Increased Plasma Glycerol Research Articles

Inhibition of lipolysis reduces β 1-adrenoceptor—mediated thermogenesis in man

The purpose of the study was to investigate whether the increase in energy expenditure and lipid oxidation during β 1-adrenergic stimulation is caused by the concomitant increase in lipolysis. Twelve healthy male subjects participated in three trials: no-LIP/-, inhibition of lipolysis by pretreatment with acipimox followed by saline infusion; -/BETA, no pretreatment, with dobutamine infusion to stimulate β 1-adrenoceptors; and no-LIP/BETA, pretreatment with acipimox followed by dobutamine infusion. Inhibition of lipolysis did not affect baseline energy expenditure, but decreased lipid oxidation and increased carbohydrate oxidation. Energy expenditure and lipid oxidation increased significantly during β 1-adrenergic stimulation, but this increase was significantly smaller when lipolysis was inhibited ([baseline v infusion period] energy expenditure: -/BETA, 5.15 ± 0.16 v 6.11 ± 0.26 kJ/min, P < .001; no-LIP/BETA, 5.28 ± 0.17 v 5.71 ± 0.19 kJ/min, P < .01; lipid oxidation: -/BETA, 0.059 ± 0.004 v 0.073 ± 0.006 g/min, P < .01; no-LIP/BETA, 0.034 ± 0.005 v 0.039 ± 0.006 g/min, P < .05). Baseline plasma glycerol and nonesterified fatty acid (NEFA) concentrations decreased after inhibition of lipolysis. Glycerol and NEFA increased significantly during β 1-adrenergic stimulation alone (glycerol, 65.0 ± 5.3 v 117.0 ± 10.9 μmol/L; NEFA, 362 ± 24 v 954 ± 89 μmol/L; both P < .001). Concomitant administration of acipimox prevented a substantial part of the increase in lipolysis during β 1-adrenergic stimulation, but the increase in plasma glycerol and NEFA remained significant (glycerol, 40.4 ± 2.2 v 44.8 ± 2.2 μmol/L; NEFA, 118 ± 18 v 160 ± 19 μmol/L; both P < .05). In conclusion, a reduced availability of plasma NEFA was associated with a reduced increase in energy expenditure and lipid oxidation during β 1-adrenergic stimulation in man.

Regulation of lipolysis by the sympathetic nervous system: A microdialysis study in normal and spinal cord—injured subjects

To evaluate the regulation of lipolysis by the sympathetic nervous system, eight spinal cord—injured (SCI) subjects with a lesion above T5 resulting in a decentralization of the lower-body sympathetic nervous system and adrenal medulla (age, 36 ± 2 years; weight, 82 ± 5 kg; body fat mass, 26.8 ± 3.0 kg; all mean ± SE) and nine control subjects (age, 33 ± 2; weight, 80 ± 3; NS; body fat mass, 16.1 ± 1.5 kg; P < .01) were investigated after fasting overnight. Each subject was studied with subcutaneous microdialysis and 133Xe-clearance adipose tissue blood flow (ATBF) in the umbilical and clavicular regions during postabsorptive rest and after sympathoexcitatory stimulation by means of mental stress and isometric handgrip exercise. SCI subjects had an increased body fat mass, hyperinsulinemia, and an elevated lipolytic rate at rest compared with control subjects. ATBF and lipolysis were activated to a normal extent following mental stress and isometric handgrip exercise in the umbilical region in control subjects. ATBF was increased in tissue above but not below the lesion level in SCI subjects following mental stress. Glycerol release was not different between groups in either tissue region despite significantly lower noradrenaline and adrenaline levels in SCI subjects. This finding argues against a significant adrenergic control of the lipolytic rate at rest. Furthermore, the small differences in stimulated glycerol release between groups, as well as the increased plasma glycerol levels in SCI subjects, cast doubt on the view that interruption of adrenergic activity below the lesion is the sole mechanism underlying the increased body fat mass in SCI subjects.

