant fall in metabolic rate (i.e. to the level of non-smokers) was thought to be partly a consequence of concomitantly increased energy intakes observed (11 percent, P less than 0.05) during this abstention period. Cigarette smoking and feeding appear to have additive rather than synergistic thermogenic effects on metabolic rate.

Body Weight↗
PubMed1985

Hepatic delta 6-desaturase activity in lean and genetically obese ob/ob mice.

Hepatic delta 6-desaturase activity is primarily located in the mitochondrial fraction in mice. Both delta 6- and delta 5-desaturase activities are increased in the liver of young (6-week-old) obese mice. The increase in hepatic delta 6-desaturase activity in obese mice does not occur until weaning. Neither restriction of food intake nor hyperinsulinaemia normalize hepatic delta 6-desaturase activity of obese mice. Both cold acclimation and tri-iodothyronine (30 micrograms/day per kg) decreased hepatic delta 6-desaturase activity of obese mice to levels observed in lean mice, whereas the increase in activity in obese mice was still maintained after the induction of hypothyroidism.

Animals↗
PubMed1985

Measurement by radioimmunoassay of the mitochondrial uncoupling protein from brown adipose tissue of obese (ob/ob) mice and Zucker (fa/fa) rats at different ages.

The concentration of the 'uncoupling protein' in brown adipose tissue mitochondria has been measured in lean and obese (ob/ob) mice and Zucker (fa/fa) rats at different ages using a specific radioimmunoassay. During the suckling period the concentration of the protein was similar in normal and mutant animals of both types, despite the decrease in mitochondrial GDP binding observed in the obese. The concentration of uncoupling protein was, however, decreased in adult ob/ob mice and adult Zucker rats compared with their respective lean siblings, in parallel with the decrease in GDP binding. It is concluded that there is a 'masked', or inactive, form of uncoupling protein in young ob/ob mice and fa/fa rats.

Adaptation, Physiological↗
PubMed1985

High affinity GDP binding sites on brown adipose tissue mitochondria of genetically obese 'fa/fa' rats.

The number of high affinity [3H]GDP binding sites in brown adipose tissue mitochondria is normal in obese (fa/fa) rats in contrast to the reduced number of low affinity GDP binding sites. Adrenalectomy corrected the loss of low affinity binding sites in fa/fa rats but had no effect on the number of high affinity sites in either lean or obese rats. Equilibrium dialysis was used to show the presence of both high and low affinity binding sites on the purified 32 kdalton protein.

Adipose Tissue, Brown↗
PubMed1985

Regulation of sympathetic activity in lean and obese Zucker (fa/fa) rats.

Norepinephrine concentration and turnover (measured by the time-dependent loss of tissue [3H]norepinephrine specific activity) were reduced in the brown adipose tissue (BAT) of obese Zucker rats but were normal in the heart. After acclimation to a 4 degrees C environment for 7 days, BAT norepinephrine turnover was increased to similar levels in lean and obese rats. After overfeeding with sucrose BAT norepinephrine turnover increased in lean rats but was unaffected in obese rats. Propranolol prevented the normalization of BAT mitochondrial GDP binding that followed adrenalectomy of obese rats. Adrenalectomy of obese rats restored BAT norepinephrine turnover to levels observed in lean rats. However, the increase in BAT GDP binding associated with sucrose overfeeding of adrenalectomized lean and obese rats was neither prevented by propranolol nor associated with a stimulation of norepinephrine turnover. The results suggest that the pituitary-adrenal endocrine axis may influence diet-related BAT thermogenesis and that this influence is only partially mediated by the sympathetic nervous system.

Acclimatization↗
PubMed1985

Regulation of brown adipose tissue thermogenesis by corticosterone in obese fa/fa rats.

The defective BAT function of obese Zucker rats has been related primarily to a loss of diet-induced thermogenesis. The normalisation of BAT function by adrenalectomy has been related to the removal of corticosterone. Experiments with propranolol-blockade and on tissue norepinephrine turnover suggest that corticosterone impairs diet-related sympathetic activity but does not alter BAT response to exogenous norepinephrine. The reduction in serum T3 in obese rats is related to the loss of sympathetic activity.

Adipose Tissue, Brown↗
PubMed1984

Effects of insulin on the lipid structure of liver plasma membrane measured with fluorescence and ESR spectroscopic methods.

Insulin increased the lipid order of rat and mouse liver plasma membrane domains sampled by the hydrophobic fluorescent probe 1,6-diphenyl-1,3,5-hexatriene in a concentration-dependent saturable manner. The ordering is half maximal at 5.1 X 10(-11) M and fully saturated at 1.7 X 10(-10) M insulin. Membranes prepared from obese hyperglycemic (ob/ob) mice demonstrated a right-shift in the dose-dependent ordering induced by insulin, such that ordering was half maximal at 1.2 X 10(-10) M and fully saturated at 2.0 X 10(-10) M. Insulin also increased the order of rat liver plasma membranes labeled with the cis- and trans-parinaric acid methyl esters. The ordering caused by insulin as detected with cis methyl parinarate was complete within approx. 15 min. after hormone addition at 37 degrees C, and the ordering was approximately double that observed with the trans isomer. Additional ESR experiments demonstrated that the addition of insulin increased the outer hyperfine splittings of spectra recorded from membranes labeled with the steroid-like spin labels, nitroxide cholestane and nitroxide androstane, but not the fatty acid spin probe, 5-nitroxide stearate. Studies utilizing model membrane systems strongly suggest that the 5-nitroxide stearate samples a cholesterol-poor domain of the membrane, while the steroid-like probes preferentially sample cholesterol-rich regions of the membrane. Finally, insulin-induced membrane ordering was dose-dependently inhibited by cytochalasin B in the range 1-50 microM. From these results, we conclude that (1) the ordering effect of insulin addition to isolated liver plasma membrane fractions occurs within the physiological range of hormone concentration, and the dose-response is right-shifted in membranes from 'insulin resistant' animals; (2) the relative responses of the fluorescent and spin probes suggest that the effects of insulin are confined to specific domains within the membrane matrix; and (3) the direct effects of insulin on the membranes may involve protein components having cytochalasin B binding sites.

Animals↗