Expression of lipolytic genes in adipose tissue is differentially regulated during multiple phases of dietary intervention in obese women.

The aim of this study was to investigate the time-course of the expression of key lipolysis-regulating genes in the subcutaneous adipose tissue (SCAT) during different phases of a 6-month dietary intervention. Fifteen obese women (BMI 34.7+/-1.0 kg.m(-2)) underwent a 6-month dietary intervention consisting of 1 month very low calorie diet (VLCD), followed by 2 months low calorie diet (LCD) and 3 months weight maintenance diet (WM). At each phase of the dietary intervention, a needle microbiopsy of the abdominal SCAT was obtained to evaluate mRNA expression of key lipolysis-regulating genes and a hyperinsulinemic euglycemic clamp (HEC) was performed. Dietary intervention induced a body weight reduction of 9.8 % and an improvement of insulin sensitivity as assessed by a HEC. Compared to pre-diet levels, mRNA levels of the adrenergic beta(2)-receptor in SCAT were higher at the end of VLCD and not different at the end of LCD and WM. In contrast, the expression of the adrenergic alpha(2)-receptor was lower at the end of VLCD and LCD compared to the pre-diet levels and did not differ at WM. Adipose triglyceride lipase and hormone-sensitive lipase levels were lower than the pre-diet levels at the end of LCD only, while phosphodiesterase-3B and the insulin receptor levels did not change throughout the dietary intervention. The results suggest that the regulation pattern of the genes that are involved in the control of lipolysis is different at the respective phases of the dietary intervention and depends on the duration of the diet and the status of energy balance.

Adrenaline but not noradrenaline is a determinant of exercise-induced lipid mobilization in human subcutaneous adipose tissue.

The relative contribution of noradrenaline (norepinephrine) and adrenaline (epinephrine) in the control of lipid mobilization in subcutaneous adipose tissue (SCAT) during exercise was evaluated in men treated with a somatostatin analogue, octreotide. Eight lean and eight obese young men matched for age and physical fitness performed 60 min exercise bouts at 50% of their maximal oxygen consumption on two occasions: (1) during i.v. infusion of octreotide, and (2) during placebo infusion. Lipolysis and local blood flow changes in SCAT were evaluated using in situ microdialysis. Infusion of octreotide suppressed plasma insulin and growth hormone levels at rest and during exercise. It blocked the exercise-induced increase in plasma adrenaline while that of noradrenaline was unchanged. Plasma natriuretic peptides (NPs) level was higher at rest and during exercise under octreotide infusion in lean men. Under placebo, no difference was found in the exercise-induced increase in glycerol between the probe perfused with Ringer solution alone and that with phentolamine (an alpha-adrenergic receptor antagonist) in lean subjects while a greater increase in glycerol was observed in the obese subjects. Under placebo, propranolol infusion in the probe containing phentolamine reduced by about 45% exercise-induced glycerol release; this effect was fully suppressed under octreotide infusion while noradrenaline was still elevated and exercise-induced lipid mobilization maintained in both lean and obese individuals. In conclusion, blockade of beta-adrenergic receptors during exercise performed during infusion of octreotide (blocking the exercise-induced rise in adrenaline but not that of noradrenaline) does not alter the exercise-induced lipolysis. This suggests that adrenaline is the main adrenergic agent contributing to exercise-induced lipolysis in SCAT. Moreover, it is the combined action of insulin suppression and NPs release which explains the lipolytic response which remains under octreotide after full local blockade of fat cell adrenergic receptors. For the moment, it is unknown if results apply specifically to SCAT and exercise only or if conclusions could be extended to all forms of lipolysis in humans.

Aerobic training improves exercise-induced lipolysis in SCAT and lipid utilization in overweight men.

