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PubMed2006

Influence of obesity on accurate and rapid arm movement performed from a standing posture.

INTRODUCTION: Obesity yields a decreased postural stability. The potentially negative impact of obesity on the control of upper limb movements, however, has not been documented. This study sought to examine if obesity imposes an additional balance control constraint limiting the speed and accuracy with which an upper limb goal-directed movement performed from an upright standing position can be executed. METHOD: Eight healthy lean subjects (body mass index (BMI) between 20.9 and 25.0 kg/m(2)) and nine healthy obese subjects (BMI between 30.5 and 48.6 kg/m(2)) pointed to a target located in front of them from an upright standing posture. The task was to aim at the target as fast and as precisely as possible after an auditory signal. The difficulty of the task was varied by using different target sizes (0.5, 1.0, 2.5 and 5.0 cm width). Hand movement time (MT) and velocity profiles were measured to quantify the aiming. Centre of pressure and segmental kinematics were analysed to document postural stability. RESULTS: When aiming, the forward centre of pressure (CP) displacement was greater for the obese group than for the normal BMI group (4.6 and 1.9 cm, respectively). For the obese group, a decrease in the target size was associated with an increase in backward CP displacement and CP peak speed whereas for the normal BMI group backward CP displacements and CP peak speed were about the same across all target sizes. Obese participants aimed at the target moving their whole body forward whereas the normal BMI subjects predominantly made an elbow extension and shoulder flexion. For both groups, MT increased with a decreasing target size. Compare to the normal BMI group, this effect was exacerbated for the obese group. For the two smallest targets, movements were on average 115 and 145 ms slower for the obese than for the normal BMI group suggesting that obesity added a balance constraint and limited the speed with which an accurate movement could be done. SUMMARY: Obesity, because of its effects on the control of balance, also imposes constraints on goal-directed movements. From a clinical perspective, obese individuals might be less efficient and more at risk of injuries than normal weight individuals in a large number of work tasks and daily activities requiring upper limb movements performed from an upright standing position.

Adult↗
PubMed2006

Quality of life in a clinical sample of obese children.

OBJECTIVES: To measure health-related quality of life (HRQoL) in a clinical sample of obese children by child self-report and parent-proxy report; to compare quality of life assessments provided by obese children and their parents; to assess differences in quality of life between the obese clinical sample and healthy control children. DESIGN: Pairwise comparison of obese children matched for age, gender and socio-economic status with non-obese controls. SUBJECTS: One hundred and twenty-six obese children (body mass index (BMI) >/=98th centile) and 71 lean control children (BMI <85th centile). Controls were matched with 71 children from the obese clinical group (mean age 8.6, standard deviation (s.d.) 1.9 years; 33 M/38 F). MEASUREMENT: The Paediatric Quality of Life Inventory (UK) version 4 was self-administered to parents and to children aged 8-12 years and interview was administered to children aged 5-7 years. This questionnaire assessed physical, social, emotional and school functioning from which total, physical and psychosocial health summary scores were derived. RESULTS: In the obese clinical group (n=126), parent proxy-reported quality of life was low for all domains. In the obese clinical group, parent-reported scores were significantly lower than child self-reported scores in all domains except physical health and school functioning. Parent-proxy reports were significantly higher for healthy controls than obese children in all domains (median total score 85.2 vs 64.7; 95% confidence interval (CI) 15.6, 24.1). For child self-reports, only physical health was significantly higher for healthy controls than obese children (median score 81.3 vs 75.0; 95% CI 3.1, 12.5). CONCLUSIONS: HRQoL is impaired in clinical samples of obese children compared to lean children, but the degree of impairment is likely to be greatest when assessed using the parent perspective rather than the child perspective.

Body Mass Index↗
PubMed2006

Prevalence of somatic small fiber neuropathy in obesity.

