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PubMed2004

Increasing the impact of European obesity research in preparation for the European research area: a report on the 2003 European Commission Obesity Workshop.

Leading obesity researchers from across Europe assembled in Aberdeen, Scotland, in January 2003 to consider how to increase the impact of European obesity research. The workshop was funded by the European Commission and hosted by the Rowett Research Institute, Aberdeen. The delegates identified the need to (i) develop a portfolio of studies that integrate genetics and mechanisms through parallel study of humans and animal models and (ii) establish major intervention studies in weight management and early life nutrition. It was recommended that these goals would be best achieved under the umbrella of a virtual European Obesity Research Institute, or Network of Excellence in Obesity Research under Framework Programme 6, that would facilitate harmonization of methodology, manage centralized standardized resources, coordinate training initiatives, workshops and working groups, and increase focus.

Diet↗

PubMed1993

Does obesity run in families because of genes? An adoption study using silhouettes as a measure of obesity.

A number of studies, including the Danish adoption study, have shown that, in adults, the familial resemblance of obesity, as measured by the body mass index (weight in kg/(height in m)2), is mainly due to genes. The body mass index may reflect both fat and fat-free body mass. In this further analysis of the Danish adoption study, the degree of obesity was assessed by a silhouette score. There was a significant relationship in scores between the adult adoptees and their biological mothers and between the adoptees and their biological full siblings reared by the biological parents. Weaker, nonsignificant associations were found for the biological fathers and for the maternal and paternal half-siblings. There were no relationships in silhouette scoring between adoptees and adoptive parents. The results confirm the results of our previous analysis of body mass index. We conclude that human obesity is under genetic control, whereas the childhood family environment has little, if any, influence on obesity in adults. It is an important task for future research to identify the genes involved.

Adoption↗

PubMed1989

Independent effects of weight change and attained body weight on prevalence of arterial hypertension in obese and non-obese men.

OBJECTIVE: To assess the relations among prevalence of arterial hypertension, history of weight change, and current body weight in the range from normal weight to severe obesity. DESIGN: Retrospective analysis of medical records of men registered with Danish military authorities from 1943 to 1977 and followed up four to 40 years later. SETTING: Draft board of Copenhagen and surrounding counties and the rest of Sjaelland and surrounding islands. SUBJECTS: 964 Men who were severely obese (body mass index greater than or equal to kg/m2 at the first examination) and 1134 random controls. MAIN OUTCOME MEASURES: Blood pressure and weight. RESULTS: Hypertension was more prevalent in subjects with an unchanged body mass index as that index increased over the range studied. At any body mass index hypertension was more prevalent in subjects who had increased to this index and less common in those who had decreased to it than in those who had stayed the same weight since the first examination. Hypertension among controls was most common in those subjects who had become obese during adulthood. CONCLUSIONS: Changes in body weight have a great influence on arterial hypertension independent of the effect of attained weight, particularly in obese subjects.

Adult↗

PubMed2005

Central orexin sensitivity, physical activity, and obesity in diet-induced obese and diet-resistant rats.

Nonexercise activity thermogenesis (NEAT), the most variable component of energy expenditure, can account for differential capacities for human weight gain. Also highly variable, spontaneous physical activity (SPA) may similarly affect weight balance in animals. In the following study, we utilized the rat model of obesity, the diet-induced obese (DIO) rat, as well as the diet-resistant (DR) rat strain, to investigate how access to a high-fat diet alters SPA and the associated energy expenditure (i.e., NEAT). DIO and DR rats showed no differences in the amount of SPA before access to the high-fat diet. After 29 days on a high-fat diet, the DIO rats showed significant decreases in SPA, whereas the DR rats did not. Next, we wanted to determine whether the DIO and DR rats showed differential sensitivity to microinjections of orexin into the paraventricular nucleus of the hypothalamus (PVN). Unilateral guide cannulae were implanted, aimed at the PVN. Orexin A (0, 0.125, 0.25, and 1.0 nmol in 500 nl) was microinjected through the guide cannula into the PVN, then SPA and energy expenditure were measured for 2 h. Using the response to vehicle as a baseline, the DR rats showed significantly greater increase in NEAT compared with the DIO rats. These data indicate that diet-induced obesity is associated with decreases in SPA and a lack of increase in NEAT. A putative mechanism for changes in NEAT that accompany obesity is a decreased sensitivity to the NEAT-activating effects of neuropeptides such as orexin.

