Adipose tissue and adipocyte dysregulation.

Obesity-associated insulin resistance is a complex disorder involving a number of candidate molecules, pathways and transduction systems possessing potential causal actions. Inflammation in adipose tissue (AT) is one mechanism proposed to explain the development of insulin resistance, while identification of factors that lead to or cause AT dysfunction when it reaches its limit of expansion represents an important challenge. Pathological expansion of AT is characterized by changes in its blood flow, and the presence of enlarged and dysfunctional adipocytes that begin an inflammatory campaign of altered adipokine and cytokine secretions. Adipocyte senescence, necrosis and death are associated with increased immune cell and macrophage infiltration of AT in obesity. This can boost inflammation and reinforce fat cell dysfunction and death. In addition, pathological fat mass expansion is also related to limited recruitment of fat cell progenitors able to proliferate and differentiate into healthy small fat cells to compensate for cell death and preserve adipocyte numbers. Limiting vascular development and enhancing fibrotic processes worsen inflammation towards chronic irreversibility. The AT expandability hypothesis states that failure of AT expansion is one of the key factors linking positive energy balance and cardiometabolic risks, not obesity per se. Besides the usual treatment of obesity based on behavioral approaches (specific dietary/nutritional approaches together with increased physical activity), a number of questions remain concerning the possible recovery of metabolic health after inflammation-preventing interventions.

[Fat mass expansion, fatty acids and adipokines: metabolic markers and risk factors for cardiovascular pathologies]. / Expansion de la masse grasse, acides gras et adipokines : des marqueurs métaboliques et des facteurs de risque de pathologies cardiovasculaires.

Obesity is described as an independent risk factor for cardiovascular disease. Fat mass expansion is often associated with occurrence of a pro-inflammatory state, which will interfere with cell metabolism in various tissues and alter noticeably insulin-signaling processes. This low-grade, systemic inflammatory response that characterizes obesity will develop towards dysfunctions which will include insulin-resistance, type 2 diabetes, dyslipidemia, hypertension and coronary and vascular pathologies and even toward some cancers. Metabolic and endocrine functions will be briefly considered as well as events related to fat mass expansion such as hypertrophy-related disturbances in adipocyte function and adipose tissue infiltration by immune cells (i.e., macrophages and lymphocytes which could secrete cytokines and chemokines). In addition to the well known function of storage and release on non esterified fatty acids (NEFAs), the adipocytes synthesize and secrete circulating hormones (called adipokines such as leptin, adiponectin and apelin) which are acting as signaling molecules and which are mediators/modulators of the inflammatory processes. The interest of adipose tissue productions as plasma metabolic markers and the dialogue and interactions between adipose tissue productions (i.e., NEFAs, adipokines and cytokines) and other target tissues will be considered. The objective of this paper is to describe adipose tissue dysfunctions observed in obesity and to delineate putative relationships, which could exist between adipose tissue dysfunctions and other tissues. The idea is to describe how adipose tissue dysfunction is involved in the development of type 2 diabetes and cardiovascular diseases.

Recommendations for healthier hydration: addressing the public health issues of obesity and type 2 diabetes.

Given the rapid increase in the prevalence of overweight, obesity, type 2 diabetes and other obesity-related conditions across the world, despite a plethora of evidence-based guidance for clinicians, innovative campaigns aimed at the general public and widespread government public health initiatives, it is clear that a novel approach is required. The importance of fluid intake has been overlooked in campaigns and guidelines and also in the clinical setting, where the question 'what do you drink?' is often omitted. It is a significant oversight that food pyramids and healthy-eating plates across the world omit fluids from their graphics and advice. While guidelines include recommendations on changes in physical activity and diet, often little or no advice is offered on the importance of healthier hydration practices, neglecting to highlight the contribution of beverages high in sugar, alcohol or additives. An interdisciplinary group of experts in medicine, nutrition, physiology and public health discussed issues surrounding healthy-hydration practices in March 2010 in Paris to create a consensus statement on hydration and gain of body weight and provide recommendations.

Neurohumoral and metabolic response to exercise in water.

