Obesity as a prospective predictor of depression in adolescent females.

Objective: Both obesity and depression are prominent during adolescence, and it is possible that obesity is a trigger for adolescent depression. The purpose of this paper is to evaluate whether overweight or obese status contributes to the development of depression in adolescent girls. Design: Participants were 496 adolescent girls who completed interview based measures of depression and had their height and weight measured at four yearly assessments. Repeated measures logistic regressions with generalized estimating equations were used to evaluate whether overweight or obese status were associated with major depression or an increase in depressive symptoms the following year. Main Outcome Measures: Major depression and depressive symptoms were evaluating using a modified version of the K-SADS interview. Overweight and obese status was determined by using standardized protocols to measure height and weight. Results: Results showed that obese status, not overweight status, was associated with future depressive symptoms, but not major depression. This study demonstrated that obesity is a risk factor for depressive symptoms, but not for clinical depression. Conclusions: As depressive symptoms are considered along the spectrum of depression with clinical depression at the high end, these results suggest that weight status could be considered a factor along the pathway of development of depression in some adolescent females. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of obesity and weight loss on cardiac function and valvular performance

OBJECTIVE: To study the consequences of long-standing obesity on myocardial function and valvular performance and to determine the effects of weight loss on these cardiovascular features. RESEARCH METHODS AND PROCEDURES: We included 41 patients with obesity referred for weight-reducing gastroplasty, 31 patients with obesity who received dietary recommendations, and 43 lean subjects. Body weight and blood pressure were measured, and cardiac function and valvular performance were estimated echocardiographically. Left ventricular ejection fraction was used to assess systolic heart function, and the ratio of transmitral early to atrial (E/A) peak flow velocity was used as an estimate of diastolic filling. All three study groups were investigated at baseline, and the two groups with obesity were re-examined at 1-year follow-up. RESULTS: Patients with obesity had higher blood pressure, greater cardiac output, lower ejection fraction, and reduced E/A ratio, compared with lean subjects (p<0.01). Surgical treatment of obesity led to significant decreases in body weight, whereas body weight remained unchanged in the group treated with dietary recommendations (p<0.001). In the weight loss group, blood pressure and cardiac output decreased and the E/A ratio increased (p<0.001). Left ventricular ejection fraction tended to increase in the weight loss group and decrease in the obese control group (p<0.01). No significant valvular disease was observed in any of the subjects with obesity at baseline or after weight loss. DISCUSSION: We conclude that weight reduction in subjects with obesity is associated with improvements in left ventricular diastolic filling and has favorable effects on left ventricular ejection fraction. Neither obesity nor weight loss seem to promote valvular heart disease.     

Obesity, dieting, and the expression of obese characteristics.

86 obese, normal, and underweight college-age males were divided into subgroups of dieters and nondieters. Consumption following a preload was found to vary as a function of dieting, not obesity, with dieters exhibiting the "obese" response (absence of caloric compensation) irrespective of weight classification. Similarly, elevated levels of free fatty acids, normally found in the obese, were associated with dieting rather than obesity per se. Implications of these findings for current theories of obesity are discussed. (25 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Final reflections: wellness after obesity surgery

The articles presented in this symposium on treatment of clinically severe obesity cover most of the topics related to obesity surgery, from basic research about genetic causes of obesity to surgical techniques and clinical results on the severely obese patient. The most striking feature of those results observed after bariatric surgery for the clinically severe obese is not the remarkable weight loss and normalization of the body mass index but the amelioration of some of the metabolic and physiologic abnormalities related to obesity. In fact, carbohydrate and lipid metabolism show improvement, as do cardiac and pulmonary function. These observations justify all efforts devoted to the design and improvement of sound bariatric surgical techniques. Moreover, surgeons seek the well-being of the ex-obese patient, and in doing so they face special discriminatory attitudes from colleges, patients' families, and the society, mainly because of negative stereotypes related to the obese individuals and the lack of information on the real benefits of bariatric procedures. Bariatric surgeons will reach their goal only when an informed society, educated physicians, and properly oriented obese patients together give to bariatric surgery its real dimension. The objective of any surgeon is the wellness of his or her patient. This is important in bariatric surgery as well; beyond excess weight loss and normalization of biochemical parameters, the ex-obese patient should be able to live a normal, productive, happy life. Approaching this goal is a task that takes months or even years. Bariatric surgeons are committed to support and help their patients until they reach wellness after obesity surgery.     