Engine and radiator: fetal and placental interactions for heat dissipation.

The 'engine' of fetal metabolism generates heat (3-4 W kg-1 in fetal sheep) which has to be dissipated to the maternal organism. Fetal heat may move through the amniotic/allantoic fluids to the uterine wall (conductive pathway; total conductance, 1.1 W degrees C-1 kg-1) and with the umbilical arterial blood flow (convective pathway) to the placenta. Because resistance to heat flow is larger than zero fetal temperature exceeds maternal temperature by about 0.5 degree C (0.3-1 degree C). Probably 85% of fetal heat is lost to the maternal organism through the placenta, which thus serves as the main 'radiator'. Placental heat conductivity appears to be extremely high and this may lead to impaired heat exchange (guinea-pig placenta). A computer simulation demonstrates that fetal temperature is essentially clamped to maternal temperature, and that fetal thermoregulatory efforts to gain thermal independence would be futile. Indeed, when the late gestational fetus in utero is challenged by cold stress, direct and indirect indicators of (non-shivering) thermogenesis (oxygen consumption, increase of plasma glycerol and free fatty acid levels) change only moderately. In prematurely delivered lambs, however, cold stress provokes summit metabolism and maximum heat production. Only when birth is imitated in utero (by cord clamping, external artificial lung ventilation and cooling) do thermogenic efforts approach levels typical of extra-uterine life. This suggests the presence of inhibitors of thermogenesis of placental origin, e.g. prostaglandins and adenosine. When the synthesis of prostaglandins is blocked by pretreatment with indomethacin, sheep fetuses react to intra-uterine cooling with vigorous thermogenic responses, which can be subdued by infusion of prostaglandin E2 (PGE2). Since the sheep placenta is known to produce sufficient amounts of PGE2, it seems that the placenta controls fetal thermogenic responses to some extent. This transforms the fetus into an ectothermic organism, and yet allows the newborn the full exploitation of thermoregulatory responses typical of endothermic animals.

Influence of prolactin on in vivo and in vitro lipolysis in rabbits.

Three experiments were conducted to assess the influence of prolactin on lipolysis in rabbits. In vivo, a single injection of 1 mg of ovine prolactin induces increased plasma glycerol and nonesterified fatty acids concentrations within 30 min (P < 0.01). On the contrary, in vitro, oPRL did not stimulate glycerol release in isolated adipocytes at physiological concentrations (under 10(-8) M). In a third experiment, the effect of chronic hyperprolactinemia on the adrenergic control of lipolysis was studied (daily subcutaneous injections of 1 mg ovine prolactin for 12 days). The weight of perirenal adipose tissue at the end of the period of injections was 27% lower in the prolactin-injected (PRL) rabbits than in the control (CTL) rabbits (88 +/- 15 g vs. 120 +/- 25 g; P < 0.05). Food intake during the period of injections was 28% lower in the PRL group than in the CTL group (177 +/- 21 g/d vs. 246 +/- 13 g/d; P < 0.05). Basal glycerol release was 157% higher in adipocytes from PRL rabbits than in those from CTL rabbits (P < 0.05). Stimulation of lipolysis with different adrenergic agonists was similar in both groups. These results suggested an indirect influence of prolactin on adipose tissue lipolysis in rabbits, but mechanisms implicated in this effect remain to be elucidated.

