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M J Stock

Publications and source records attributed to M J Stock.

At least 163 records · Page 9Linked to original sources
PubMed1983

Effects of age on diet-induced thermogenesis and brown adipose tissue metabolism in the rat.

Measurements of energy balance, thermogenic responses to noradrenaline and brown adipose tissue (BAT) activity were performed in male Lister-hooded rats aged 3.5 and 6.5 months, and fed either a pelleted control diet or a palatable cafeteria diet for 15 d. Cafeteria feeding produced increases in energy intake of 34 and 30 per cent in 3.5 and 6.5-month-old rats respectively, and energy expenditure was elevated by 25 and 10 per cent in these groups. Three-and-a-half-month-old cafeteria-fed rats gained more energy than their controls, but net energetic efficiency was significantly reduced, while in the older cafeteria rats, body energy gain was markedly increased without any apparent effect on net efficiency. The thermogenic response to noradrenaline was enhanced by cafeteria feeding at both ages. The younger cafeteria-fed rats showed significant increases in the mass, protein content and mitochondrial yield of BAT, and the activity of the mitochondrial proton conductance pathway, assessed from GDP-binding, was greater than their controls. The 6.5-month-old cafeteria group also showed hypertrophy of BAT and small, but not significant, increases in the protein content of the tissue and mitochondrial GDP-binding. These results demonstrate that rats aged 3.5 months can exhibit diet-induced thermogenesis and activate BAT in response to overfeeding, but the capacity for thermogenesis declines with age and was virtually absent in 6.5-month-old rats.

Adipose Tissue, Brown↗
PubMed1982

Dopaminergic mechanisms in diet-induced thermogenesis and brown adipose tissue metabolism.

The role of dopamine (DA) in diet-induced thermogenesis was examined. DA was found in, and released from the sympathetic nerves supplying brown adipose tissue. However, the release of DA was only approximately 10% of that of noradrenaline. No significant re-uptake of DA was observed. Hyperphagic, cafeteria-fed rats exhibited higher rates of resting oxygen consumption (VO2) and increased DA release and turnover in brown adipose tissue relative to control animals. Pimozide completely abolished the difference in VO2 between the two groups and DA (0.5 mg . kg-1 s.c.) stimulated VO2 in control and cafeteria animals.

Adipose Tissue, Brown↗
PubMed1982

Effect of chronic food restriction on energy balance, thermogenic capacity, and brown-adipose-tissue activity in the rat.

Young male rats were fed a pelleted stock diet either ad libitum (control) or in restricted amounts (65% of control intake) for 17 d. Body energy gain and energy expenditure, determined from energy balance measurements, were reduced by 73 and 27% respectively compared to controls. Resting oxygen consumption was similar for both groups during the light phase but was significantly depressed in energy-restricted rats at night, and the thermogenic response to noradrenaline was also reduced in these animals. Brown-adipose-tissue mass, protein content, and mitochondrial protein were all decreased in the food-deprived rats, and specific and total depot mitochondrial GDP-binding capacity were 29 and 53% lower than controls. The reduced energy expenditure which occurs during food restriction may be due partly to a lower activity of brown adipose tissue which is associated with a decrease in thermogenic capacity.

Adipose Tissue, Brown↗
PubMed1982

Catecholamine and thyroid hormone influence on brown fat Na+, K+-ATPase activity and thermogenesis in the rat.

Resting oxygen consumption (VO2) before and after injection of noradrenaline (NA), and plasma triiodothyronine levels were elevated in hyperthyroid and hyperphagic cafeteria fed rats, but were reduced in 4d-fasted and hypothyroid animals compared to controls. Refeeding fasted rats with a single carbohydrate meal caused all of these parameters to increase towards control levels. In vivo turnover, and in vitro release of NA brown adipose tissue (BAT) was elevated in cafeteria fed rats but remained unaltered in other groups and levels and uptake of NA in BAT were similar for all rats. Basal and NA stimulated Na+,K+-ATPase activity in BAT was increased in cafeteria and hyperthyroid rats and reduced in fasted and hypothyroid animals compared to control and refed groups. A highly significant correlation (r = 0.977), (P less than 0.001), found between the in vitro activity of this enzyme and resting VO2 in all rats, indicates that BAT Na+,K+-ATPase may be involved in the thermogenic responses to diet, catecholamines and thyroid hormones.