BACKGROUND: Somatic cutaneous small sensory fiber neuropathy (SSFN) can be an early manifestation of impaired glucose tolerance and diabetes mellitus and/or insulin resistance among obese subjects and is often associated with pain, wound occurrence and impaired wound healing. It is yet unclear as to whether SSFN is prevalent among obese individuals without glucose and/or insulin dysregulation despite abundant evidence of delayed wound healing. OBJECTIVE: To observe whether there is hypofunctioning of stimulated capsaicin-sensitive cutaneous nerves (small sensory fibers) in obese subjects with/without hyperglycemia and hyperinsulinemia. DESIGN, SETTING AND PARTICIPANTS: Fifty-eight morbidly obese and 15 lean subjects were recruited for small fiber testing of the forearm in a cross-sectional study. Hyperglycemia was observed in 35 obese subjects. Of 25 obese subjects, hyperinsulinemia was noted in 15, 14 of which were hyperglycemic. No subjects demonstrated symptoms/signs of neuropathy over the hairy skin of the forearm. In fact, a neurological examination revealed that 37 subjects were asymptomatic in the legs and only four complained of a neuropathic pain in the foot. Virtually all subjects were exposed to a set of capsaicin-sensitive tests and measures which were identified by capsaicin desensitization procedures. These tests, conducted while in a supine position in bed at the Banner Good Samaritan Medical Center, Phoenix, examined the two principle roles of cutaneous SSFs, namely conveying pain signals to the CNS and controlling local neurogenic vasodilatation (flare; axon-reflex). MAIN OUTCOME MEASURES: Heat-induced pain was assessed by verbal reports of sensation after accommodation and heat-, capsaicin-, and transcutneous stimulation- induced blood flow was measured by laser Doppler flowmetry with probes placed at the site of stimulation and 1 cm remote from the site, the latter to evaluate flare latency and intensity of flare. RESULTS: Significant depression of pain and flare responses were observed in the obese subjects in all but one test. Decreased pain and flare responses were noted in all subjects without hyperglycemia and hyperinsulinemia. Age negatively correlated with capsaicin-induced flare in both the obese and normal groups. CONCLUSION: SSFN was prevalent in the cohort of morbidly obese subjects in a skin area without neurological symptoms or signs and in subjects with/without hyperglycemia and hyperinsulinemia. SSFN may be a serious factor in observations of impaired wound healing among obese subjects, a particularly worrisome problem in an obese aging population given the propensity for small fiber impairment in aging subjects. Small fiber impairment in the younger obese population may signal an early aging phenomenon.

Adult↗
PubMed2006

Testing a model of physical activity and obesity tracking from youth to adulthood: the cardiovascular risk in young Finns study.

OBJECTIVE: To test a potential model of the relationship between physical activity and obesity from youth to adulthood. DESIGN: Longitudinal study data from the cardiovascular risk in young Finns study. SUBJECTS: A total of 1319 boys (n=626) and girls (n=693) aged 9, 12, 15 and 18 years were randomly selected from five university towns and their rural surroundings in 1980. They were followed up for 21 years. In 2001 they were 30, 33, 36 and 39 years old. MEASUREMENTS: Physical activity was assessed by a short questionnaire at two measurement points. Obesity was measured by body mass index (BMI) and sum of skinfolds in 1980 and BMI and waist circumference in 2001. RESULTS: Structural equation analysis (LISREL) indicated that the prevalence of abdominal obesity in adulthood was directly affected by adult physical activity (beta (beta)=-0.16, t=-4.02, P< 0.05 for men, beta=-0.12, t=-3.35, P<0.05 for women) and indirectly via youth physical activity (beta=-0.10, t=-4.68, P< 0.05 for men, beta=-0.07, t=-4.54, P<0.05 for women). Obesity tracked significantly from youth to adulthood (beta=0.41, t=11.13, P<0.05 for men, beta=0.34, t=9.39, P<0.05 for women). Youth physical activity might reduce body weight in youth but was not directly associated with adult abdominal obesity in either men or women. The model accounted 19% of abdominal obesity in men and 13% in women. The path from youth physical activity to adult obesity through youth obesity seemed to be stronger than the path through adult physical activity. CONCLUSIONS: This study lends general support to the hypothesized model that abdominal obesity in adulthood is directly related to adult physical activity and youth overall obesity in both sexes. Youth physical activity had an indirect effect on abdominal obesity through the maintenance of physical activity in adulthood. Participation in and maintaining physical activity from youth to adulthood may have an important role in reducing obesity in adulthood.

Adolescent↗
PubMed2001

Difference in leptin response to a high-fat meal between lean and obese men.