The aim of this study was to investigate whether endurance training improves lipid mobilization and oxidation in overweight subjects. Eleven young men (25.6 +/- 1.4 yr and body mass index 27.7 +/- 0.2) performed a 4-mo training program consisting of practicing aerobic exercise 5 days/wk. Before and after the training period, lipid oxidation was explored during a 60-min exercise at 50% of peak O2 consumption by use of indirect calorimetry. Lipid mobilization and antilipolytic alpha2-adrenoceptor effect were also studied using the microdialysis method in abdominal subcutaneous adipose tissue (SCAT). After training, plasma nonesterified fatty acid (NEFA) levels, at rest and during exercise, were significantly lower than before (P < 0.001). Lipolysis in SCAT was significantly higher after than before training. An antilipolytic alpha2-adrenoceptor effect in SCAT was underlined during exercise before training and disappeared after. The respiratory exchange ratio was lower after training, i.e., the percentage of lipid oxidation was higher only at rest. The amount of lipid oxidized was higher after training, at rest, and during exercise. Although exercise power was higher after training, the relative intensity was equivalent, as suggested by a similar increase in plasma catecholamine concentrations before and after training. In conclusion, 4-mo training in overweight men improved lipid mobilization through a decrease of antilipolytic alpha2-adrenoceptor effect in SCAT and lipid oxidation during moderate exercise. Training induced a decrease of blood NEFA, predicting better prevention of obesity.

Post-exercise increase of lipid oxidation after a moderate exercise bout in untrained healthy obese men.

The aim of the study was to examine whether a moderate exercise increases the utilization of fatty acids during the recovery period in obese men. Six healthy obese participated in a randomized crossover investigation, one with exercise and one without exercise. At 8 a. m., the subjects had a standardized breakfast and they rested in a sitting position for 3 hours. The subjects were maintained in the sitting position for 4 additional hours in one session. In a second session, they exercised for 60 min at 50 % of their VO(2) max and then returned to the sitting position for 3 hours. Respiratory exchange ratio (RER) values were calculated by indirect calorimetry. During the resting session, plasma non-esterified fatty acids (NEFA) and glycerol concentrations rose progressively, whereas RER progressively decreased. During the exercise, plasma catecholamines, NEFA, glycerol, growth hormone and cortisol levels and RER increased while insulin decreased. During the recovery, plasma NEFA increased and glycerol decreased. During the first hour of recovery, RER values were lower and fatty acid utilization higher than during the same period of the resting session. The study shows that exercise induces modifications in hormonal factors promoting lipid mobilization and suggests that exercise provide substantial amounts of NEFA for muscle oxidation during recovery from an exercise bout in obese subjects.

Effect of a long-duration physical exercise on fat cell lipolytic responsiveness to adrenergic agents and insulin in obese men.

OBJECTIVE: The aim of the study was to investigate whether a long-lasting bout of exercise modifies the lipolytic beta- and antilipolytic-alpha(2)-adrenergic effect and the antilipolytic effect of insulin in obese subjects. DESIGN: Biopsies of abdominal subcutaneous adipose tissue were performed before and immediately after 2 h exercise (at 50% of VO(2max)) on an ergometric bicycle. SUBJECTS: Nine healthy obese male subjects (mean age 38.0+/-3.5 y; mean body mass index (BMI) 35.6+/-3.9 kg/m(2)) were included in the experiment. METHODS: :The lipolytic responsiveness to adrenaline, isoprenaline (beta-adrenergic agonist), UK-14304 (alpha(2)-adrenergic agonist) and insulin was studied in the isolated fat cell obtained by biopsies of subcutaneous adipose tissue from the peri-umbilical region before and after exercise. RESULTS: After exercise, an increase was observed in spontaneous lipolytic rate, and in the lipolytic effect of isoprenaline, but no modification in the lipolytic action of adrenaline. Antilipolytic effects of UK-14304 and insulin were not changed by the single bout of exercise. CONCLUSION: A single bout of long-term exercise increased the responsiveness of adipose tissue to beta-adrenergic stimulation of lipolysis in obese subjects.