Adipose Tissue, Brown↗
PubMed1982

The effects of physical exercise on metabolic rate and dietary-induced thermogenesis.

1. The energy metabolism of ad lib.-fed adult male Wistar rats receiving daily running exercise (0.9 km/d; 8 degrees incline) on a motor-driven treadmill, over a period of 56 d, was compared with that of sedentary ad lib.-fed rats and sedentary restricted-fed rats of similar body-weight (approximately 420 g). 2. The metabolizable energy of the diet (Oxoid 41 B) was 11.44 +/- 0.05 kJ/g. This value was not affected by restricted feeding (70% ad lib.), exercise training or exercise itself. 3. Exercise-trained rats ate 5% more food than the sedentary ad lib.-fed rats but their equilibrium body-weight was 60 g lower than that of the latter group. 4. Resting metabolic rate, measured over 22 h in a respiration chamber was increased by 10% in exercise-trained animals. 5. Feeding increased energy expenditure (dietary-induced thermogenesis) and this effect was potentiated by performance of an exercise task. 6. Exercise-trained rats exhibited anticipatory rises in energy expenditure (approximately 40%) when placed on a stationary treadmill. 7. Treadmill work increased energy expenditure by a factor of 1.9-2.4. 8. The energy cost of the exercise, determined by respiration calorimetry was 66-80 J/g per km. These energy costs did not account for all the differences observed in food energy consumption of exercise-trained and sedentary rats of equal body-weight. 9. It is concluded that regular physical exercise increases energy expenditure by factors additional to the energy requirement directly related to the physical work. These factors include an increased resting metabolic rate in exercise-trained rats, increased dietary thermogenesis induced by exercise and anticipatory increases in energy metabolism during the period preceding exercise.

Animals↗
PubMed1982

Effects of feeding a palatable "cafeteria' diet on energy balance in young and adult lean (+/?) Zucker rats.

1. The effects of feeding a palatable and varied "cafeteria' diet on energy balance were studied in young (5.5 week) and adult (5.5 month) lean male Zucker (+/?) rats. 2. Estimates of metabolizable energy (ME) intake derived from food composition tables were almost identical to values obtained from bomb calorimetry of foods, urine and faeces, and ME intake was elevated by approximately 73% in all "cafeteria' animals compared to stock-fed controls. 3. "Cafeteria' feeding had no effect on the body-weight of young rats but induced excess weight gains in the older animals and resulted in increased deposition of fat and energy in both groups. Energy expenditure, calculated from ME intake and body-energy gain, was elevated by 77 and 57% in young and adult-cafeteria rats respectively. The energy cost of fat deposition could account for only a small proportion of this increased expenditure. 4. The present results confirm previous findings in another strain of rat and show that the increased energy expenditure (i.e. diet-induced thermogenesis, DIT) which occurs in response to hyperphagia is not restricted to young animals but is also seen in older rats. Measurements of resting oxygen consumption after injections of noradrenaline or a beta-adrenergic antagonist (propranolol), and changes in brown adipose tissue mass are consistent with the suggestion that the DIT of "cafeteria'-fed rats results from sympathetic activation of brown fat.

Adipose Tissue, Brown↗
PubMed1982

Effects of early overnutrition and undernutrition in rats on the metabolic responses to overnutrition in later life.