The aim of this study was to compare the leptin responses to a high-fat meal in lean and obese men, and to investigate whether the net leptin response (area under the incremental curve) after the meal was related to the thermic effect of food (TEF). Blood samples were collected after an overnight fast and every 2 h for 8 h after a high-fat breakfast (60 g of fat/m(2) body surface area) in 12 lean and 12 obese men for determination of glucose, insulin and leptin. The TEF was calculated as postprandial energy expenditure minus fasting energy expenditure, as measured by indirect calorimetry. Fasting plasma glucose levels were similar in lean and obese men, and increased in the same way after the meal. Fasting and postprandial plasma insulin concentrations were significantly greater in obese than in lean men (P<0.01 and P<0.05 respectively). Accordingly, obese men showed a significantly higher net insulin response than lean subjects (P<0.001). Fasting plasma leptin levels were greater in obese than in lean men (P<0.001). After the meal, plasma leptin increased significantly in lean men, whereas it decreased in obese men (group by time interaction, P<0.01). The net response of leptin was greater in lean than in obese men, but this did not reach statistical significance (P=0.07). Moreover, the TEF was similar in the two groups. No significant relationship was observed between either the net insulin response or the net leptin response after the high-fat meal and the TEF of lean subjects (-0.05 <r<0.31). In obese men, the net response of insulin was correlated significantly with TEF (r=0.70, P<0.05), whereas the net response of leptin was not (r=-0.40). These results suggest that obesity is related to an impaired regulation of leptin by insulin, since leptin levels increased in lean men but decreased in obese men following a high-fat meal. Moreover, the fact that the postprandial leptin responses of both lean and obese men were not significantly related to the TEF suggests that the ob gene product is probably not acutely involved in the control of this energy expenditure component in humans.

Adult↗
PubMed2004

Rofecoxib decreases renal injury in obese Zucker rats.

The present study tested the hypothesis that altered vascular regulation of arachidonic acid enzymes in obese Zucker rats contributes to renal damage. Protein expression of CYP450 (cytochrome P450) and COX (cyclo-oxygenase) enzymes in renal microvessels was studied in obese and lean Zucker rats at 20-21 weeks of age. Body weight and blood glucose averaged 649+/-13 g and 142+/-10 mg/dl in obese Zucker rats compared with 437+/-10 g and 111+/-5 mg/dl in age-matched lean Zucker rats. Renal microvascular CYP4A and COX-2 protein levels were increased and CYP2C protein levels decreased in obese Zucker rats. TX (thromboxane) B2 excretion was 2-fold higher and PG (prostaglandin) E2 excretion significantly lower in obese Zucker rats. Additional studies investigated the ability of the COX-2 inhibitor, rofecoxib, to slow the progression of renal injury in obese Zucker rats. Rofecoxib treatment decreased urinary PGF2alpha and 8-isoprostane levels in obese Zucker rats. Renal microvessel mRNA expression of pro-inflammatory chemokines was decreased in COX-2-inhibitor-treated obese Zucker rats. Urinary albumin excretion, an index of kidney damage, averaged 95+/-11 mg/day in vehicle-treated and 9+/-1 mg/day in rofecoxib-treated obese Zucker rats. Glomerulosclerosis, characterized by mesangial expansion, tubulo-interstitial fibrosis and extracellular matrix accumulation, was prominent in obese Zucker rats compared with a lack of damage in age-matched lean Zucker rats and rofecoxib-treated obese Zucker rats. These results suggest that altered vascular arachidonic acid enzymes contribute to the renal damage, and that COX-2 inhibition decreases glomerular injury in obese Zucker rats.

Animals↗
PubMed2002

A dose-response relationship between short sleeping hours and childhood obesity: results of the Toyama Birth Cohort Study.

BACKGROUND: Short sleeping hours could cause obesity through increased sympathetic activity, elevated cortisol secretion and decreased glucose tolerance. The aim of this study was to clarify parental and lifestyle factors, particularly sleeping habits, associated with obesity in Japanese children. METHODS: Between June and July 1996, 8274 children (4194 males and 4080 females) aged 6-7 years living in Toyama prefecture, Japan, were investigated by questionnaire survey and the collection of anthropometric data. Subjects with a body mass index (BMI; weight in kg divided by square of height in m) greater than the age- and sex-specific cut-off points linked to adulthood overweight (BMI of 25 kg/m2 or more) were defined as obese subjects. Parental obesity was defined as a BMI of 25 kg/m2 or more. Logistic regression analysis was performed to evaluate the strength of the relationships between parental obesity or lifestyle factors and childhood obesity, adjusted for possible confounding factors. RESULTS: Parental obesity, long hours of TV watching and physical inactivity were significantly associated with childhood obesity. Although wake-up time was not related to obesity, there was a significant dose-response relationship between late bedtime or short sleeping hours and childhood obesity. Compared with children with 10 or more hours of sleep, the adjusted odds ratio was 1.49 (95% confidence interval 1.08-2.14) for those with 9-10 h sleep, 1.89 (1.34-2.73) for those with 8-9 h sleep and 2.87 (1.61-5.05) for those with <8 h sleep, after adjustment for age, sex, parental obesity and other lifestyle factors. CONCLUSION: A strong inverse association was observed in the relationship between sleeping hours and childhood obesity. Longitudinal research will be required to confirm this causality.

