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M J Stock

Publications and source records attributed to M J Stock.

At least 145 records · Page 8Linked to original sources
PubMed1983

Parasympathethic effects on diet-induced thermogenesis.

Injection of atropine methyl nitrate or atropine sulphate enhanced the acute thermogenic response to food in rats. The main effector of diet-induced thermogenesis is brown adipose tissue (BAT), but acetylcholine (determined by bioassay) and acetylcholinesterase activity (determined histochemically) were not detected in BAT. This suggests that BAT has no parasympathetic innervation, and atropine must therefore act elsewhere to affect thermogenesis.

Acetylcholinesterase↗
PubMed1983

Protein synthesis in liver, skeletal muscle, and brown adipose tissue of rats fed a protein-deficient diet.

Feeding protein-deficient diets to rats is known to stimulate diet-induced thermogenesis and activate brown adipose tissue (BAT). The fact that BAT protein content, unlike that of other tissues, is unnaffected by protein deficiency prompted us to measure tissue protein synthesis in vivo in animals maintained on normal- (18.8%) and low- (7.6%) protein (LP) diets. Protein synthesis was depressed in the liver of the LP rats due to a fall in RNA activity, with no change in RNA content, and synthesis was also reduced in skeletal muscle from the LP group, but this was due to decreased RNA content with no change in RNA activity. Conversely, protein synthesis, RNA, DNA, and protein content of interscapular BAT were all unaltered in protein-restricted animals. These data indicate that, unlike liver, skeletal muscle, and whole carcass, BAT protein synthesis is not reduced in protein-restricted rats, and this may be related to activation of thermogenesis in the tissue.

Adipose Tissue, Brown↗
PubMed1983

Reduced lipogenesis in cafeteria-fed rats exhibiting diet-induced thermogenesis.

Fatty-acid synthesis has been measured in vivo with 3H2O in cafeteria-fed rats exhibiting diet-induced thermogenesis. Synthesis was decreased in brown adipose tissue, the liver, white adipose tissue, and the carcass of the cafeteria-fed animals compared to rats fed the normal stock diet. Whole-body synthesis was also decreased in the cafeteria-fed group. Diet-induced thermogenesis, in contrast to cold-induced non-shivering thermogenesis, does not lead to increased fatty-acid synthesis and this is presumably due to the inhibitory effects on lipogenesis of the high dietary fat intake characteristic of cafeteria diets. The results also indicate that the energy cost of body fat deposition in cafeteria-fed rats is lower than in animals fed a low-fat/high-carbohydrate stock diet.

Adipose Tissue↗
PubMed1983

Identification of two mitochondrial GDP-binding sites in rat brown adipose tissue.

Scatchard analysis of specific guanosine-diphosphate-([3H]GDP-) binding to rat brown-adipose-tissue mitochondria revealed two distinct binding sites with apparent dissociation constants (Kd) of approximately 0.05 and 2.0 microM. Binding to both sites was insensitive to atractyloside. Reducing the pH of the binding medium from 7.1 to 6.6 caused marked reductions in the Kd of both sites, but at pH 7.6, the dissociation constants were increased about 3-fold. Acute treatment of rats with noradrenaline, 1 h before sacrifice, increased the maximum number of binding sites (Bmax, pmol/mg mitochondrial protein) of both sites and also increased the dissociation constants. The Bmax of the lower-affinity site was elevated in rats exposed to 5 degrees C or fed a palatable cafeteria diet for 10 d, compared to control animals, with the greater changes occurring in the cold-adapted group. The high-affinity site was unaltered by cold adaptation or cafeteria feeding. These results indicate the presence of two distinct nucleotide-binding sites in brown-fat mitochondria, both of which may be involved in thermogenesis.

Adenosine Diphosphate↗
PubMed1983

Acute effects of fat and carbohydrate on metabolic rate in normal, cold-acclimated and lean and obese (fa/fa) Zucker rats.