Atrial natriuretic peptide (ANP) stimulates lipid mobilization and lipid oxidation in humans. The mechanism appears to promote lipid mobilization during exercise. We tested the hypothesis that water immersion augments exercise-induced ANP release and that the change in ANP availability is associated with increased lipid mobilization and lipid oxidation. In an open randomized and cross-over fashion we studied 17 men (age 31+/-3.6 years; body mass index 24+/-1.7 kg/m(2); body fat 17+/-6.7%) on no medication. Subjects underwent two incremental exercise tests on a bicycle ergometer. One test was conducted on land and the other test during immersion in water up to the xiphoid process. In a subset (n=7), we obtained electromyography recordings in the left leg. We monitored gas exchange, blood pressure, and heart rate. In addition, we obtained blood samples towards the end of each exercise step to determine ANP, norepinephrine, epinephrine, lactate, free fatty acids, insulin, and glucose concentrations. Heart rate, systolic blood pressure, and oxygen consumption at the anaerobic threshold and during peak exercise were similar on land and with exercise in water. The respiratory quotient was mildly reduced when subjects exercised in water. Glucose and lactate measurements were decreased whereas free fatty acid concentrations were increased with exercise in water. Water immersion attenuated epinephrine and norepinephrine and augmented ANP release during exercise. Even though water immersion blunts exercise-induced sympathoadrenal activation, lipid mobilization and lipid oxidation rate are maintained or even improved. The response may be explained by augmented ANP release.

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.

Use of the microdialysis technique to assess lipolytic responsiveness of femoral adipose tissue after 12 sessions of mechanical massage technique.

BACKGROUND: Adipocytes in femoral areas are known to be metabolically 'silent'. Changes related to fat cell hypertrophy may be involved in the formation of cellulite. A mechanical massage technique, with circulatory and dermotrophic properties, has been shown to have an impact on clinical evaluations (i.e. changes in morphometric measurements) in cellulite areas. Whether this technique affected lipolytic responsiveness in subcutaneous adipose tissue of cellulite areas was not known. OBJECTIVE: Using a microdialysis technique in subcutaneous adipose tissue, a study was carried out to test the in situ incidence of a mechanical massage technique in terms of adipose tissue responsiveness to a lipolytic challenge. MATERIALS AND METHODS: Nine healthy women volunteers with cellulite (grade > or = 2) were included and treated with 12 sessions of mechanical massage technique (Endermologie). Microdialysis has been carried out in the femoral adipose tissue in order to assess lipolytic responsiveness via glycerol determination following perfusion of a lipolytic agent (0.1, 1 and 10 microm isoproterenol). Clinical evaluations (measurements of waist, thighs and skin fold) were carried out in parallel. All evaluations were performed before and after treatment. RESULTS: The studied intervention lowered resting dialysate glycerol levels in femoral adipose tissue. The lipid-mobilizing effect of isoproterenol was enhanced after 1 month of treatment. In addition, a clear decrease of morphometric measurements (mean decrease on thighs perimeter: 3.1 to 3.3 cm, P < 0.01) was observed. CONCLUSION: These results suggest an increase in the lipolytic responsiveness of femoral adipose tissue in women with cellulite having undergone 12 sessions of mechanical massage.

Impact of visceral adipose tissue on liver metabolism. Part I: heterogeneity of adipose tissue and functional properties of visceral adipose tissue.

Excess visceral adipose tissue is associated with anomalies of blood glucose homoeostasis, elevation of plasma triglycerides and low high-density lipoprotein cholesterol that contribute to the later appearance of type 2 diabetes and cardiovascular syndromes. Visceral adipose tissue releases a large amount of free fatty acids and hormones/cytokines in the portal vein that are delivered to the liver, and interact with hepatocytes and various immune cells in the liver. The functional characteristics of visceral adipose tissue will be compared with subcutaneous adipose tissue to clarify the major mechanisms affecting free fatty acid metabolism and cytokine production.

Impact of visceral adipose tissue on liver metabolism and insulin resistance. Part II: Visceral adipose tissue production and liver metabolism.