Weanling rats fed a palatable "cafeteria" diet consumed 40-70% more energy than stock fed controls but also showed a marked (80%) increase in energy expenditure (diet-induced thermogenesis) so that body weight and body energy gain were almost identical in both groups. Animals previously fed the cafeteria diet for 30 days after weaning exhibited lower weight gains when re-exposed to the cafeteria diet at 90 days of age than either naive rats or rats which had been fed the cafeteria diet continuously from weaning. Rats which had been undernourished for 30 days form weaning and allowed to recover for 30 days showed similar responses to the cafeteria diet as normal animals. Hypertrophy of brown adipose tissue (BAT) was seen in all cafeteria fed rats but hyperplasia (increased DNA content) was observed only in rats which had been overfed in early life. These results suggest that overfeeding young, weanling rats can result in a lower fat content, a greater thermogenic capacity and resistance to obesity later in life and may be due to a permanent increase in BAT cell number.

Adipose Tissue, Brown↗
PubMed1982

Effects of feeding a "cafeteria" diet on energy balance and diet-induced thermogenesis in four strains of rat.

Genetic influences on energy, balance and body weight were studied in four strains of rat (male Sprague-Dawley, Lister Hooded and Alderley Park, and male and female hybrid wild/Sprague-Dawley), maintained for 15 days on either a stock or cafeteria diet. Metabolizable energy intake (kiloJoule/W0.75) was similar for all stock-fed groups, and intake was increased by 34% in Alderly Park rats on the cafeteria diet, but by 50-60% in all other strains. Sprague-Dawley and Alderley Park rats were heavier and fatter than other strains, and gained 16 g more fat during cafeteria feeding compared to 8 g in the wild hybrid and only 4 g in the Lister rats. These variations in weight and fat gain resulted from differences in energetic efficiency and energy expenditure. Compared to their controls, expenditure was elevated by 63 and 21% in Lister and Alderley Park cafeteria-fed rats, respectively, and by 50-60% in other groups. Brown adipose tissue mass and protein content was increased in all cafeteria-fed groups. In the laboratory strains, resting oxygen consumption, before and after norepinephrine injections (250 micrograms/kg, s.c.), was significantly increased by the cafeteria diet. Variations in fat and weight gains among strains therefore appeared to be mainly due to differences in metabolic efficiency, and these were exaggerated by cafeteria feeding.

Adipose Tissue↗
PubMed1982

Energy balance and mitochondrial function in liver and brown fat of rats fed "cafeteria" diets of varying protein content.

Rats fed "cafeteria" diets with low (7%, LP) normal (23%, NP) or high (33%, HP) protein contents showed increases in metabolizable energy intake (kJ/kg 0.75, 23-41%) and in energy expenditure (36%) compared to controls fed stock diet (27% protein). The high metabolic rates were inhibited by beta-adrenergic blockade with propranolol. All rats fed cafeteria diets deposited more fat than controls, but the LP diet depressed growth, and these animals also showed the lowest energetic efficiency. Brown adipose tissue (BAT) mass and protein content were increased in all groups fed cafeteria diets, but the largest changes occurred in LP-fed animals, and the smallest in the HP group. Hepatic mitochondrial alpha-glycerophosphate shuttle activity and plasma triiodothyronine levels were elevated twofold in rats fed LP cafeteria diet compared to controls, but the other cafeteria diet groups showed little or no changes, and shuttle activity in BAT was not affected by any of the diets. Blood glucose and plasma insulin levels were similar for control, NP and HP animals, whereas glucose levels were slightly lower and insulin levels were very much lower in the rats fed LP cafeteria diet.

Adipose Tissue, Brown↗
PubMed1982

Effects of diet and acute noradrenaline treatment on brown adipose tissue development and mitochondrial purine-nucleotide binding.