The rise in metabolic rate after intragastric feeding with fat and carbohydrate was enhanced in cold-acclimated (5 degrees C) rats and diminished in warm-acclimated (30 degrees C) rats compared to controls (24 degrees C), but the response was largest in cold-acclimated animals intubated with fat. These acute effects of nutrients were almost completely abolished by beta-adrenergic blockade with propranolol in all groups, while the parasympathetic antagonist atropine sulphate enhanced the responses in control rats, but had little effect in cold-acclimated animals. Feeding carbohydrate produced similar increases in interscapular brown adipose tissue (BAT) temperature in control and cold-acclimated rats, but fat caused a much greater rise in the latter group. The thermic effects of both nutrients were lower in genetically obese Zucker rats than in their lean littermates. Atropine slightly increased the thermic responses to fat and carbohydrate in the lean Zucker rats and caused marked potentiation in obese rats intubated with fat, but did not alter the effect of carbohydrate in the obese animals These data suggest that the size of the acute rise in metabolic rate after fat and carbohydrate is dependent on the thermogenic capacity of the animal. The response to fat was particularly large in cold-acclimated rats, where BAT activity is high, possibly due to a direct action of fat on the tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1983

Mechanisms of thermogenesis induced by low protein diets.

Weanling (22-day-old) rats fed a low protein (8% casein) diet consumed the same amount of energy as controls (22% casein diet), but intake corrected for body size (kJ/kg0.75) was increased in the former group. Weight gain and the efficiency of gain (g gain/MJ) were markedly reduced in low protein fed rats. Resting oxygen consumption (VO2) was elevated by 15% in the low protein group but this difference was completely abolished by beta-adrenergic blockade with propranolol. Interscapular brown adipose tissue (BAT) mass, protein content, mitochondrial yield and GDP binding were increased in low protein fed rats but mitochondrial alpha-glycophosphate shuttle activity of BAT was unaltered, although shuttle activity was elevated in liver mitochondria. Plasma triiodothyronine levels were increased by 64% in the low protein group, whereas insulin levels were markedly reduced in spite of normal blood glucose levels. Resting VO2 and BAT mass were also increased in older (55-day-old) rats fed the low protein diet, but the changes were smaller than in weanling rats. These data suggest that the decreased metabolic efficiency seen in rats fed protein deficient diets involves sympathetic activation of BAT, and is therefore similar to the thermogenic responses seen in cold adapted and cafeteria-fed animals.

Adaptation, Physiological↗
PubMed1983

Diurnal variations in circulating hormone levels and brown adipose tissue activity in "cafeteria"-fed rats.

Circulating hormone levels and interscapular brown adipose tissue (BAT) mitochondrial GDP-binding capacity were measured at 4-hr intervals over 24 hr in rats fed a stock diet or a palatable "cafeteria" diet. Plasma thyroxine, insulin and glucagon levels were unaffected by diet, but plasma triiodothyronine, BAT mass, mitochondrial protein content and GDP-binding were higher in cafeteria-fed rats. Blood glucose levels and BAT mitochondrial GDP-binding were higher at night in the cafeteria rats. The diurnal variations in these parameters correlated with changes in diet-induced thermogenesis previously observed in cafeteria-fed rats.

Adipose Tissue, Brown↗
PubMed1983

Influence of thyroid hormone on diet-induced thermogenesis in the rat.

Energy balance and brown adipose tissue (BAT) metabolism were studied in rats maintained on stock or 'cafeteria' diet, and injected with either saline or triiodothyronine (T3, 10 micrograms/100 g b.wt./d) for 14 d. Cafeteria-fed rats showed large increases in metabolizable energy intake, energy expenditure and BAT mass, Na+, K+-ATpase activity and mitochondrial GDP binding. In stock fed rats, T3 also stimulated energy intake, metabolic rate and BAT mass and Na+, K+-ATPase activity, but did not affect GDP binding. Hyperthyroidism potentiated the effects of cafeteria feeding on energy expenditure and BAT mass, but BAT Na+, K+-ATPase activity was only slightly higher than that of the euthyroid cafeteria rats, and GDP binding was similar for both groups. These results confirm the involvement of BAT in diet-induced thermogenesis and show that this is potentiated by hyperthyroidism. The data also suggest that thyroid thermogenesis may result, at least partly, from stimulation of BAT.

Adipose Tissue, Brown↗
PubMed1983

Energy balance, diet-induced thermogenesis and brown adipose tissue in lean and obese (fa/fa) Zucker rats after adrenalectomy.