Obesity and hypertension

An increasing number of clinical trials have demonstrated that obese patients are more likely than lean individuals to be hypertensive. Moreover, both obesity and arterial hypertension have been identified as independent risk factors for cardiovascular disease. Pathophysiologically, obesity appears to have a major influence on the hemodynamic changes associated with hypertension. The available evidence suggests that at any given level of arterial pressure, obese hypertensive patients have a higher cardiac output and lower total peripheral resistance than do lean patients. Recent reports have indicated that obesity exerts a disparate effect on target organs in hypertension. Whereas at rest obesity seems to mitigate cardiovascular changes in the systemic vascular bed caused by hypertension, no such mitigation was observed in the renovasculature; left ventricular hypertrophy as a major cardiovascular risk factor was even exacerbated by the presence of obesity. The different hemodynamic patterns in obese hypertensive patients have recently been shown clinically relevant for treating hypertensive patients.     

Cardiac autonomic nerve function and insulin sensitivity in obese subjects

OBJECTIVE: To investigate whether obesity influences cardiac autonomic nerve function. DESIGN: Comparing two groups of subjects with different degrees of obesity to normal weight controls. SUBJECTS: 19 healthy controls (mean age 33 y, BMI 21.7 +/- 0.2 kg/m2) and 17 obese non-diabetic subjects (mean age 39 y, BMI 33.7 +/- 1.8 kg/m2). MEASUREMENTS: Insulin sensitivity was calculated by an oral glucose tolerance test. Autonomic nerve function was evaluated by analysing the variation of the heart frequency at rest (coefficient variation of R-R intervals, REST 1), during deep respiration, at a Valsalva maneuver (longest/shortest R-R interval during inspiration hold) and by the Ewing test (ratio between the 30th and 15th R-R interval after reaching up-right position). RESULTS: The obese showed a lower insulin sensitivity than healthy controls (3.09 vs 4.60 mg x l2/mmol x mU x min, P < 0.001). Their variation in heart frequency was reduced (REST 1: 1.95 vs 2.9, P < 0.01, Valsalva: 1.30 vs 1.52 and Ewing test: 1.03 vs 1.14, P < 0.05). However, patients with moderate (BMI 31.7 kg/m2) or severe obesity (39.0 kg/m2) with identical insulin sensitivity had no significant difference in autonomic nerve function. Except for the Ewing test all measured parameters for the evaluation of cardiac autonomic nerve function correlated with the degree of diminished insulin sensitivity (REST 1: r = 0.475, P < 0.001). CONCLUSION: Moderate obesity with significantly decreased insulin sensitivity is associated with impaired cardiac autonomic nerve function.     

Dietary magnesium supplementation attenuates ethanol-induced myocardial dysfunction

Hypomagnesemia is positively correlated with a number of cardiovascular abnormalities and recent evidence suggests that magnesium supplementation prevents ethanol-induced development of hypertension. The purpose of our study was to assess whether dietary magnesium supplementation effectively reverses or attenuates chronic ethanol-induced cardiac dysfunction, both at the tissue and the cellular level. Therefore, the influence of dietary magnesium supplementation during chronic ethanol ingestion on the mechanical properties of cardiac muscle was studied using isolated papillary muscles and ventricular myocytes from rat heart. In addition, the acute effects of ethanol on cardiac muscle from animals chronically exposed to ethanol in the absence and presence of dietary magnesium supplementation were also examined. Chronic ethanol exposure caused significant cardiac, hepatic, and renal enlargement, increased systolic blood pressure, and produced hypomagnesemia. After chronic ethanol exposure, the baseline force generating capacity of papillary muscles was markedly depressed and was associated with a significant slowing in the maximum velocities of contraction and relaxation. By contrast, in isolated myocytes, long-term ethanol exposure increased the extent of cell shortening associated with a significant reduction in the duration of relengthening and an increase in both the maximum velocities of shortening and relengthening. Dietary magnesium supplementation among animals chronically ingesting ethanol effectively normalized heart size, systolic blood pressure, and reduced plasma ethanol concentration. Magnesium supplementation also attenuated chronic ethanol-induced depression of contractile force and increased the extent of cell shortening. As expected, acute ethanol exposure caused a dose-dependent inhibition of both isometric force and isotonic shortening associated with a decrease in the intracellular calcium transient. However, the extent of the acute ethanol-induced reduction in isometric force and isotonic shortening was always slightly greater among preparations from animals chronically exposed to ethanol. Dietary magnesium supplementation normalized the acute inhibitory action of ethanol on isometric force, isotonic shortening, and the intracellular calcium transient. Our results suggest that dietary magnesium supplementation may attenuate chronic ethanol-induced alterations in baseline myocardial mechanical function and normalize the cardiac response to acute ethanol exposure.     