The effects of a selective Alpha-1 adrenergic blockade on the activity of adipose tissue lipoprotein lipase in female hamsters

Lipoprotein lipase, is an enzyme responsible for the hydrolysis of triacylglycerols at the surface of endothelial cells. Its regulation is not completely elucidated and seems, among other things, under the influence of the sympathetic nervous system. The adrenergic regulation of lipoprotein lipase activity is complex and the α 1 adrenergic pathway appears involved in this regulation. In the present study, adipose tissues of female hamsters are investigated following a single injection of doxazosin and phenylephrine and are compared to controls for the activity of lipoprotein lipase. After an acute treatment with a selective α 1 antagonist (doxazosin), lipoprotein lipase activity was decreased in the parametrial white adipose tissue and increased in brown adipose tissue (p <- 0.05). Moreover, a treatment with phenylephrine,' an α 1 adrenergic agonist, increased the activity of lipoprotein lipase, in the parametrial fat pad only. On the other hand, the activity of lipoprotein lipase in heart and in skeletal muscle was not modified by an α 1, stimulation or blockade. In this study, calcium and norepinephrine did not appear involved in the regulation of lipoprotein lipase activity. On the contrary, the increase of plasma glycerol after an acute treatment with doxazosin suggests that the lipolytic activity of white adipose tissue could be involved in the decrease of lipoprotein lipase activity in the parametrial white adipose tissue.

A comparison of the β1–selectivity of conventional metoprolol and metoprolol CR during exercise in healthy volunteers

This paper reports on a randomized double-blind crossover study to compare the effects of daily treatment with 100 mg conventional metoprolol (M100), 50 or 100 mg slow-release metoprolol CR (CR50, CR100) and placebo on the response to treadmill walking exercise in 12 healthy volunteers. Twenty minutes of exercise was undertaken at 1.5 h post-dose (Ex1) and again at 4 h (Ex2). During Ex1 all metoprolol preparations caused a reduction in the exercise-induced increase in heart rate when compared to placebo (P < 0.001). The exercise-induced increase in plasma glycerol, an indicator of lipolysis, was diminished by all metoprolol preparations but to a greater extent by M100 (P < 0.05). Rises in plasma ammonia were used to assess the net degradation of energy-rich adenine nucleotides by skeletal muscle during exercise. When compared to placebo, a significant elevation in plasma ammonia was seen only during exercise with M100 (P < 0.05). The perceived exertion at the end of exercise was also greatest on conventional metoprolol. The differences between the effects of conventional and CR formulations of metoprolol were less when exercise was repeated 4 h post dosing. We conclude that metoprolol CR may offer advantages over the conventional preparation, in subjects regularly engaging in exercise, by reducing the metabolic stress imposed upon skeletal muscle.

Importance of beta-adrenoceptor function in fat cells for lipid mobilization.

The role of peripheral catecholamine sensitivity in lipid mobilization was investigated in 78 healthy non-obese subjects by comparing beta-adrenergic regulation of lipolysis in isolated adipocytes with circulating catecholamines and glycerol (lipolysis index). Small intra-individual variations (5-7%) in adipocyte lipolytic beta-adrenoceptor sensitivity (ED50) for isoprenaline were found. However, large inter-individual variations (almost 10(5)-fold) in isoprenaline ED50 were observed in abdominal or gluteal adipocytes, which correlated (r = 0.52) negatively with the resting plasma noradrenaline levels. A correlation was also observed between circulating noradrenaline and adipocyte ED50 for noradrenaline (r = -0.38). In subjects with high (ED50 less than 10(-11) mol l-1) as compared to low isoprenaline sensitivity (ED50 greater than 10(-10) mol l-1) physical exercise induced a two times greater increase in plasma glycerol (P less than 0.01), in spite of a 50% less marked increase of plasma noradrenaline (P less than 0.01). Findings with beta-adrenoceptor mRNA and with total beta-adrenoceptor number or affinity for agonist did not show any strong correlation with the resting plasma noradrenaline level (r less than 0.25). In conclusion, inter-individual variations in beta-adrenoceptor sensitivity and its relation to circulating noradrenaline can be ascribed to specific modulations of either BAR-subtypes or in the postreceptor activation of lipolysis. These variations in adipocyte beta-adrenoceptor sensitivity may participate in the regulation of peripheral nervous activity and play a putative role in lipolysis during exercise when subjects with high beta-adrenoceptor sensitivity increased their ability to mobilize lipids despite a reduced noradrenaline response.