Lack of alpha(2)-adrenergic antilipolytic effect during exercise in subcutaneous adipose tissue of trained men.

The aim of this study was to investigate the involvement of the antilipolytic alpha(2)-adrenergic receptor pathway in the regulation of lipolysis during exercise in subcutaneous abdominal adipose tissue (SCAAT). Seven trained men and 15 untrained men were studied. With the use of microdialysis, the extracellular glycerol concentration was measured in SCAAT at rest and during 60 min of exercise at 50% of maximal oxygen consumption. One microdialysis probe was perfused with Ringer solution; the other was supplemented with phentolamine (alpha(2)-adrenergic receptor antagonist). No differences in baseline extracellular or plasma glycerol concentrations were found between the two groups. The exercise-induced extracellular and plasma glycerol increase was higher in trained compared with untrained subjects (P < 0.05). Addition of phentolamine to the perfusate enhanced the exercise-induced response of extracellular glycerol in untrained subjects but not in trained subjects. The exercise-induced increase in plasma norepinephrine and epinephrine concentrations and the decrease in plasma insulin were not different in the two groups. These in vivo findings demonstrate higher exercise-induced lipolysis in trained compared with untrained subjects and show that, in trained subjects, the alpha(2)-mediated antilipolytic action is not involved in the regulation of lipolysis in SCAAT during exercise.

A single bout of exercise induces beta-adrenergic desensitization in human adipose tissue.

This study was designed to assess whether physiological activation of the sympathetic nervous system induced by exercise changes adipose tissue responsiveness to catecholamines in humans. Lipid mobilization in abdominal subcutaneous adipose tissue was studied with the use of a microdialysis method in 11 nontrained men (age: 22. 3 +/- 1.5 yr; body mass index: 23.0 +/- 1.6). Adipose tissue adrenergic sensitivity was explored with norepinephrine, dobutamine (beta(1)-agonist), or terbutaline (beta(2)-agonist) perfused during 30 min through probes before and after 60-min exercise (50% of the maximal aerobic power). The increase in extracellular glycerol concentration during infusion was significantly lower after the exercise when compared with the increase observed before the exercise (P < 0.05, P < 0.02, and P < 0.01, respectively, for norepinephrine, dobutamine, and terbutaline). In a control experiment realized without exercise, no difference in norepinephrine-induced glycerol increase between the two infusions was observed. To assess the involvement of catecholamines in the blunted beta-adrenergic-induced lipolytic response after exercise, adipose tissue adrenergic sensitivity was explored with two 60-min infusions of norepinephrine or epinephrine separated by a 60-min interval. With both catecholamines, the increase in glycerol was significantly lower during the second infusion (P < 0.05). The findings suggest that aerobic exercise, which increased adrenergic activity, induces a desensitization in beta(1)- and beta(2)-adrenergic lipolytic pathways in human subcutaneous adipose tissue.

Recent developments on lipolysis regulation in humans and discovery of a new lipolytic pathway.

In man, the major hormones controlling the lipolytic function are insulin (inhibition of lipolysis) and catecholamines (stimulation of lipolysis). Catecholamines are of major importance for the regulation of lipid mobilization in human adipose tissue and for the increase of non-esterified fatty acid supply to the working muscle. In vitro studies have shown that there are differences in the catecholaminergic control of fat cells from various fat deposits and a number of physiological and pathological alterations of catecholamine-induced lipolysis have been reported. Lipolytic resistance to catecholamines has been reported in subcutaneous adipose tissue, the major fat depot in obese subjects. Multiple alterations in catecholamine signal transduction pathways have been reported. In situ microdialysis allows a physiological exploration of adipose tissue biology. Recent data obtained on the catecholaminergic regulation of lipolysis and lipid mobilization, using microdialysis in humans, will be analysed. A potent lipolytic and lipomobilizing effect of atrial natriuretic peptide has recently been discovered; the mechanisms of action and physiological relevance will also be discussed.