Control of prolactin and growth hormone secretion in mice by obesity

Prolactin (PRL) and growth hormone (GH) secretions in mice rendered obese by the administration of gold thioglucose (GTG) are abnormal. The objective of the present experiments was to determine whether the effects were related to the drug or to the resultant obesity. Perphenazine-induced PRL release in normal mice and in GTG-injected non-obese mice was compared to that of GTG-injected obese mice after the initial development of obesity, after body weight reduction by diet control and after the resumption of obesity by ad lib. feeding. The GTG-injected mice which did not become obese had greater (50%) than normal levels of serum PRL following perphenazine stimulation in 2 of 3 experiments. This suggested that the injection of GTG directly affected the control mechanism for PRL secretion, but that the abnormal PRL secretion was probably not the cause of obesity that develops after GTG treatment. Perphenazine-induced PRL levels in mice rendered obese with GTG were much greater (2-3 times higher than normal). However, the unusually high levels of PRL were totally abolished when the body weights of these mice were brought down to normal by dietary restriction. Conversely, when obesity was permitted to recur by giving the mice free access to food, PRL levels reverted back to the original obese pattern. The concentrations of GH were usually lower than normal in GTG-obese mice, and these levels were also more often associated with the development of obesity than with the injection of GTG. The data show a marked influence of obesity on the control of PRL and GH secretions in the mouse.     

Left atrial size in hypertensive men: influence of obesity, race and age. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents

OBJECTIVES: We sought to determine the relations of left atrial (LA) size to blood pressure, obesity, race, age and left ventricular (LV) mass in hypertension. BACKGROUND: Although obesity, race and age may influence LV mass, their effects on LA size have not been defined in hypertension. METHODS: Left atrial size was measured in 690 men (58% African-Americans) with mild to moderate hypertension (mean [+/-SD] blood pressure 152 +/- 15/98 +/- 6 mm Hg) and a high prevalence of LV hypertrophy. Effects of LV mass, adiposity, race, age, physical activity, height, weight, sodium excretion, plasma renin activity and heart rate were examined. RESULTS: Left atrial size was greater (p < or = 0.0001) in obese (44.2 +/- 5.7 mm) than in overweight (41.6 +/- 5.9 mm) or normal weight (38.9 +/- 6.2 mm) patients. Left atrial enlargement (> or = 43 mm) was present in 56% of obese patients compared with 42% of overweight and 25% of normal weight hypertensive men. As age increased, white patients had a greater LA size than African-American patients. Although there was no relation between LV mass and LA size in normal weight patients, there was a significant positive relation in obese patients. On multiple regression analysis, obesity was the strongest independent predictor of increased LA size. CONCLUSIONS: Obesity is the strongest predictor of LA size in patients with hypertension and amplifies the relation between LA size and LV mass. Race influences effects of age and hypertension on LA size. Because increased LA size and LV mass (also influenced by obesity) are associated with an adverse outcome, these findings underscore the importance of obesity, race and age with regard to the cardiac effects of hypertension.     

Compliance with universal precautions among emergency department personnel caring for trauma patients

INTRODUCTION: Low intake of the fat-soluble antioxidants alpha-tocopherol and beta-carotene has been linked to greater risks of cardiovascular disease in epidemiologic studies. Obesity in adults is associated with lower levels of alpha-tocopherol and beta-carotene, which may contribute to the increased risk of cardiovascular disease associated with obesity. AIM: To examine serum concentrations of fat-soluble antioxidants in a large, nationally representative sample of obese and nonobese children. METHODS: Serum levels of alpha-tocopherol and beta-carotene were measured in 6139 children between the ages of 6 and 19 years enrolled in the National Health and Examination Survey, cycle III. Serum alpha-tocopherol levels were adjusted for fasting cholesterol and triglyceride levels. Nutritional intake was assessed by 24-hour dietary recall and food frequency questionnaires. RESULTS: Serum levels of beta-carotene were significantly lower in obese children compared with those found in normal weight children (0.22 0.14 micromol/L vs 0.29 0.17 micromol/L, P <.001). After adjustment was done for serum triglyceride and cholesterol levels, alpha-tocopherol levels were also significantly lower in obese children (2.68 0.59 vs 3.17 0.60, P <.001). Approximately one half of obese children had serum levels of beta-carotene and adjusted alpha-tocopherol in the lowest quartile compared with approximately one quarter of normal weight children (P <.001). No significant differences were seen in reported intake of beta-carotene, alpha-tocopherol, fruit, or vegetables between obese and nonobese children. CONCLUSION: Reduced serum levels of fat-soluble antioxidants are present in obese children.     