Five-week-old male, lean (+/?) and genetically obese (fa/fa) Zucker rats received either bilateral adrenalectomy or sham operations, and energy balance was measured over the subsequent 21 days. Body weight and energy intake were similar for intact lean and obese rats, but the latter group showed a marked increased in body energy gain and energetic efficiency, and reduced energy expenditure. Adrenalectomy did not significantly influence energy balance in lean rats but caused decreases in food intake and body weight gain in obese rats, and restored their energetic efficiency and body energy gain to the level of lean animals. The lower thermic response to a single meal (40 kJ) in intact obese rats was restored to normal by adrenalectomy. Brown adipose tissue (BAT) mass was larger in sham-operated obese rats, but tissue protein concentration, mitochondrial yield and mitochondrial GDP binding were all markedly reduced in obese rats. BAT mass, composition and GDP binding were almost identical in adrenalectomized obese and all lean rats. These findings demonstrate that the reduced fat deposition in Zucker rats after adrenalectomy is mainly due to the large decrease in the efficiency of energy utilization associated with a restoration of brown fat activity.

Adipose Tissue, Brown↗
PubMed1983

Influence of chronic administration of ciclazindol on energy balance and brown adipose tissue in adult 'cafeteria'-fed rats.

The effects of chronic oral administration of ciclazindol on energy balance and brown adipose tissue (BAT) activity were studied in adult rats maintained on a palatable cafeteria diet. Treatment with 1 mg ciclazindol/kg/day produced small, but not significant, reductions in body energy gain and increases in BAT mass and protein content. Administration of 3.4 and 11 mg/kg/day of ciclazindol depressed weight gain and caused a substantial (42%) reduction in body energy gain. These effects were partly due to a lower food intake, but also resulted from a marked decrease in energetic efficiency. Rats treated with 3.4 and 11 mg/kg/day of the drug showed significant increases in BAT protein content, Na+, K+-ATPase activity and mitochondrial proton conductance, assessed from GDP-binding capacity. These results show that the reduced body weight produced by ciclazindol is due to a lower energetic efficiency, which is associated with activation of BAT, and also a depressed food intake.

Adipose Tissue, Brown↗
PubMed1983

Decerebration activates thermogenesis in the rat.

Under fluothane anaesthesia, suction decerebration was performed at the immediate pre-pontine level in adult, male, Sprague-Dawley rats; this resulted in a large and sustained rise in rectal temperature from 35.6 +/- 0.2 (control) to 38.8 +/- 0.5 degrees C (decerebrate) following recovery from anaesthesia. Propranolol inhibited this rise. In a separate group of continuously (urethane) anaesthetized rats, brain transection at the immediate pre-pontine level produced marked increases in rectal temperature and oxygen consumption, both of which were inhibited by injection of the beta-adrenergic antagonist propranolol (10 mg/kg). The rise in rectal temperature (2.8 +/- 0.4 degrees C) after transection was preceded by a greater increase (3.6 +/- 0.3 degrees C) in the temperature of the interscapular brown adipose tissue (i.b.a.t.). Skin temperature on the tail showed no immediate response. In anaesthetized lean (+/?) male Zucker rats, rectal and i.b.a.t. temperatures showed similar responses to Sprague-Dawley rats after decerebration, but in the genetically obese (fa/fa) Zucker rat, temperatures were not significantly altered by decerebration. The above results, together with macroscopic examination of the transected brains, suggest that descending pathways (possibly arising in the mid-brain tegmentum) normally inhibit a sustained thermogenic drive from areas in the lower brain stem. Decerebration can release this inhibition and cause a large rise in body temperature and in metabolic rate, which apparently result from sympathetic activation of i.b.a.t. The genetically obese Zucker rat exhibits an impaired thermogenic response to decerebration.

Adipose Tissue, Brown↗
PubMed1983

Role of insulin in thermogenic responses to refeeding in 3-day-fasted rats.