Determination of appendicular muscle mass by dual energy X-ray absorptiometry method in women with sarcopenia and Alzheimer's disease.

OBJECTIVES: To study appendicular muscle mass in women with Alzheimer's disease (AD) to investigate the association between sarcopenia and AD. To examine the AD associated changes in body fat distribution. DESIGN: a cross-sectional study of 32 women with AD and 32 healthy age and bone mineral density matched women. SETTING: Toulouse, France. RESULTS: No differences were noted in fat free soft tissue mass or Appendicular Skeletal Muscle (ASM) mass between AD women and control women. The difference of ASM (kg) /height2 (m)2, used as an index of relative skeletal muscle mass, was not statistically significative between the two groups. The prevalence of sarcopenia increased from 21.9 % in healthy elderly women to 40.6 % in AD women but the difference was not statistically significant. No statistically significant relationship emerged between sarcopenia and AD (OR= 0.41, CI 0.12-1.4). Moreover, total body fat mass was significantly lower in women with AD than in the age -, sex - and bone mineral density - matched controls. CONCLUSION: AD are not necessary linked to sarcopenia. The decrease in adipose tissue in women with AD could be one more factor involving estrogen deficiency in the etiology of the disease.

Activation of alpha(2)-adrenergic receptors impairs exercise-induced lipolysis in SCAT of obese subjects.

With the use of the microdialysis method, exercise-induced lipolysis was investigated in subcutaneous adipose tissue (SCAT) in obese subjects and compared with lean ones, and the effect of blockade of alpha(2)-adrenergic receptors (ARs) on lipolysis during exercise was explored. Changes in extracellular glycerol concentrations and blood flow were measured in SCAT in a control microdialysis probe at rest and during 60-min exercise bouts (50% of heart rate reserve) and in a probe supplemented with the alpha(2)-AR antagonist phentolamine. At rest and during exercise, plasma norepinephrine and epinephrine concentrations were not different in obese compared with lean men. In the basal state, plasma and extracellular glycerol concentrations were higher, whereas blood flow was lower in SCAT of obese subjects. During exercise, the increase of plasma glycerol was higher in obese subjects (115 +/- 35 vs. 65 +/- 21 micromol/l). Oppositely, the exercise-induced increase in extracellular glycerol concentrations in SCAT was five- to sixfold lower in obese than in lean subjects (50 +/- 14 vs. 318 +/- 53 micromol/l). The exercise-induced increase in extracellular glycerol concentration was not significantly modified by phentolamine infusion in lean subjects but was strongly enhanced in the obese subjects and reached the concentrations found in lean sujects (297 +/- 46 micromol/l). These findings demonstrate that the physiological stimulation of SCAT adipocyte alpha(2)-ARs during exercice-induced sympathetic nervous system activation contributes to the blunted lipolysis noted in obese men.

Natriuretic peptides: a new lipolytic pathway in human adipocytes.

Atrial natriuretic peptide (ANP) receptors have been described on rodent adipocytes and expression of their mRNA is found in human adipose tissue. However, no biological effects associated with the stimulation of these receptors have been reported in this tissue. A putative lipolytic effect of natriuretic peptides was investigated in human adipose tissue. On isolated fat cells, ANP and brain natriuretic peptide (BNP) stimulated lipolysis as much as isoproterenol, a nonselective beta-adrenergic receptor agonist, whereas C-type natriuretic peptide (CNP) had the lowest lipolytic effect. In situ microdialysis experiments confirmed the potent lipolytic effect of ANP in abdominal s.c. adipose tissue of healthy subjects. A high level of ANP binding sites was identified in human adipocytes. The potency order defined in lipolysis (ANP > BNP > CNP) and the ANP-induced cGMP production sustained the presence of type A natriuretic peptide receptor in human fat cells. Activation or inhibition of cGMP-inhibited phosphodiesterase (PDE-3B) (using insulin and OPC 3911, respectively) did not modify ANP-induced lipolysis whereas the isoproterenol effect was decreased or increased. Moreover, inhibition of adenylyl cyclase activity (using a mixture of alpha(2)-adrenergic and adenosine A1 agonists receptors) did not change ANP- but suppressed isoproterenol-induced lipolysis. The noninvolvement of the PDE-3B was finally confirmed by measuring its activity under ANP stimulation. Thus, we demonstrate that natriuretic peptides are a new pathway controlling human adipose tissue lipolysis operating via a cGMP-dependent pathway that does not involve PDE-3B inhibition and cAMP production.