Changes in plasma adenosine during simulated birth of fetal sheep

Adenosine is known to inhibit nonshivering thermogenesis in adult brown fat. These experiments were undertaken to test whether fetal adenosine, normally present in high concentrations, suppresses lipolysis in utero and then falls after birth, permitting thermogenesis to begin. To test this hypothesis, we measured fetal plasma adenosine concentration [ADO] using high-performance liquid chromatography in 11 fetal sheep at 135-140 days gestation during simulated birth. During an initial control period, fetal [ADO] averaged 1.9 +/- 0.3 microM, about four times maternal [ADO] (0.4 +/- 0.1 microM, P less than 0.001). The fetus was then cooled by circulating cold water through a plastic coil encircled about the fetal torso. One hour later, when fetal core temperature had decreased 2.3 degrees C, fetal [ADO] averaged 2.8 +/- 0.5 microM, a 50% increase (P less than 0.05), while thermogenesis remained inactive. Next the fetal lungs were ventilated with O2 to raise arterial Po2 to greater than or equal to 150 Torr. Fetal [ADO] decreased only slightly, and thermogenic responses were modest. Finally, the umbilical cord was occluded. Fetal [ADO] decreased rapidly and 60 min later averaged 1.1 +/- 0.2 microM, 40% below initial control (P less than 0.05) and 57% below the previous period (P less than 0.001). As [ADO] fell, strong thermogenic responses became apparent, as indicated by seven- to eightfold increases in plasma glycerol (P less than 0.001) and a doubling in fetal O2 consumption (P less than 0.001). These results are consistent with the hypothesis that high fetal [ADO] inhibits thermogenesis before birth but then decreases after cord occlusion, allowing thermogenesis to begin.(ABSTRACT TRUNCATED AT 250 WORDS)

Altered cardiovascular responsiveness to adrenoceptor agonists in endurance-trained men

The influence of physical training on responses to intravenous infusions of phenylephrine (Phe) and isoproterenol (Iso) were investigated in 10 well-trained runners (WT) and 10 age-matched untrained controls (UT). The latter were reinvestigated after a 4-mo training period. The venous plasma Iso and Phe concentrations attained during infusions were lower in WT than in UT. Responses were related to the corresponding plasma concentrations. Phe-induced decreases and Iso-induced increases in heart rate were less pronounced (P less than 0.01) in WT than in UT. At venous plasma concentrations of 100 nM Phe and 0.8 nM Iso, the responses were -9 +/- 1 and 30 +/- 2, and -17 +/- 2 and 44 +/- 4 beats/min, respectively. Increases in blood pressures during Phe infusions were greater in WT than in UT (100 nM Phe: systolic 36 +/- 3 vs. 25 +/- 3 mmHg, P less than 0.05). The Iso-induced decrease in diastolic blood pressure was also more pronounced in WT (0.8 nM Iso: -29 +/- 3 vs. -15 +/- 2 mmHg, P less than 0.01). Iso-induced changes in systolic time intervals showed no consistent differences between training states. Increases in plasma adenosine 3',5'-cyclic monophosphate during Iso infusions were smaller (P less than 0.05) in WT than in UT, whereas increases in plasma glycerol were larger (P less than 0.05). Lymphocyte beta 2-adrenoceptor function and binding characteristics did not differ between training states. In summary, the present results indicate that beta-adrenergic vasodilator and alpha-adrenergic vasopressor responses are enhanced in endurance-trained subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Metabolic adjustments of an air‐breathing teleost, Channa maculata, to acute and prolonged exposure to hypoxic water