Refeeding 3-day-fasted rats with 40 kJ carbohydrate (CHO; corn flour) or protein (gelatin) caused a rise in plasma insulin levels 3 h later, but refeeding fat or injection of norepinephrine (400 micrograms/kg) had no effect. Injection of insulin (0.25 U) caused a 15% rise in metabolic rate 24 h later in fasted rats that could be inhibited by treatment with propranolol. Refeeding rats with a single CHO meal produced an increase in oxygen consumption (15%) 24 h later that was inhibited by injection of diazoxide or 2-deoxy-D-glucose given at the time of the meal. The thermogenic response to insulin injection was unaffected by treatment with diazoxide or 2-deoxy-D-glucose. Genetically obese Zucker rats failed to increase metabolic rate after insulin or CHO. In normally fed lean rats, maintained on a stock diet or a palatable cafeteria diet, insulin (4 U) enhanced the thermogenic response to norepinephrine and stimulated resting metabolic rate (16%) in the cafeteria-fed rats. These data suggest that insulin is involved in the thermogenic responses to food and catecholamines.

Animals↗
PubMed1983

Metabolic responses to fasting and refeeding in lean and genetically obese rats.

Injection of norepinephrine (NE) (25 micrograms/100 g body wt) caused a similar rise in metabolic rate in lean and obese (fa/fa) Zucker rats, but 3-day fasting suppressed the response in lean rats and enhanced the rise in obese mutants. Triiodothyronine (T3) injection (10 micrograms/100 g body wt) caused a significantly greater rise in oxygen consumption (Vo2) in obese than lean rats, but the response was attenuated by fasting in all animals. The thermic response to a single meal of either mixed composition, carbohydrate, or protein (40 kJ) was much smaller in obese rats than lean, but the response to the mixed nutrient meal was similar for all rats after a 3-day fast. Refeeding 3-day fasted lean rats with a single carbohydrate meal (40 kJ) caused a rise in plasma T3 levels after 3 h and a delayed increase in metabolic rate 24 h later. Injection of NE instead of refeeding caused a similar delayed rise in metabolic rate. Carbohydrate refeeding had no effect on plasma T3 levels or oxygen consumption in 3-day fasted obese Zuckers, but injection of NE did produce a significant increase in metabolic rate after 24 h. Refeeding 3-day fasted rats with protein (40 kJ) caused a rise in oxygen consumption 24 h later in lean animals but had no effect in obese animals. The data from lean Zucker rats confirm previous findings in Sprague-Dawley rats and suggest that the thermic response to refeeding involves a complex interaction between the sympathetic nervous system and thyroid hormones. Obese Zuckers responded normally to NE and T3, indicating that their reduced thermogenesis after food may be due to insensitivity to nutrient availability or an inability to activate the sympathetic nervous system.

Animals↗
PubMed1983

Physical changes associated with the onset of precocious puberty in rats after treatment with PMSG.

Body dimensions, composition, oxygen consumption and core temperature were measured in 2 groups of immature rats treated with PMSG. The first group weighed over 60 g on Day 27 of life and responded to PMSG treatment by ovulating; the second group weighed less than 60 g and did not ovulate after PMSG. Body composition, expressed as a percentage of body weight, was identical in the two groups, but growth rate, oxygen consumption and body temperature were all lower in the lighter animals. Oxygen consumption and body temperature were manipulated by altering temperature (i.e. 5, 22 and 30 degrees C) or by hyperphagia, and a positive correlation was found between body temperature and the occurrence of ovulation.

Animals↗
PubMed1983

The effect of high fat and high carbohydrate cafeteria diets on diet-induced thermogenesis in the rat.

Young rats fed cafeteria diets of mixed composition, high fat or high carbohydrate (CHO) content exhibited hyperphagia, but the high-fat diet produced the largest, and the high-CHO the smallest increases in energy intake compared to stock-fed controls. Energy expenditure was increased and energetic efficiency reduced by all forms of the cafeteria diet, thus minimizing excess body energy and weight gains. Hypertrophy of brown adipose tissue (BAT) occurred in all cafeteria-fed rats. In separate rats fed a mixed composition cafeteria diet, the acute thermic response to fat was slightly greater than that to CHO, but for stock-fed controls the response to both nutrients was similar. Fat produced increases in thermogenesis in the acute and chronic experiments that were as large as those due to CHO, and these could be due to activation of the sympathetic nervous system or to direct stimulation of BAT metabolism.

Animals↗