Anthropometry↗
PubMed2002

Effect of withdrawal of somatostatin plus GH-releasing hormone as a stimulus of GH secretion in obesity.

OBJECTIVES: Somatostatin (SS) may not merely be inhibitory to GH secretion but, under appropriate temporal conditions, may act in a paradoxically positive manner to sensitize somatotroph responsiveness to GH-releasing hormone (GHRH). SS infusion withdrawal (SSIW) produces a rebound GH rise in humans and increases GHRH-induced GH release. Theoretically, SSIW leaves the somatotroph cell in a situation of low endogenous SS. In obesity, there is markedly decreased GH secretion. In both children and adults, the greater the body mass index (BMI), the lower the GH response to provocative stimuli. It has been postulated that increased hypothalamic somatostatin secretion is the main mechanism responsible for the blunted GH secretion of obesity. There are no data evaluating GH responsiveness to SSIW plus GHRH in obese adults. The aim of the present study was to evaluate the GH response to SSIW plus GHRH in a group of control subjects and a group of obese patients. PATIENTS AND MEASUREMENTS: Seven obese patients (six female, one male) with a BMI of 36.1 +/- 7.7 kg/m2 were studied. As a control group, seven normal subjects (six female, one male) with a BMI of 20.3 +/- 0.9 kg/m2 were also studied. Two tests were performed. On one day, somatostatin (SS) i.v. infusion (500 microg from 0-90 min) was performed followed by a placebo i.v. bolus 90 min after SS withdrawal (SSIW). On another day, SS i.v. infusion (500 microg from 0-90 min) was performed followed by a GHRH (100 microg) i.v. bolus 90 min after SS withdrawal. A second group of seven obese patients (six female, one male) with a BMI of 32.2 +/- 2.3 kg/m2 were studied. As a second control group, seven normal healthy subjects (six female, one male) with a BMI of 20.1 +/- 0.6 kg/m2 were also studied. On one day, saline infusion was performed followed by a placebo i.v. bolus at 90 min. On another day, saline infusion was performed followed by a GHRH (100 microg) i.v. bolus at 90 min. Blood samples were taken at appropriate intervals for determination of GH. Serum GH was measured by chemiluminescent immunometric assay. Statistical analysis was performed by Wilcoxon and Mann-Whitney tests. RESULTS: GHRH-induced GH secretion in normal subjects showed a mean peak of 15.8 +/- 2.1 microg/l. Normal control subjects had a mean peak of 3.1 +/- 1.5 microg/l after SSIW-induced GH secretion. When GHRH was administered after SSIW there was an increased GH secretion with a mean peak of 23.3 +/- 4.4 microg/l, significantly greater than the response after SSIW alone (P < 0.05) and GHRH alone (P < 0.05). GHRH-induced GH secretion in obese patients was decreased with a mean peak of 3.9 +/- 1.5 microg/l. In obese patients, GH secretion after SSIW was markedly decreased with a mean peak of 1.0 +/- 0.4 microg/l. When GHRH was administered after SSIW, an increase in GH secretion was observed with a mean peak of 4.3 +/- 0.9 microg/l, significantly greater than SSIW alone (P < 0.05) but not GHRH alone (P = NS), and significantly less than in normal subjects (P < 0.05). CONCLUSIONS: This study demonstrates a significantly blunted peak GH response to somatostatin infusion withdrawal plus GHRH in obese patients compared to normal subjects. In this theoretical situation of decreased somatostatinergic tone, there is persistence of GH hyposecretion in obesity, suggesting the existence of multiple defects responsible for decreased GH secretion in obesity. We also found that in obese patients, in contrast to normal subjects, SSIW did not increase GHRH-induced GH secretion.