Adipose tissue lipolysis is increased during a repeated bout of aerobic exercise.

The goal of the study was to examine whether lipid mobilization from adipose tissue undergoes changes during repeated bouts of prolonged aerobic exercise. Microdialysis of the subcutaneous adipose tissue was used for the assessment of lipolysis; glycerol concentration was measured in the dialysate leaving the adipose tissue. Seven male subjects performed two repeated bouts of 60-min exercise at 50% of their maximal aerobic power, separated by a 60-min recovery period. The exercise-induced increases in extracellular glycerol concentrations in adipose tissue and in plasma glycerol concentrations were significantly higher during the second exercise bout compared with the first (P < 0.05). The responses of plasma nonesterified fatty acids and plasma epinephrine were higher during the second exercise bout, whereas the response of norepinephrine was unchanged and that of growth hormone lower. Plasma insulin levels were lower during the second exercise bout. The results suggest that adipose tissue lipolysis during aerobic exercise of moderate intensity is enhanced when an exercise bout is preceded by exercise of the same intensity and duration performed 1 h before. This response pattern is associated with an increase in the exercise-induced rise of epinephrine and with lower plasma insulin values during the repeated exercise bout.

Weight loss in Alzheimer disease.

BACKGROUND: Epidemiologic studies have shown that weight loss is commonly associated with Alzheimer disease (AD) and is a manifestation of the disease itself. The etiology of weight loss in AD appears multifactorial. Hypotheses to explain the weight loss have been suggested (eg, atrophy of the mesial temporal cortex, biological disturbances, and higher energy expenditure); however, none have been proven. OBJECTIVE: In the first part of this article, we describe weight loss in AD (epidemiologic data and hypotheses to explain weight loss and anorexia in AD). In the second part we report the results of a longitudinal study of the changes in nutritional variables in a cohort of patients with a probable diagnosis of AD. DESIGN: We followed subjects with AD (based on criteria of the National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer's Disease and Related Disorders Association) who were recruited from the Alzheimer's Disease Center in Toulouse. All subject underwent a nutritional, neuropsychologic, and functional evaluation. The Zarit scales were used to assess caregiver burden and caregiver reactions to the patients' behavioral and autonomic disorders. RESULTS: We showed that only results of the Burden Interview and the Memory and Behavior Problems Checklist, which explored caregiver burden, predicted weight loss in AD. It is possible that caregivers who consider themselves overburdened by the disease process are not willing to invest adequate resources to allow AD patients to properly nourish themselves. CONCLUSION: Nutritional education programs for the caregivers of AD patients seem to be the best way to prevent weight loss and improve the nutritional status of these patients.

Activation of antilipolytic alpha(2)-adrenergic receptors by epinephrine during exercise in human adipose tissue.