New knowledge about obesity--news for obese patients?]

This review explains and surveys very recent findings and experimental results concerning molecular pathology and genetics of overweight and obesity and also evaluates their relevance for the actual treatment of obesity at present. Most of these studies were done on inbred obese mice or rats and it is yet unknown to what extent the results do apply to human overweight. Nevertheless these studies led to the discovery of a new hormone--OB-protein or leptin--produced by adipocytes of animals. It does not only increase satiety by influencing feeding centers and decrease body weight but it also interferes with several peripheral metabolic functions. Mutations of leptin expression or expression of leptin receptors as observed in animals are, however, very rare in humans. In obese individuals (and animals) there is a yet unexplained resistance to the effects of leptin which interferes with successful therapeutic use of leptin in human obesity. Various other recently discovered transmitters modifying feeding habits may, however, become targets of future drugs making dietary weight loss and its maintenance more acceptable and successful. At present obese people and patients have to rely, however, on traditional methods of weight loss though these are known to yield poor results over prolonged periods of time. Orlistat, a recently introduced drug results in malabsorption of fat from the gut by inhibiting lipases. Though it is not based on recent insights to regulation of body weight it is promising primarily for educating patients to reduce their nutritional fat intake.     

Cardiovascular depressant effects of the neomycin-streptomycin group of antibiotics

Cardiovascular depressant effects of the neomycin-streptomycin group of antibiotics (aminoglycoside antibiotics) were examined during pentobarbital anesthesia in cats, dogs, and 4 species of nonhuman primates: owl (Aotus trivirgatus), squirrel (Saimiri sciureus), and rhesus (Macaca mulatta) monkeys, and dog-faced baboons (Papio cynocephalus). Intravenous administration of kanamycin, streptomycin, gentamicin, or neomycin produced various degrees of hypotension and relative bradycardia in all species examined. In surgically prepared (open-chest) baboons, neomycin consistently induced a dose-related depression of myocardial contractile force, maximum dF/dt of myocardial contraction, cardiac output, heart rate, and systolic and diastolic blood pressures. Maximum depression of hemodynamic values usually occurred within 2 to 5 minutes after administration of neomycin; cardiovascular function then gradually returned to control or near control levels within 30 to 60 minutes. Intravenous administration of calcium chloride rapidly reversed the neomycin-mediated alterations of cardiovascular function. Present findings indicated that aminoglycoside antibiotics altered cardiovascular dynamics in anesthetized animals, and indicated that this deleterious action(s) may be related to modification of calcium ion function.     

Modification of insulin resistance by diazoxide in obese Zucker rats

Hyperinsulinism, insulin resistance, and decreased number of insulin receptors are characteristic of obesity in both humans and experimental animals. To assess the role of insulin in developing obesity, diazoxide (DZ), an inhibitor of glucose-stimulated insulin secretion, was administered for 8 weeks to 7-week-old female Zucker rats in two concentrations, 50 mg/kg.day (LD-DZ), and 100 mg/kg.day (HD-DZ). The obese and lean rats were divided into three subgroups: diazoxide (DZ), pair-fed (PF), and control (C) groups (n = 6 rats/subgroup-genotype). Diazoxide-treated obese and lean animals showed significantly lower postabsorptive plasma insulin concentrations (P < 0.005) than their respective obese and lean PF and C subgroups. HD-DZ obese rats consumed more calories (P < 0.001), yet gained less weight (P < 0.05) than PF and C rats. The plasma glucose concentrations in the postabsorptive state and during glucose tolerance tests in HD-DZ obese rats were significantly lower than those in PF and C rats (P < 0.01) despite a decrease in their plasma insulin concentrations (P < 0.01), whereas HD-DZ lean rats displayed a diabetic response (P < 0.01). The adipocyte-specific insulin receptor binding was dose-dependently increased in both lean and obese DZ animals (P < 0.01). DZ had a dual effect on insulin metabolism; it decreased insulin secretion and increased insulin receptor binding. This dual effect was associated with improved glucose tolerance and a decrease in weight gain in obese rats.     