Plasma and tissue metabolite levels were measured in the air‐breathing Channa maculata during acute and prolonged exposure to normoxic and hypoxic water. Exposure of the fish to hypoxic water (water oxygen partial pressure, PwO2= 50 mmHg) for 1 h caused increases in plasma glucose and lactate, liver and brain lactate, liver a‐amino acid, heart and brain alanine and brain succinate levels. The metabolic changes in heart, brain and muscle could only be detected when PwO2 was 30 or 10 mmHg. Heart glycogen and liver lipid decreased during acute exposure. Prolonged exposure to hypoxic water (PwO2= 30 mmHg) for 3 days caused an increase in plasma glycerol and liver lactate dehydrogenase activity, and a depletion of glycogen store in all tissues investigated. However, metabolite levels which had been elevated during acute hypoxic exposure were observed to return to their normoxic values after prolonged exposure. It was concluded that anaerobic metabolism was triggered by acute exposure to hypoxic water. Prolonged exposure to hypoxic water induced a metabolic readjustment involving mobilisation of lipid and glycogen stores, which is probably a reflection of the high metabolic load of aerial respiration imposed on the fish during exposure to hypoxic water.

Role of the availability of substrates on hepatic and renal gluconeogenesis in the fasted late pregnant rat

Studies were conducted to examine the role of gluconeogenetic substrate availability on glucose production in the fasted late pregnant rat. Virgin and 21-day pregnant rats were studied after 24 hours' food deprivation. Pregnant animals showed decreased circulating glucose and gluconeogenic amino acid and increased plasma glycerol concentration. Glucose formation was studied in vivo two, five, and ten minutes after the intravenous administration of two concentrations of 14C-alanine, 14C-pyruvate, or 14C-glycerol. Concentrations of 0.2 mmols of 14C-glycerol or 14C-pyruvate, but not of 14C-alanine, enhanced 14C-glucose production in pregnant rats, whereas 1 mmol of any of the three 14C-substrates always enhanced 14C-glucose production in these rats. Both 1 mmol/L and 5 mmol/L 14C-alanine increased 14C-glucose formation in 90-minute-incubated liver slices of fasted pregnant rats, in spite of decreased cytosolic activity of alanine aminotransferase. The three substrates enhanced “in vitro” renal gluconeogenesis in pregnant rats. Under all experimental conditions studied, labeled glycerol was converted more efficiently into glucose than equivalent amounts of any other substrate used, and this difference was greater in pregnant, than in virgin animals. Results indicate that, in spite of enhanced gluconeogenetic activity, maternal glucose production in the fasted state at late gestation is limited by the deficiency of certain substrates, such as amino acids. It is proposed that glycerol derived from enhanced maternal adipose tissue lipolysis constitutes a preferential gluconeogenetic substrate in comparison with others, such as alanine, that are more efficiently transferred through the placenta to the fetus.

Food intake and blood fuels after oil consumption: Differential effects in normal and diabetic rats

The mechanisms by which fat feeding suppresses the hyperphagia of diabetic rats were examined. Rats that were allowed to consume a small amount (1.5 ml) of corn oil decreased subsequent food intake within 6 hr after ingesting. Diabetic rats decreased food intake much more than normal rats. Similar results were obtained when oil was given intragastrically. Analysis of blood samples revealed that diabetic rats showed greater increases in plasma ketones and triglycerides and smaller increases in plasma glycerol than normal rats following consumption of 1.5 ml corn oil. This difference between diabetic and normal rats appeared when rats were allowed to eat after oil ingestion as well as when they were fasted. Brief periods of food deprivation (2.5–4.5 hr) substantially increased plasma ketones and glycerol and decreased plasma triglycerides in both diabetic and normal rats. The results indicate that diabetic rats decrease food intake more than normal rats after fat feeding because they oxidize more of the ingested fat.

Influence of circulating NE and Epi on adipose tissue vascular resistance and lipolysis in humans.