Adult↗
PubMed2003

Comparisons of leptin, incretins and body composition in obese and lean patients with hypopituitarism and healthy individuals.

OBJECTIVE: To identify possible abnormalities specific for obesity in hypopituitary patients. STUDY DESIGN: Cross-sectional case-control study. MEASUREMENTS AND STUDY SUBJECTS: Body composition (DEXA) and measurements of fasting plasma levels of glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptides (GLPs), insulin, C-peptide, glucose, leptin and lipids were performed in 25 hypopituitary patients (15 obese, 10 normal weight) and 26 BMI and age-matched healthy controls (16 obese, 10 normal weight). All hypopituitary patients had GH deficiency and received adequate substitution therapy on this and other deficient axes (3 +/- 1). RESULTS: Fasting GIP-levels were significantly higher in obese hypopituitary patients compared to lean hypopituitary patients (P < 0.01), while the fasting concentrations of GLP-1 and GLP-2 were comparable between obese and lean hypopituitary patients. The same trend was seen in obese healthy controls vs. lean controls. No differences were observed in glucose, insulin or C-peptide between the hypopituitary patients and the controls. Leptin levels were increased in obese hypopituitary patients compared to lean hypopituitary patients when adjusted for gender. At least a 2-fold higher level of leptin was observed in women compared to men in both patient groups and healthy controls. Lean female hypopituitary patients had higher leptin levels than matched controls. CONCLUSIONS: Fasting levels of GIP were elevated in obese substituted hypopituitary patients, while fasting concentrations of GLPs were similar. Obese hypopituitary patients had the same degree of hyperinsulinaemia, affected glucose tolerance, dyslipoproteinaemia and central obesity as obese healthy controls. Further studies are required to identify the possible biochemical reasons for obesity in patients with apparently well-substituted hypopituitarism.

Adult↗
PubMed1999

The different effects of a Gln27Glu beta 2-adrenoceptor gene polymorphism on obesity in males and in females.

OBJECTIVES: To investigate the role of a polymorphism in codon 27 (Gln27Glu) of the beta 2-adrenoceptor gene for obesity in males compared to previously investigated females with an association of this polymorphism to obesity. DESIGN: Population-based study. SETTING: Medical department at a University Hospital. SUBJECTS: A total of 138 non-related Swedish males with body mass indexes (BMI) in the range 19.4-53.4 kg m-2 were recruited as: healthy volunteers, healthy obese subjects and subjects undergoing surgery for uncomplicated gallstone or abdominal hernia. In order to investigate the impact of gender, the results were compared with a subset of an earlier investigated female population of 109 Swedish females. Obesity was defined as a BMI > 27 kg m-2. MAIN OUTCOME MEASURES: Genotype examination of beta 2-adrenoceptor polymorphism in codon 27 with polymerase chain reaction and restriction fragment length polymorphism. RESULTS: The allele frequency of Gln27 and Glu27 did not differ between males and females when obese and non-obese subjects were investigated together. However, in obese males, the frequency of the Glu27 allele was significantly decreased (P = 0.034), whereas the frequency of this allele was increased in obese females (P = 0.013). No impact of the female androgen status on the distribution of the Gln27Glu polymorphism could be demonstrated in the obese females. CONCLUSION: A positive association between obesity and the Glu27 genetic variant in the beta 2-adrenoceptor exists in females, whereas in males there is a negative correlation between Glu27 and obesity. The findings suggest that different genetic factors contribute to obesity in males and females.

Adult↗
PubMed2002

Association between overweight or obesity and household income and parental body mass index in Australian youth: analysis of the Australian National Nutrition Survey, 1995.