Excess visceral adipose tissue is associated with anomalies of blood glucose homoeostasis, elevation of plasma triglycerides and low levels of high-density lipoprotein cholesterol that contribute to the development of type-2 diabetes and cardiovascular syndromes. Visceral adipose tissue releases a large amount of free fatty acids and hormones/cytokines in the portal vein that are delivered to the liver. The secreted products interact with hepatocytes and various immune cells in the liver. Altered liver metabolism and determinants of insulin resistance associated with visceral adipose tissue distribution are discussed, as well as, determinants of an insulin-resistant state promoted by the increased free fatty acids and cytokines delivered by visceral adipose tissue to the liver.

Remodeling phenotype of human subcutaneous adipose tissue macrophages.

BACKGROUND: Adipose tissue macrophages (ATMs) have become a focus of attention recently because they have been shown to accumulate with an increase in fat mass and to be involved in the genesis of insulin resistance in obese mice. However, the phenotype and functions of human ATMs are still to be defined. METHODS AND RESULTS: The present study, performed on human subcutaneous AT, showed that ATMs from lean to overweight individuals are composed of distinct macrophage subsets based on the expression of several cell surface markers: CD45, CD14, CD31, CD44, HLA-DR, CD206, and CD16, as assessed by flow cytometry. ATMs isolated by an immunoselection protocol showed a mixed expression of proinflammatory (tumor necrosis factor-alpha, interleukin-6 [IL-6], IL-23, monocyte chemoattractant protein-1, IL-8, cyclooxygenase-2) and antiinflammatory (IL-10, transforming growth factor-beta, alternative macrophage activation-associated cc chemokine-1, cyclooxygenase-1) factors. Fat mass enlargement is associated with accumulation of the CD206+/CD16- macrophage subset that exhibits an M2 remodeling phenotype characterized by decreased expression of proinflammatory IL-8 and cyclooxygenase-2 and increased expression of lymphatic vessel endothelial hyaluronan receptor-1. ATMs specifically produced and released matrix metalloproteinase-9 compared with adipocytes and capillary endothelial cells, and secretion of matrix metalloproteinase-9 from human AT in vivo, assessed by arteriovenous difference measurement, was correlated with body mass index. Finally, ATMs exerted a marked proangiogenic effect on AT-derived endothelial and progenitor cells. CONCLUSIONS: The present results showed that the ATMs that accumulate with fat mass development exhibit a particular M2 remodeling phenotype. ATMs may be active players in the process of AT development through the extension of the capillary network and in the genesis of obesity-associated cardiovascular pathologies.

Advances in adipose tissue metabolism.

This review will focus on the recent findings in adipose tissue metabolism with special attention to human adipocyte biology and physiology. There are major advances stemming from the concomitant results obtained from studies on mature human adipocytes, human preadipocytes differentiated in vitro and murine adipose cell lines. Physiological developments have been based on the expanded utilization of various kinds of murine transgenic models and physiological techniques such as microdialysis, open-flow microperfusion, arteriovenous techniques and the utilization of deuterium- or tritium-labelled metabolites that have provided a number of physiological advances in the understanding of human adipose tissue physiology. Gene expression profiling studies and nutrigenomics are emerging methods that herald interesting approaches for the future. An overview of recent discoveries in the mechanisms involved in the control of free fatty acid uptake, triacylglycerol synthesis and fat deposition will be discussed, as well as recent advances in the mechanisms involved in the lipolytic pathways, the role of lipases and perilipins. In addition, the in vivo validation of catecholamine action and the discovery of the lipolytic effects of natriuretic peptides will also be covered.

Phosphodiesterase-5A and neutral endopeptidase activities in human adipocytes do not control atrial natriuretic peptide-mediated lipolysis.