Effects of antibodies to adipocytes on body weight, food intake, and adipose tissue cellularity in obese rats

Female Wistar rats were fed on a high fat diet for 18 weeks, during which their energy intake increased by 25% and body weight by 50% due to a doubling of adipose tissue tissue stores. Animals were then treated with increasing doses of a sheep polyclonal antiserum to rat adipocytes on days 1-4 and 7 after which they remained untreated for 14 weeks. Antibody treatment reduced body weight by 10% and the weight of parametrial and subcutaneous adipose tissue by 30-40%. This decrease was explicable entirely in terms of a decrease in the number of adipocytes presumably due to adipocyte lysis. These favourable changes in body fat mass were accompanied by improvement in at least one metabolic factor associated with obesity - serum leptin concentrations were significantly reduced in treated animals compared with high fat controls. Genetically obese Zucker rats also showed decreases in the number of adipocytes after treatment with antibodies but in contrast to diet-induced obese rats, they showed a compensatory increase in adipocyte volume which attenuated the effects on body fat mass. These results demonstrate for the first time, the potential to treat diet-induced obesity with antibodies to adipocytes by producing long-term reductions in the number of adipocytes, with minimal side-effects.     

Insulin resistance: lessons from animal models of obesity]

The insulin resistance of animal models of obesity (the gold thioglucose obese mouse and the o b/o b mouse) is characterized by several abnormalities. At the receptor step, both the binding function (decreased number of sites) and the enzymatic, tyrosine kinase function (decreased insulin activation) are altered. At postreceptor steps, phosphatidylinositol 3-kinase (PI3-K) plays an important role in insulin signalling, particularly for the stimulation of glucose transport in muscle and adipocyte. Insulin activation of PI3-K is markedly diminished in obese mice; starving the obese animals restores normal responses of PI3-K, glucose transport, and glycogen synthesis, to insulin. These observations emphasize the multi-site, and largely reversible, nature of insulin resistance in these animal models of obesity. Similar alterations have been reported in the literature with regard to the sites of insulin resistance in human obesity and non insulin-dependent diabetes.     

Cardioprotective and hypolipidemic effects of nisoldipine in the JCR:LA-cp rat

The JCR:LA-cp rat exhibits the obesity/insulin resistance/hypertriglyceridemia syndrome in an extreme form. These normotensive rats spontaneously develop advanced atherosclerosis and ischemic myocardial lesions. The calcium channel antagonist, nisoldipine, was administered to obese rats of the JCR:LA-cp strain in drinking water at a dose of 1 mg/kg from age 6 weeks. Nisoldipine-treated rats showed no change in food consumption or body weight compared with control animals. Plasma glucose and insulin levels also were unchanged in the nisoldipine-treated rats. Insulin-mediated total glucose turnover, an index of insulin sensitivity as measured by euglycemic insulin clamp, was similarly not improved. Serum triglyceride levels in obese male rats were markedly reduced (57%; p < 0.001, at age 12 weeks), whereas obese female rats showed no significant change in triglyceride levels and an increase in esterified cholesterol in response to nisoldipine treatment. The impaired endothelium-dependent (nitric oxide-mediated) vascular relaxation of the male cp/cp rats was not improved by nisoldipine treatment. The severity of atherosclerotic raised lesions in the aortic arch of male cp/cp rats was significantly reduced (p < 0.01) by nisoldipine treatment, and this was accompanied by a major reduction in the incidence of ischemic myocardial lesions (85%; p < 0.01). Thus nisoldipine treatment ameliorates atherosclerotic damage and myocardial injury even in the presence of gross obesity, hyperinsulinemia, and significant hyperlipidemia. This effect appears to involve protection of the vascular wall from atherogenesis and probably antivasocontractile effects at the smooth muscle level as well.     