This study is a secondary data analysis based on the 1995 Australian National Nutrition Survey (NNS). A random subsample of 1581 school children aged 7-15 years old from the NNS was studied. The results show the prevalence of overweight, obesity and combined overweight and obesity was 10.6-20.9%, 3.7-7.2% and 15.6-25.7%, respectively. The odds ratio of overweight or obese boys with highest household income was significantly smaller than those with the lowest household income. The proportion of combined overweight and obesity in children whose parents were overweight or obese was significantly greater compared with those whose parents were not. The trend of increasing prevalence of overweight or obesity among children with increasing parental body mass index (BMI) was significant after adjusting for age except the trend of father's BMI for boys. This study provided baseline data on the recent prevalence of overweight or obesity of Australian school children using new international absolute BMI cut-off points. It indicated that young school girls (7-9 years) were more likely to be overweight or obese compared with boys, the prevalence rates of overweight or obesity in older boys (13-15 year) was significantly greater than in other age groups while in girls it was the opposite. The boys with lowest household income ($0-17 500) were more likely to be overweight or obese compared with those with the highest household income (greater than $67 500). Having parents especially mothers who were overweight or obese may increase the risk of children being overweight or obese.

Adolescent↗
PubMed2003

Effect of Trp64Arg mutation of the beta3-adrenergic receptor gene and C161T substitution of the peroxisome proliferator activated receptor gamma gene on obesity in Japanese children.

OBJECTIVE: Obesity is a multifactorial syndrome influenced by both genetic and behavioral factors. Trp64Arg mutation of the beta3-adrenergic receptor (AR) gene and C161T substitution of the peroxisome proliferator-activated receptor (PPAR) gamma gene have been reported to be associated with obesity or lipid metabolism in adults. However, the effects of these mutations on children have not yet been clarified. For this reason, we studied the effects of Trp64Arg mutation of the beta3-AR gene and C161T substitution of the PPARgamma gene on obesity in Japanese children. SUBJECTS AND METHODS: In order to determine the effects of Trp64Arg mutation of the beta3-AR gene and C161T substitution of the PPARgamma gene on obesity in children, 105 obese Japanese children were screened by the polymerase chain reaction and restriction fragment-length polymorphism analysis. Plasma lipid, apolipo-protein (apo), glucose, insulin and leptin levels were also determined. RESULTS: Obese boys with Trp64Arg showed a higher obesity index and lower plasma levels of high-density lipoprotein cholesterol (HDL-C), apoA-I and apoA-II than those of them without the mutation. Obese boys with both mutations showed a higher plasma leptin level than those with only the beta3-AR gene mutation or PPARgamma gene mutation. No significant effect of these mutations was found in obese girls. CONCLUSION: All of these data suggest that Trp64Arg mutation of the beta3-AR gene might affect obesity and HDL metabolism in obese boys. In contrast, C161T mutation of the PPARgamma gene, by itself, is unlikely to influence obesity, lipid metabolism or plasma leptin levels.

Apolipoproteins↗
PubMed2002

Neuronal activation and corticotropin-releasing hormone expression in the brain of obese (fa/fa) and lean (fa/?) Zucker rats in response to refeeding.

The present study was conducted to investigate the pattern of neuronal activation and corticotropin-releasing hormone (CRH) expression in fed, food deprived and refed lean (Fa/?) and obese (fa/fa) Zucker rats. The pattern of neuronal activation was studied by measuring the expression of the immediate-early gene c-fos. Expression of c-fos and CRH mRNA was determined by in situ hybridization histochemistry. In both lean and obese rats, one hour of refeeding led to a transient increase in c-fos mRNA levels which was detected in the paraventricular hypothalamic nucleus (PVH), the dorsomedial hypothalamic nucleus, the supraoptic nucleus, the paraventricular thalamic nucleus, the central nucleus of amygdala (CeA), the lateral and medial parabrachial nuclei, the nucleus of the solitary tract, and the area postrema. In addition, refeeding led to strong activation of the arginine-vasopressin neurons located in the magnocellular part of the PVH. Following 24 h of food deprivation, CRH expression in the parvocellular division of the PVH was significantly higher in obese rats compared to lean animals. During refeeding, PVH CRH mRNA levels in obese rats decreased to reach control values. The decrease in CRH expression in obese rats was accompanied by the alleviation of the hypercorticosteronemia that characterized obese Zucker rats. CRH mRNA levels in the central nucleus of the amygdala were significantly higher in lean rats than in obese animals, when the rats were fed ad libitum During food deprivation, CeA CRH mRNA levels decreased in lean rats and gradually returned to predeprivation values during refeeding. In refed obese rats, CeA levels of CRH mRNA were higher than those of ad libitum fed or food-deprived obese mutants. In the perifornical region of the lateral hypothalamic area (LHA), the expression of CRH mRNA rose significantly in response to refeeding in lean rats, but not in obese animals. Following the first hour of refeeding, the number of neurons expressing CRH mRNA in the LHA in lean rats almost doubled. The present results demonstrate that refeeding has a stimulating effect in obese Zucker rats in a pattern of activation similar to that seen in lean Fa/? rats. They also demonstrate differences in CRH expression between Fa/? and fa/fa rats after refeeding. The most apparent of these differences was seen in the lateral hypothalamus in which refeeding failed to up-regulate CRH expression in obese rats.