BACKGROUND AND PURPOSE: Atrial natriuretic peptide (ANP) stimulates lipolysis in human adipocyte through a cGMP signalling pathway, the regulation of which is poorly known. Since phosphodiesterases (PDE) and neutral endopeptidase (NEP) play a major role in the regulation of the biological effects of natriuretic peptides in the cardiovascular and renal systems, we investigated whether these mechanisms could regulate cGMP signalling and ANP-mediated lipolysis in human adipocytes. EXPERIMENTAL APPROACH: The presence of cGMP-specific PDE and NEP in differentiated pre-adipocytes and in mature adipocytes was evaluated by real-time qPCR and Western blot. The effect of non-selective and selective inhibition of these enzymes on ANP-mediated cGMP signalling and lipolysis was determined in isolated mature adipocytes. KEY RESULTS: PDE-5A was expressed in both pre-adipocytes and adipocytes. PDE-5A mRNA and protein levels decreased as pre-adipocytes differentiated (10 days). PDE-5A is rapidly activated in response to ANP stimulation and lowers intracellular cGMP levels. Its selective inhibition by sildenafil partly prevented the decline in cGMP levels. However, no changes in baseline- and ANP-mediated lipolysis were observed under PDE-5 blockade using various inhibitors. In addition, NEP mRNA and protein levels gradually increased during the time-course of pre-adipocyte differentiation. Thiorphan, a selective NEP inhibitor, completely abolished NEP activity in human adipocyte membranes but did not modify ANP-mediated lipolysis. CONCLUSIONS AND IMPLICATIONS: Functional PDE-5A and NEP activities were present in human adipocytes, however these enzymes did not play a major role in the regulation of ANP-mediated lipolysis.

Effects of CB1 antagonist on the control of metabolic functions in obese type 2 diabetic patients.

Clinical reports (RIO trials) have shown that chronic administration of a CB-cannabinoid receptor antagonist (rimonabant) provides improvements of disturbed metabolic parameters observed in overweight and obese patients with type 2 diabetes. The production of endocannabinoid and the expression of CB1-cannabinoid receptors are largely distributed in the different organs aside from the brain. It is now clearly established that endocannabinoids act both through orexigenic effects and peripheral metabolic effects in various tissues involved in the control of metabolism and energy expenditure (i.e. adipose tissue, liver, gastrointestinal tract, skeletal muscle and pancreas). This review will consider: i) the disturbances of glucose and lipid metabolisms in obese type 2 diabetics; ii) an overview of the pharmacological properties of rimonabant and iii) the various mechanisms involved in tissues and organs to explain the therapeutic efficacy of rimonabant. A special attention will be paid to its utilization in obese type 2 diabetics. The emerging concept of endocannabinoids acting as metabolic regulators is the more likely explanation of the success of rimonabant treatments in phase III studies.

Integrated physiology and pathophysiology of CB1-mediated effects of the endocannabinoid system.

The discovery of the endocannabinoid system (ECS) has raised a large interest in the scientific community providing us with a strikingly long list of apparently independent multi organ effects. As a result, in most reviews on this issue the main function of the ECS is considered as modulatory. Unfortunately, this vision does not add much to our understanding of the specific biological function of the ECS. Thus, modulatory is what in general all biological systems are or should be. In this review we will show that the apparent inconsistent puzzle of the very different tissue specific effects of endocannabinoids (ECs) can be reconstructed in one unitary picture. This picture clearly shows that all the different CB1-mediated effects of ECs sub-serve one major physiological function: to facilitate and increase energy storage. We will also analyze the implications of this unitary vision of the ECS in different contexts. First, in the context of the systems that regulate energy balance, introducing a new systematization based on two homeostatic systems: an endostatic and an exostatic system. Second, in the context of evolution, showing how the function of the ECS has shifted from essential to survival to almost pathological in current times. Finally, in a pathophysiological context, introducing the new concept of "proactive evolution diseases", which can explain the current obesity epidemic and the role the ECS plays in it.

Atrial natriuretic peptide inhibits the production of adipokines and cytokines linked to inflammation and insulin resistance in human subcutaneous adipose tissue.