Cloning and sequence analysis of rhp51+, a Schizosaccharomyces pombe homolog of the Saccharomyces cerevisiae RAD51 gene

Elevation or depression of the ST segment of the 12-lead electrocardiogram is an important and established marker of myocardial ischemia or injury. The ST segment deviation in normal individuals using standard cardiac monitoring equipment in the clinical setting of prehospital transport has not been studied. The hypothesis that we tested is that ST segment changes do not occur in normal subjects on standard prehospital cardiac monitors during transport. During a simulated transport, we monitored healthy volunteers of both sexes between the ages of 20 and 30 who had a normal cardiovascular history, physical examination, and 12-lead electrocardiogram. Fourteen of 34 subjects (41%) who qualified as normal exhibited ST segment deviation on the monitor. Of these 14, 11 exhibited ST segment depression, and 3 exhibited ST segment elevation. We conclude that normal individuals can exhibit ST segment deviation on standard prehospital cardiac monitoring equipment during routine transport.     

Uncoupling of obesity from insulin resistance through a targeted mutation in aP2, the adipocyte fatty acid binding protein

Fatty acid binding proteins (FABPs) are small cytoplasmic proteins that are expressed in a highly tissue-specific manner and bind to fatty acids such as oleic and retinoic acid. Mice with a null mutation in aP2, the gene encoding the adipocyte FABP, were developmentally and metabolically normal. The aP2-deficient mice developed dietary obesity but, unlike control mice, they did not develop insulin resistance or diabetes. Also unlike their obese wild-type counterparts, obese aP2-/- animals failed to express in adipose tissue tumor necrosis factor-alpha (TNF-alpha), a molecule implicated in obesity-related insulin resistance. These results indicate that aP2 is central to the pathway that links obesity to insulin resistance, possibly by linking fatty acid metabolism to expression of TNF-alpha.     

Abdominal obesity and its metabolic complications: implications for the risk of ischaemic heart disease

Although the health hazards of obesity are well established, obese individuals are not all at equal risk of developing a disease, which reflects the heterogeneity of this condition. The regional distribution of body fat is now recognized as a very important component of the obesity-related health hazards. Epidemiological studies have shown that abdominal obesity, that is, a preponderance of fat in the abdominal area, is a better predictor of both cardiovascular disease and type 2 diabetes than obesity per se. It is now generally accepted that the fat located within the abdominal cavity, the visceral fat, is the best correlate of most of the highly atherogenic metabolic complications seen in individuals with abdominal obesity. These include, among others, insulin resistance and hyperinsulinaemia, hypertriglyceridaemia, reduced plasma high-density lipoprotein (HDL) cholesterol concentrations and an increased number of small, dense low-density lipoprotein (LDL) particles. This review summarizes the evidence that these metabolic complications may account to a large extent for the increased risk of cardiovascular disease associated with abdominal/visceral obesity. Abdominal obesity may be the most prevalent denominator of highly atherogenic dyslipidaemic and hyperinsulinaemic/insulin-resistant states in affluent, sedentary societies. Targeting individuals with this high-risk trait in primary prevention is therefore crucial if we are truly to have an impact on the incidence of cardiovascular disease.     

Combined effect of obesity and aging on feeding-induced monoamine release in the rostromedial hypothalamus of the Zucker rat

OBJECTIVE: The obesity of the Zucker rat is associated with numerous metabolic and neurochemical disturbances involving the central transmitters regulating feeding behaviour. Among them, the release of satiety-related monoamines from the median hypothalamus in response to a meal is enhanced in obese, as compared to normal, rats as though larger amounts of these amines were necessary to bring about satiety in obese rats. Besides, the obese Zucker rat has often been described as shorter-living than its lean congener. One of the reasons for the shorter longevity of the obese rat was investigated in this study: it could be an aggravation of its obesity-related central disturbances with age. METHODS: We assessed the response to a meal of the hypothalamic monoamines, dopamine and serotonin, in young (four month old) and old (twelve month old) lean (Fa-Fa) and obese (fa-fa) Zucker rats. The in vivo technique of microdialysis was used to combine behavioural recordings and continuous neurochemical assays. RESULTS: The exacerbation of monoamine release observed in young obese rats in response to a meal was no longer found in old obese rats. Serotonin increase during a meal weakened with aging, especially in obese rats. Dopamine (DA) response to a meal was completely reversed in old obese rats, with a decrease instead of the increase observed in the three other groups. CONCLUSION: The decrease of monoaminergic response to a meal with age is apparently the opposite to the enhanced release related to obesity. However, this does not correspond to an amelioration of the hyperphagia of the obese rats with age, as we could observe in parallel behavioural experiments, but rather to a decrease in neurotransmitter metabolism and thus in neuronal functioning.