The effects of circulating norepinephrine (NE) and epinephrine (Epi) on vascular resistance in subcutaneous adipose tissue and the calf as well as on plasma glycerol, an indicator of lipolysis, were studied in healthy volunteers. Adipose tissue blood flow was determined by the local clearance of 99mTcO-4 or 133Xe. The two isotopes gave similar results. Calf blood flow was determined by venous occlusion plethysmography. Intravenous infusion of NE caused increases in systolic and diastolic blood pressures, adipose tissue and calf vascular resistances, and plasma glycerol and a decrease in plasma insulin and heart rate, all of which were significant when arterial plasma NE was elevated from 1.17 +/- 0.14 to 8.38 +/- 0.30 nM (n = 16). Epi reduced diastolic and mean arterial pressures and adipose tissue and calf vascular resistances and increased plasma glycerol without affecting systolic blood pressure or plasma insulin. An increase of arterial plasma Epi from 0.20 +/- 0.03 to 1.15 +/- 0.05 nM (n = 6) was sufficient to induce vasodilatation in adipose tissue and lipolysis. Human adipose tissue differs from canine adipose tissue inasmuch as Epi causes vasodilatation in humans (present results) but vasoconstriction in the dog (previous results), presumably due to a predominance of vascular beta 2-adrenoceptors in human and beta 1-adrenoceptors in canine adipose tissue. Furthermore, Epi is a considerably more potent lipolytic hormone than NE in humans but not in the dog. Our results indicate that both NE and Epi may influence human adipose tissue blood flow and lipolysis as circulating hormones.

Effects of adrenal demedullation combined with chemical sympathectomy on cold-induced responses of endocrine pancreas in rats.

Adrenal demedullation combined with chemical sympathectomy with 6-hydroxydopamine (ACS) lowered plasma glucagon and insulin levels in rats. Acute cold exposure increased plasma glucagon in both ACS and control rats, while it increased plasma insulin only in ACS rats. ACS rats responded to cold with a smaller increase in plasma glycerol and a more pronounced elevation of plasma free fatty acids.

Increases in plasma glycerol levels precede the hypophagia following subcutaneous glycerol injection in rats

Cumulative food intake and plasma glycerol levels following subcutaneous glycerol injections were investigated in rats, because increases in plasma glycerol have been suspected to contribute to glycerol-induced hypophagia. Besides plasma glycerol, plasma non-esterified fatty acids (NEFA), plasma D-(−)-3-hydroxybutyrate (3-HB), blood glucose, and liver glycogen content were also measured. Two daily injections of 80 mg/kg body wt. glycerol did not affect food intake and failed to increase plasma glycerol 30 min after the injection. A single injection of 660 mg/kg body wt. glycerol reduced food intake and increased plasma glycerol 1–2 hours after the injection. This glycerol dose also increased liver glycogen content 1–2 hours after the injection but did not affect plasma NEFA and 3-HB. Rats injected with 660 mg/kg body wt. glycerol did not reduce feeding within the first 2 hours following the injection, when plasma glycerol levels were increased. Inhibition of feeding began at about 3 hours and continued up to 6 hours although plasma glycerol levels had declined to control values 5–6 hours after the injection. It is concluded that metabolic consequences of elevated plasma glycerol levels rather than increases in plasma glycerol levels per se elicit the food intake reduction following exogenous glycerol loads in rats.

Plasma fat metabolites and hunger

In order to test the hypothesis that the fat metabolites are the blood-borne signals which suppress hunger during recovery from reversible obesity, experiments were designed to manipulate plasma fat metabolite levels directly. In order to elevate plasma glycerol levels, glycerol was infused intravenously into relatively unrestrained rats for 36 hours; this treatment greatly increased plasma glycerol levels but reduced voluntary food intake only slightly. Similar results were obtained when glycerol was mixed with powdered rat food. These results suggest that glycerol is not the “lipostatic hormone” although it may contribute to regulation. Similar experiments with a synthetic precursor of the ketone bodies (1,3 butanediol), suggest that the ketone bodies contribute to the decrease in food intake after reversible obesity, but cannot be a complete explanation. Dietary fat consumption raised plasma free fatty acid (FFA) levels to the range seen during recovery from reversible obesity, suggesting that plasma FFAs may be a blood-borne signal of fat utilization in both cases. Intralipid, a synthetic triglyceride emulsion designed for intravenous administration, also increased plasma FFA levels but suppressed food intake by less than predicted. However, Intralipid may tend to cause spuriously high plasma FFA readings for reasons which are discussed. These results suggest that plasma fat metabolites, especially FFAs, may be blood-borne signals which contribute to the voluntary dieting after reversible obesity.