Feeding rats a highly palatable 'cafeteria' diet resulted in a two-fold increase in interscapular brown adipose tissue (b.a.t.) mass after only 3 d on the diet. No significant difference in DNA content of b.a.t. was noted between control and cafeteria-fed rats at this time but DNA content was elevated 2-3-fold in the latter group by day 30, and incorporation rates of tritiated thymidine into DNA were elevated in these animals after 5, 15 and 30 d of cafeteria feeding. A doubling of specific GDP (per mg protein) to b.a.t. mitochondria was seen in cafeteria-fed rats on days 3, 15 and 30 and total GDP binding in the interscapular depot was increased by 3-4-fold. Injection of the animals with noradrenaline (25 micrograms/100 g body weight) 1 h before killing caused 180 and 430% increases in b.a.t. mitochondrial GDP binding in control and cafeteria-fed rats respectively. Linear Scatchard plots of binding data obtained from 15 d control and cafeteria groups indicated a single class of receptor, with the same affinity for GDP in all animals, but the maximum number of binding sites was markedly elevated in cafeteria rats and was increased further after treatment with noradrenaline 1 h prior to sacrifice. When cafeteria-fed rats were returned to stock diet alone the differences in b.a.t. mass and GDP binding diminished but after 10 d brown fat mass and noradrenaline-stimulated GDP binding were still significantly higher than control levels. These data provide further evidence for the involvement of b.a.t. and its mitochondrial proton conductance pathway in diet-induced changes in thermogenic capacity.

Adipose Tissue, Brown↗
PubMed1982

Energy expenditure of 'cafeteria'-fed rats determined from measurements of energy balance and indirect calorimetry.

1. Energy expenditure was determined in rats fed a standard laboratory diet or a varied and palatable 'cafeteria' diet, from metabolizable energy intake and body energy gain over a 15 d experiment. This was compared with measurements of oxygen consumption (Vo2) made over 24 h during the first and second weeks of the experiment. 2. Metabolizable energy intake was elevated by 50% in 'cafeteria'-fed rats and these animals gained more weight and had a higher body fat content than stock-fed controls. Energy expenditure derived from these measurements was 45% higher in the 'cafeteria' group, and the net efficiency for energy gain was significantly reduced. 3. Vo2 was increased by 45% in the 'cafeteria' group and the daily energy expenditure, estimated from Vo2, was identical to that derived from the energy balance for controls, and differed by only 3% for the 'cafeteria' group. 4. These results confirm the high levels of diet-induced thermogenesis previously seen in hyperphagic, 'cafeteria'-fed rats and reaffirm the validity of the carcass balance method for estimating energy expenditure.

Animals↗
PubMed1982

Sympathetic and thyroid influences on metabolic rate in fed, fasted, and refed rats.

Twice daily subcutaneous injections of norepinephrine (NE, 25 micrograms/100 g body wt) for 16 days, in adults rats, produced significant increases in resting oxygen consumption (VO2), thermogenic responses to NE, plasma triiodothyrone (T3) levels, interscapular brown fat mass, and hepatic mitochondrial alpha-glycerophosphate dehydrogenase activity. These responses were absent in hypothyroid rats. Rats fasted for 72 h showed significant decreases in VO2 and plasma T3. Refeeding with carbohydrate (CHO, 40 kJ) produced a rapid rise in plasma T3 within 3 h and a delayed rise in VO2 (peak rise at 24 h). Treatment with the beta-adrenergic antagonist propranolol (2 mg/100 g body wt, sc) at the time of the meal blocked the rises in T3 and VO2. Injecting fasted rats with T3 (365 ng/100 g body wt, ip) had no effect on subsequent VO2 but NE (40 micrograms/100 g body wt, sc) produced similar increases in plasma T3 and VO2 to CHO refeeding. The delayed rise in VO2 after CHO refeeding was blocked by propranolol (0.5 mg/100 g body wt, sc) when given 24 h after the meal. These results provide evidence for catecholamine-induced changes in thyroid hormone metabolism and for a sympathetic involvement in thyroid-dependent responses to nutritional manipulations.

Adipose Tissue, Brown↗
PubMed1982

Changes in metabolic rate and brown adipose tissue composition during nutritional rehabilitation of postnatally undernourished rats.