AIMS/HYPOTHESIS: Increased adipose tissue secretion of adipokines and cytokines has been implicated in the chronic low-grade inflammation state and insulin resistance associated with obesity. We tested here whether the cardiovascular and metabolic hormone atrial natriuretic peptide (ANP) was able to modulate adipose tissue secretion of several adipokines (derived from adipocytes) and cytokines (derived from adipose tissue macrophages). SUBJECTS AND METHODS: We used protein array to measure the secretion of adipokines and cytokines after a 24-h culture of human subcutaneous adipose tissue pieces treated or not with a physiological concentration of ANP. The effect of ANP on protein secretion was also directly studied on isolated adipocytes and macrophages. Gene expression was measured by real-time RT-quantitative PCR. RESULTS: ANP decreased the secretion of the pro-inflammatory cytokines IL-6 and TNF-alpha, of several chemokines, and of the adipokines leptin and retinol-binding protein-4 (RBP-4). The secretion of the anti-inflammatory molecules IL-10 and adiponectin remained unaffected. The cytokines were mainly expressed in macrophages that expressed all components of the ANP-dependent signalling pathway. The adipokines, leptin, adiponectin and RBP-4 were specifically expressed in mature adipocytes. ANP directly inhibited the secretion of IL-6 and monocyte chemoattractant protein-1 by macrophages. The inhibitory effects of ANP on leptin and growth-related oncogene-alpha secretions were not seen under selective hormone-sensitive lipase inhibition. CONCLUSIONS/INTERPRETATION: We suggest that ANP, either by direct action on adipocytes and macrophages or through activation of adipocyte hormone-sensitive lipase, inhibits the secretion of factors involved in inflammation and insulin resistance.

Dynamic strength training improves insulin sensitivity and functional balance between adrenergic alpha 2A and beta pathways in subcutaneous adipose tissue of obese subjects.

AIMS/HYPOTHESIS: The aim of this study was to investigate whether dynamic strength training modifies the control of lipolysis, with particular attention paid to the involvement of the antilipolytic adrenergic alpha 2A receptor (ADRA2A) pathway. METHODS: Twelve obese men (age: 47.4+/-2.8 years; BMI: 32.7+/-0.9) were investigated during a 210-min euglycaemic-hyperinsulinaemic clamp conducted before and after 3 months of dynamic strength training. Before and during the third hour of the clamp, the lipolytic effect of a perfusion of isoproterenol or adrenaline (epinephrine) alone or associated with the ADRA2A antagonist phentolamine was evaluated using the microdialysis method of measuring extracellular glycerol concentration (EGC) in subcutaneous abdominal adipose tissue (SCAAT). In addition, biopsies of SCAAT were carried out before and after training to determine mRNA levels RESULTS: The training increased insulin sensitivity in adipose tissue. The decrease of EGC was more pronounced during the clamp conducted after the training period than during the clamp done in pre-training conditions. Before and after the training, catecholamines induced an increase in EGC, the increase being lower during the clamp on each occasion. The isoproterenol-induced increase in EGC was higher after the training. Adrenaline-induced lipolysis was potentiated by phentolamine after but not before the training. There were no training-induced changes in mRNA levels of key genes of the lipolytic pathway in SCAAT. CONCLUSIONS/INTERPRETATION: In obese subjects, dynamic strength training improves whole-body and adipose tissue insulin responsiveness. It increases responsiveness to the adrenergic beta receptor stimulation of lipolysis and to the antilipolytic action of catecholamines mediated by ADRA2As.

[High frequency ultrasonography and celluscore: an improvement in the objective evaluation of cellulite phenomenon]. / L'ultrasonographie à haute fréquence et le celluscore : un progrès dans l'évaluation objective du phénomène de cellulite.

As they usually do not have any serious effect on health condition, cellulite phenomenons are not considered as potentially hazardous by general practitioners; unfortunately they involve almost all the feminine population after the forties and may really induce bad side effects either psychological or physical whatever the confusing origin of that cutaneous deformation: heredity, nutrition, circulatory and hormonal diseases etc. Trying to appreciate in a more scientific way this superficial skin disorder, we have developed a computerised questionnaire which can be combined with the finest upto date way of skin exploration, high frequency ultrasonography. It seems possible to consider now cellulite as the result of various disorders which can be separate into fibrotic or retentional phenomenons (surrounding superficial fat tissues) and the direct adipocyte reaction (adiposis). We hope to be able in the future to extend the treatment of cellulite beyond the limits of liposuction which seems until today the only way to bring some improvement to that phenomenon in spite of the very delicacy of the surgical approach.