Prematurity in the rat. II. Effect of hypothermia.

The time-courses of liver glycogen, plasma glucose, lactate, alanine and glycerol concentrations in term and preterm rats undergoing hypothermia (30 degrees C) during the first 2 h after delivery have been studied. Hypothermia prevented liver glycogenolysis and the neonatal decrease of plasma glucose concentration in term and preterm rats during the first 2 h after delivery. Hypothermia decreased plasma glucose, lactate and alanine utilization but increased plasma glycerol concentration. These results suggest that hypothermia blunts the utilization of the main metabolic substrates but increases brown adipose tissue lipolysis for thermogenesis.

Effect of metoprolol on blood glycerol, free fatty acids, triglycerides and glucose in relation to plasma catecholamines in hypertensive patients at rest and following submaximal work.

Studies were performed in nine male patients with moderate hypertension. Treatment with metoprolol, 50--150 mg three times daily for 4--17 weeks, had no effect on the plasma level of glycerol, free fatty acids, triglycerides or glucose under basal conditions, neither in the supine nor in the upright position. Submaximal work, performed postprandially, increased plasma glycerol before medication but not during metoprolol, in spite of a marked increase in plasma noradrenaline. The work load employed caused no change in free fatty acids, triglycerides or glucose, neither before medication nor during metoprolol.

Physical training in human hyperplastic obesity. IV. Effects on the hormonal status

Severely obese subjects and sex- and age-matched controls underwent physical training during a 6-wk period. Evidence of training was shown in all subjects by increased aerobic power. Before training the obese subjects were characterized by the following abberations: decreased glucose tolerance, hyperinsulinemia, elevated blood glycerol and plasma free fatty acids, and a blunted plasma growth hormone response during glucose tolerance. Noradrenaline output was elevated, a finding of potential interest for the explanation of increased lipolysis, blood pressure, and heart size in obesity. With training the following changes were found: In the controls there was evidence for the beginning of a decrease of adipose tissue mass. In the obese, however, body weight, body fat, or fat cell size did not decrease during training. Plasma insulin decreased, and a corresponding increase of plasma glycerol was seen. Glucose tolerance was not changed, and this, together with decreased plasma insulin, indicated an increase insulin sensitivity of the periphery. Changes in noradrenaline or growth hormone during training could not explain this increased sensitivity. Urinary cortisol output was found to decrease after training in the obese; this might be interpreted as a decrease in cortisol secretion allowing a more effective insulin action on the periphery.

Effect of acute temperature stress on the plasma catecholamine, corticosterone and metabolite levels in the pigeon

1. Adult pigeons of both sexes were exposed to either +2°C or +32°C for 5, 15, 30 or 60 min. Furthermore, 2 groups of pigeons were housed at these temperatures for 3 weeks. 2. Acute cold or heat stress produced biphasic changes in the blood NA, A and corticosterone concentrations. Both at cold and heat an immediate rise in A level was seen, but corticosterone level increased only at cold, which was followed by a fall at 30 min. Thereafter the corticosterone levels were recovered and at 60 min even exceeded the initial values. In NA level an immediate and controversial fall both at cold and heat was seen. However, at cold, an unexpected and significant elevation above the pre-exposure level was seen at 30 min. 3. In FFA, glycerol and glucose levels an immediate fall at heat but a controversial elevation at cold was observed. 4. Our findings show that there are increased plasma glycerol, FFA, A and NA levels in cold-acclimated pigeon compared with heat-acclimated pigeon.