Rats previously undernourished (PU) during the first 3 postnatal weeks gained less weight than controls during the subsequent rehabilitation period, in spite of similar levels of food intake per body weight 0.75. Resting oxygen consumption (ml/min/kg0.75) was significantly elevated (15-22%) in the PU group after 36 days of age but this difference was almost completely abolished by beta-adrenergic blockade with propranolol. PU rats also showed a greater thermogenic activity after noradrenaline (25 micrograms/100 g b.wt.) than controls. The mass of brown adipose tissue (BAT, mg/100 g b.wt.) was reduced by undernutrition but during rehabilitation BAT increased in PU rats to a value greater than that of controls. These results indicate that the low weight gain of PU rats may result partly from a high metabolic rate due to sympathetic activation of BAT.

Adipose Tissue, Brown↗
PubMed1982

Effect of diet and cold exposure on norepinephrine turnover in brown adipose tissue of the rat.

Brown adipose tissue (BAT) is an important site of adaptive changes in thermogenesis in the rat. The sympathetic nervous system, which richly supplies BAT, is thought to play an important role in the regulation of BAT thermogenesis because catecholamines stimulate and beta adrenergic blocking agents inhibit oxygen consumption in this tissue. The present studies were carried out to assess directly sympathetic activity in BAT in response to cold exposure and to changes in dietary intake, both of which alter heat production in the rat. Sympathetic activity was determined from the rate of norepinephrine (NE) turnover in interscapular brown adipose tissue (IBAT) after preliminary experiments validated the use of NE turnover techniques in IBAT. Acute exposure to 4 degrees C increased NE turnover in IBAT 4- to 12-fold compared with ambient temperature controls, depending upon the interval over which the turnover measurement was made, while in the heart NE turnover doubled in response to the same cold stimulus. In animals exposed to cold continuously for 10 d before study, NE turnover measurements in IBAT and in the heart were elevated comparably to those obtained during acute exposure. Alterations in feeding were also associated with changes in NE turnover in IBAT. Fasting for 2 d decreased NE turnover in IBAT (-35% from 29.2+/-4.2 ng NE/h to 18.9+/-5.9) and in heart (-52%). In animals fed a "cafeteria" diet, a model of voluntary overfeeding in the rat, NE turnover was increased in both IBAT (+108% from 24.8+/-4.5 ng NE/h to 51.7+/-6.8) and heart (+66%). Because ganglionic blockade exerted a greater effect on NE turnover in IBAT in cafeteria-fed rats than in controls, the increase in NE turnover in IBAT with this overfeeding regimen reflects enhanced central sympathetic outflow. Thus NE turnover techniques can be satisfactorily applied to the assessment of sympathetic nervous system activity in IBAT. The experiments reported here demonstrate changes in sympathetic activity in IBAT that parallel known adaptive changes in heat production in the rat. These studies, therefore, support the concept that the increased thermogenesis of chronic cold exposure and of cafeteria feeding occur by similar mechanisms and imply an important role for the sympathetic nervous system, mediated in part through BAT, in the regulation of energy balance in the rat.

Adipose Tissue, Brown↗
PubMed1982

Factors influencing the acute effect of food on oxygen consumption in the rat.

The rise in resting oxygen consumption (VO2) during the 2-3 h following intragastric feeding (50 kJ [12 kcal]) was significantly greater in hyperphagic cafeteria-fed rats and hyperthyroid rats, but was markedly reduced in 3-day fasted and genetically-obese Zucker rats, compared to their respective stock-fed controls. In control and hyperthyroid animals this response was almost completely abolished by administration of propranolol. In another group of rats, resting VO/ was elevated by 8 per cent after 12 h of cafeteria feeding and was maximally increased by 20 per cent after 2.5 days on the diet. In rats previously cold-adapted (15 days at 5 degrees C) the maximal response (20 per cent) to cafeteria feeding was seen after only 12 h on the diet. These results suggest that the acute thermic response to food involves a sympathetic activation of thermogenesis, similar to that induced by chromic hyperphagia and cold-exposure, and can be influenced by genetic background plane of nutrition and thyroidal status.

Adaptation, Physiological↗