Animals↗
PubMed2000

Change of cytokine balance in diet-induced obese mice.

Although decreased T-cell function has been observed in obese human subjects and genetically obese animals, the precise role of immune functions in obesity is still unclear. To investigate immune functions in obesity, we examined the proliferative responses of splenic lymphocytes and their capacity to produce cytokines in the presence or absence of leptin, the protein produced by the obese gene, in diet-induced obese and control mice. For induction of obesity, C57BL/6J mice were fed a high-fat diet for 13 weeks. In mice fed the high-fat diet, body weight, fat pad weight, and tumor necrosis factor (TNF) alpha production by adipocytes were significantly increased relative to mice fed the normal diet. Lipopolysaccharide (LPS) stimulated proliferation of cultured splenocytes from diet-induced obese mice was also increased. However, production of interleukin (IL)-2 by splenic lymphocytes from obese mice was suppressed, whereas interferon (IFN)-gamma and IL-4 production was increased. Exogenous lepitn regulated the cytokine production by cultured splenocytes from control and obese mice, respectively (upregulation of IFN-gamma and downregulation of IL-2 in control mice, and downregulation of IL-4 in obese mice). These results suggest that changes in cytokine production by splenic lymphocytes in obesity are indicative of altered immune functions that might contribute to related complications, although the effect of difference in nutrient intake (macro and micro) may also have contributed to the changes.

Animals↗
PubMed2002

Crohn's disease clinical course and severity in obese patients.

BACKGROUND AND AIMS: Obesity is unusual in Crohn's disease and the particularities of the disease in obese patients have not been studied. METHODS: 2065 patients were studied retrospectively. Obesity was defined by a BMI value >25.0 at disease onset and >30.0 at any time during the course of the disease. Disease characteristics, therapeutic needs, and year-by-year disease activity were determined in patients with and without obesity. RESULTS: 62 patients (3%) were obese. When compared with non-obese patients, obese patients did not show differences regarding sex, intestinal disease location, and disease behavior, but at diagnosis they were older (32 vs 28 years, P = 0.01) and a larger proportion had anoperineal disease (35 vs 24%, P = 0.03). When the 62 obese patients were paired for sex, location of disease at onset, date of birth, and date of diagnosis with 124 non-obese patients, the disease severity assessed by the importance of medical therapy and excisional surgery did not differ in the two groups but time to development of anoperineal abscess or fistula was shorter in obese patients, and obese patients were more prone to develop an active disease (OR 1.50, 95% CI 1.07-2.11) and to require hospitalization (OR 2.35, 95% CI 1.56-3.52) CONCLUSION: Obesity in Crohn's disease is associated with more frequent anoperineal complications and a more marked year-by-year disease activity, but does not alter significantly the long-term course of the disease.

Adult↗
PubMed1998

Societal and personal costs of obesity.

The economic costs of obesity can be broken down into three levels: 1. DIRECT COSTS: Costs to the community, related to the diversion of resources to the diagnosis and treatment of diseases directly related to obesity, as well as the treatment of obesity itself. These costs have been estimated to vary between 1-5% of total healthcare costs for various countries. Usually, the cost of obesity alone has been calculated, although it is known that the costs associated with being overweight [body mass index (BMI) 25-30 kg/m2] are also substantial because of the large proportion of individuals involved. These constitute costs to the health service (visits to general practitioners, consultations with medical specialists, hospital admissions and medication). 2. SOCIETAL OR INDIRECT COSTS: These costs are related to the loss of productivity caused by absenteeism, disability pensions and premature death. There is a lack of good economic analysis on this subject, although research from Sweden, Finland and the Netherlands has clearly shown that obesity is associated with increased sick leave and disability pensions. 3. PERSONAL COSTS: Obese subjects may earn less than their lean counterparts because of job discrimination (related to the stigma associated with obesity, or due to diseases and disabilities caused by obesity). Many insurance companies (particularly life insurance) charge higher premiums with increasing degrees of overweight. Obesity is further related to poor physical functioning and limitations in daily life. Some of these require assistance or adaptations which may be costly for an individual. In conclusion, there is much indirect information that obesity and overweight contribute substantially to healthcare-related costs. Data on aspects such as societal costs and personal costs are too fragmentary to allow calculation of the expenses involved. An appropriate analysis of all costs associated with obesity is important in order to persuade responsible bodies to develop strategies towards the prevention and long-term management of obesity.