Effect of endurance training on adrenergic control of lipolysis in adipose tissue of obese women.

The effect of a 12-wk training program on sc abdominal adipose tissue (SCAAT) was studied in 11 obese women. Before and after the training, biopsies of SCAAT were performed for mRNA levels determination. Using the microdialysis method, involvement of alpha(2)- and beta-adrenergic receptor (ARs) in the control of lipolysis in SCAAT was studied using local perfusion of epinephrine alone or supplemented with phentolamine, an alpha(2)-AR antagonist. In addition, the variation in dialysate glycerol concentrations during exercise (50% peak oxygen consumption at 40 min) in a probe perfused with Ringer's solution was compared with that obtained in a probe perfused with Ringer's solution plus phentolamine. Training did not promote changes in the expression of key genes of the lipolytic pathway. The epinephrine-induced rise in the dialysate glycerol concentration was identical before and after training and was similarly potentiated by phentolamine. During exercise, the potentiating effect of phentolamine on the glycerol response was apparent before, but not after, training. The exercise-induced increase in plasma norepinephrine was lower after training (P = 0.04). In conclusion, training did not modify either the expression of genes involved in the control of lipolysis or alpha(2)- and beta-ARs in situ sensitivity to epinephrine in SCAAT. Training reduced the antilipolytic action of catecholamines mediated by alpha(2)-ARs during exercise, probably due to a reduction of exercise-induced catecholamine increase.

Effect of testosterone on lipolysis in human pre-adipocytes from different fat depots.

AIM/HYPOTHESIS: Regional differences in lipolysis, with higher lipolytic activity in visceral than subcutaneous fat, are important for the development of insulin resistance and might be influenced by testosterone. METHODS: We studied testosterone-regulated lipolysis and protein expression (by western blot) in fully differentiated pre-adipocytes from visceral (omental) and abdominal subcutaneous adipose tissue from 52 human subjects. These cells were isolated and cultured in a serum-free medium. RESULTS: Testosterone caused a specific, time- and concentration-dependent 50% reduction of catecholamine-stimulated lipolysis in the subcutaneous depot. Half of the maximum effect occurred at 10 nmol/l. The inhibitory effect was due to the inability of beta-adrenoceptors and cyclic AMP to stimulate the protein kinase A, hormone-sensitive lipase complex. Testosterone caused a depot-specific 50% reduction of the protein expression of hormone-sensitive lipase and beta(2)-adrenoceptors in differentiated subcutaneous pre-adipocytes, but no change in beta(1)-adrenoceptors, protein kinase A subunits or perilipin expression. In contrast, testosterone had no effect on lipolysis or protein expression in the visceral depot. However, testosterone receptors were present in both depots, and the hormone inhibited adipocyte leptin secretion. Similar effects on lipolysis were observed with dihydrotestosterone. CONCLUSIONS/INTERPRETATION: Testosterone in physiological concentrations causes a depot-specific reduction of catecholamine-stimulated lipolysis in subcutaneous fat cells, probably due to reduced protein expression of beta(2)-adrenoceptors and hormone-sensitive lipase. This could be an important pathogenic factor underlying regional differences in lipolysis and development of insulin resistance and hyperandrogenic polycystic ovary syndrome.

[Metabolic and secretory activities of adipocytes]. / Activités métaboliques et sécrétoires des adipocytes.

White fatty tissue represents 10 to 25% of the total body weight in a normal person. It is the principal site of storage and release of lipids: the stockpile of organism's energy. Adipocytes play an essential role in the lipid metabolism and participate in endocrine and in autoparacrine regulations. Numerous molecules synthesized and released by adipocytes have been described but their precise roles have to be studied in vivo before their potential application in treatment of obesity or type II diabetes can be proposed.