The involvement of the antilipolytic alpha(2)-adrenergic pathway and the specific role of epinephrine in the control of lipolysis during exercise in adipose tissue (AT) were investigated in healthy male subjects (age: 24.1 +/- 2.2 yr; body mass index: 23.0 +/- 1.6). An in vitro study carried out on isolated adipocytes showed that the weak lipolytic effect of epinephrine was potentiated after blockade of alpha(2)-adrenergic receptor (AR) by an alpha(2)-AR antagonist and reached that of isoproterenol, a beta-AR agonist. The effect of the nonselective alpha(2)-AR antagonist phentolamine on the response of the extracellular glycerol concentration (EGC) in AT during two successive bouts of aerobic exercise (50% maximum O(2) uptake, 60 min duration) was evaluated using the microdialysis method. The metabolic responses measured in perfused probes with Ringer solution were compared with those obtained in perfused probes with Ringer plus 0.1 mmol/l phentolamine. Plasma norepinephrine level was not different during the two exercise bouts, whereas that of epinephrine was 2.5-fold higher during the second exercise. EGC in AT was twofold higher in the second compared with the first exercise, and the same response pattern was found for plasma glycerol. The exercise-induced increase in EGC was higher in the probe perfused with phentolamine compared with the control probe in both bouts of exercise. However, the potentiating effect of phentolamine on EGC was significant during the second exercise bout but did not reach a significant level during the first. These results suggest that epinephrine is involved in the control of lipid mobilization through activation of antilipolytic alpha(2)-AR in human subcutaneous AT during exercise.

[Alzheimer's disease and nutrition]. / Maladie d'Alzheimer et nutrition.

Weight loss is a nutritional problem commonly associated with Alzheimer disease. Two types of weight loss have been described. A severe weight loss correlated with a decrease in daily caloric intake and with increased difficulties in performing the activities of daily living. A slowly progressive but clinically significant loss, not associated with either a decrease in caloric intake or an inflammatory syndrome. It is difficult to explain this type of weight loss as subjects have adequate caloric intakes. Several hypothesis are however considered as increased energy requirements (which can result from increased energy expenditure, from increased metabolic disorder, or from increased growth hormone secretion), or mesial temporal cortex atrophy. But, at the present time, no study can give a proper explanation. Vitamin deficiencies, specially vitamin B6, B12 and folates, high homocysteine level, antioxidants deficiencies (especially, vitamin E deficiency), iron, counter, and phenol derived could also influence the memory capacities and have an effect upon cognitive impairment, as reported in epidemiological studies. The prevention of nutritional deficiencies in patients with Alzheimer's disease, could be one of the strategies to improve the caregiver and the patients quality of life.

Lack of antilipolytic effect of lactate in subcutaneous abdominal adipose tissue during exercise.

The purpose of our study was to evaluate the potential inhibition of adipose tissue mobilization by lactate. Eight male subjects (age, 26. 25 +/- 1.75 yr) in good physical condition (maximal oxygen uptake, 59.87 +/- 2.77 ml. kg-1. min-1; %body fat, 10.15 +/- 0.89%) participated in this study. For each subject, two microdialysis probes were inserted into abdominal subcutaneous tissue. Lactate (16 mM) was perfused via one of the probes while physiological saline only was perfused via the other, both at a flow rate of 2.5 microl/min. In both probes, ethanol was also perfused for adipose tissue blood flow estimation. Dialysates were collected every 10 min during rest (30 min), exercise at 50% maximal oxygen consumption (120 min), and recovery (30 min) for the measurement of glycerol concentration. During exercise, glycerol increased significantly in both probes. However, no differences in glycerol level and ethanol extraction were observed between the lactate and control probes. These findings suggest that lactate does not impair subcutaneous abdominal adipose tissue mobilization during exercise.

Endurance training increases the beta-adrenergic lipolytic response in subcutaneous adipose tissue in obese subjects.