Absenteeism↗
PubMed2006

Increased aldosterone/renin quotient in obese hypertensive women: a novel role for low-density lipoproteins?

Obesity, especially visceral obesity, is strongly associated with arterial hypertension. Indeed, obesity hypertension has to be considered as the most common form of essential hypertension. However, the exact nature of the relationship between obesity and increased blood pressure remains poorly understood. Involvement of renin-independent mechanisms has been suggested in adrenal stimulation of aldosterone secretion in obese patients. This investigation examined the plasma levels of renin, aldosterone, insulin, and HDL and LDL in obese hypertensive and obese normotensive women. The group of hypertensive obese women showed significantly reduced plasma levels of renin and increased aldosterone/renin quotient (ARQ) compared to obese normotensive women. Plasma aldosterone levels were not significantly different between hypertensive and normotensive obese women. In addition, plasma levels of LDL-cholesterol in the hypertensive obese group were significantly increased in comparison to the obese normotensive group. No differences were observed in HDL-cholesterol or total cholesterol/HDL-C ratios between the two groups. We therefore examined the effect of LDL on angiotensin II-stimulated aldosterone release from human adrenocortical H295R cells. Treatment of adrenocortical cells with LDL led to a sensitization towards stimulation by angiotensin II, dramatically increasing angiotensin II-induced aldosterone production, so the increased aldosterone/renin ratio observed in the hypertensive group may be due to the enhanced LDL levels in these patients and/or other adipocyte-derived mineralocorticoid-stimulating factors.

Adolescent↗
PubMed1998

Obesity-related overexpression of fatty-acid synthase gene in adipose tissue involves sterol regulatory element-binding protein transcription factors.

Elevated lipogenesis is a key determinant of exaggerated fat deposition in adipose tissue of obese Zucker rats. We previously delineated a region in the fatty-acid synthase promoter, which was responsible for obesity-related overexpression of the fatty-acid synthase (FAS) gene, by negatively regulating the activity of the downstream promoter in lean but not obese rat fat cells. The present study aimed to identify the transcriptional factors acting on this target region. First, functional analysis of mutated FAS promoter constructs in transiently transfected lean and obese rat adipocytes showed that the activity of the obesity-related region relied on the presence of a transcriptionally inactive sterol regulatory element at -150, which counteracted activation through the downstream E-box. Adenovirus-mediated overexpression of a dominant negative form of adipocyte determination and differentiation factor 1 (ADD1) was used to neutralize endogenous ADD1/ sterol regulatory element-binding protein (SREBP) transcriptional activity in fat cells, by producing inactive dimers unable to bind target DNA. With this system, we observed that overexpression of FAS in obese rat adipocytes was ADD1/SREBP-dependent. SREBP isoforms expression was assessed in lean and obese rat fat cells and showed no differences in the level of ADD1/SREBP1 mRNA. In addition, equivalent amounts of immunoreactive ADD1/SREBP1 were found in nuclear extracts from lean and obese rat fat cells. In contrast, immunoreactive SREBP2, which was very low in nuclear extracts from lean rats, was induced in obese rat fat cells. Finally, using in vitro binding studies, we showed that SREBP2 was able to displace ADD1/SREBP1 binding from the sterol regulatory element (SRE) site. Thus, we propose a mechanism for obesity-related overexpression of FAS gene in rat adipocyte. ADD1/SREBP1-activated transcription proceeding from the E-box motif is counterbalanced by a negative SRE site acting by limiting the availability of ADD1/SREBP1 in normal fat cells. The negative effect of this site is abolished in obese rat adipocyte nuclei where SREBP2 is induced and can substitute for ADD1/SREBP1 binding to the inactive SRE. These results provide evidence for the implication of SREBPs in the dysregulation of adipocyte metabolism characteristic of the obese state.

Adipose Tissue↗