OBJECTIVE: The aim of this study was to assess, by longitudinal follow-up, the influence of aerobic training on the in vivo lipolytic activity of adipose tissue in obese male subjects. SUBJECTS: Eleven obese non-diabetic males, aged 41.5+/-5.77 (range 27-49 y) with body mass index (BMI) 36.5+/-4.5 kg/m2 (range 29.4-47.1 kg/m2) participated in the study. DESIGN: Subjects took part in a 12-week aerobic training program. Before and after training, microdialysis of abdominal subcutaneous adipose tissue (SCAT) was carried out, using perfusion with graded doses of the beta-adrenergic agonist isoprenaline and a single dose of the phosphodiesterase inhibitor theophylline. In addition, the response of plasma glycerol and free fatty acids (FFAs) to intravenous infusion of graded doses of isoprenaline was tested. RESULTS: The training did not induce significant weight loss and promoted an increase in maximum aerobic capacity (P<0.05). The increase of extracellular glycerol in SCAT in response to isoprenaline perfusion was enhanced after the training (P<0.05), while no change in the response of interstitial glycerol to theophylline action was observed. The training did not elicit a change in the isoprenaline-induced changes of blood flow in adipose tissue. The increases of plasma FFAs and glycerol in response to intravenous isoprenaline infusion, were significantly enhanced after training. CONCLUSION: The present study shows that aerobic training induced an increase in the response of plasma and subcutaneous adipose tissue concentration of glycerol to beta-adrenergic stimulation. The effect of an agent acting at the post-receptor level (theophylline) in SCAT was not modified by training.

Decrease of subcutaneous adipose tissue lipolysis after exposure to hypoxia during a simulated ascent of Mt Everest.

The purpose of this study was to examine the effects of prolonged hypoxia on adipose tissue lipolysis, in relation to the weight loss usually observed at high altitude. Eight male subjects were exposed for 31 days to gradually increasing hypobaric hypoxia up to the equivalent altitude of 8848 m (Mt Everest) in a decompression chamber, after 7 days at 4350 m for altitude pre-acclimatization. A biopsy of subcutaneous adipose tissue was performed before and after hypoxic exposure, to study in vitro changes in adipose tissue sensitivity. Fat mass, adipocyte volume and spontaneous lipolysis were not impaired by the exposure to hypoxia. The in vitro lipolytic response to epinephrine, isoproterenol, growth hormone (GH) and parathormone (PTH) decreased significantly (P<0.01, P<0.05, P<0.01 and P<0.01 respectively), as did the plasma concentration of free fatty acid (P<0.01). The anti-lipolytic effect promoted by alpha2-adrenergic receptor stimulation (epinephrine with propranolol) was greater after hypoxia (P<0.05), while the anti-lipolytic activity of insulin was decreased (P<0.01). In conclusion, prolonged exposure to hypobaric hypoxia led to a potent reduction in lipid mobilization, through a decrease in the efficiency of beta-adrenergic, GH and PTH lipolytic pathways, as well as an increment in the alpha2-adrenergic-receptor-mediated anti-lipolytic effects.

Endurance training changes in lipolytic responsiveness of obese adipose tissue.

The aim of this study was to investigate the effect of aerobic exercise training on the lipolytic response of adipose tissue in obese subjects. Thirteen men (body mass index = 36.9 +/- 1.3 kg/m2) were submitted to aerobic physical training on a cycloergometer (30-45 min, 4 days a wk) for 3 mo. Adipocyte sensitivity to the action of catecholamines and insulin was studied in vitro before and after training. Training induced a decrease in the percentage of fat mass (P < 0.05) without changing the body weight. Basal lipolysis and hormone-sensitive lipase activity were significantly decreased after training (P < 0.05). The lipolytic effects of epinephrine, isoprenaline (beta-adrenoceptor agonist), and dobutamine (beta1-adrenoceptor agonist) were significantly increased (P < 0.05) but not those of procaterol (beta2-adrenoceptor agonist). The antilipolytic effects of alpha2-adrenoceptor and insulin were significantly decreased (P < 0.05). Lipolysis stimulation by agents acting at the postreceptor level was unchanged after training. In conclusion, aerobic physical training in obese male subjects modifies adipose tissue lipolysis through an enhancement of beta-adrenergic response and a concomitant blunting of adipocyte antilipolytic activity.