Animals↗

PubMed2002

Anti-obesity effect of SR141716, a CB1 receptor antagonist, in diet-induced obese mice.

Because the CB1 receptor antagonist SR141716 was previously reported to modulate food intake in rodents, we studied its efficacy in reducing obesity in a diet-induced obesity (DIO) model widely used for research on the human obesity syndrome. During a 5-wk treatment, SR141716 (10 mg. kg(-1). day(-1) orally) induced a transient reduction of food intake (-48% on week 1) and a marked but sustained reduction of body weight (-20%) and adiposity (-50%) of DIO mice. Furthermore, SR141716 corrected the insulin resistance and lowered plasma leptin, insulin, and free fatty acid levels. Most of these effects were present, but less pronounced at 3 mg. kg(-1). day(-1). In addition to its hypophagic action, SR141716 may influence metabolic processes as the body weight loss of SR141716-treated mice was significantly higher during 24-h fasting compared with vehicle-treated animals, and when a 3-day treatment was compared with a pair feeding. SR141716 had no effect in CB1 receptor knockout mice, which confirmed the implication of CB1 receptors in the activity of the compound. These findings suggest that SR141716 has a potential as a novel anti-obesity treatment.

Animals↗

PubMed1992

Skeletal muscle composition in dietary obesity-susceptible and dietary obesity-resistant rats.

The intent of this study was to determine whether a relationship exists between susceptibility to high-fat diet (HFD)-induced obesity and skeletal muscle fiber type. Forty-four adult male Wistar rats were given ad libitum access to a HFD (60% of calories from fat) for 4 wk. Rats were then grouped into quartiles for total weight gain, and the top-quartile [obesity prone (OP)] rats were compared with the bottom-quartile [obesity resistant (OR)] rats. OP rats gained 1.5 times as much weight as OR rats. OR rats had a significantly higher proportion of type I muscle fibers in the medial head of the gastrocnemius muscle than OP rats both before (determined from a muscle biopsy) and after the HFD feeding period. A greater proportion of type I fibers may be associated with a greater capacity for fat oxidation, which would favor resistance to body fat accumulation. Preexisting differences in muscle fiber composition may play a role in determining susceptibility to dietary obesity.

Animals↗

PubMed1993

Obesity-associated decrease in growth hormone-releasing hormone gene expression: a mechanism for reduced growth hormone mRNA levels in genetically obese Zucker rats.

The secretion of growth hormone (GH) is impaired in the genetically obese Zucker rat where GH gene expression and plasma GH levels are depressed; however, the underlying mechanism of this abnormality remains unclear. We have evaluated the potential causative role of hypothalamic GH-releasing hormone (GHRH) and somatostatin (SRIH) gene expression in the onset of the decreased GH mRNA levels by studying both GHRH and SRIH mRNA and peptide levels in obese and lean rats at 5 weeks of age when the decrease in GH mRNA is first detected. At that age both GHRH content and GHRH mRNA were significantly reduced in obese rats as compared to lean controls; hypothalamic SRIH content was also decreased in obese rats, but SRIH mRNA levels did not differ. Since GHRH is capable of stimulating GH gene expression, the decreased GHRH mRNA level could be a critical factor in causing the attenuation in GH gene expression and consequent diminution of circulating plasma GH.

Animals↗

PubMed1995

Molecular cloning of rat obese cDNA and augmented gene expression in genetically obese Zucker fatty (fa/fa) rats.

The obese (ob) gene has recently been isolated through a positional cloning approach, the mutation of which causes a marked hereditary obesity and diabetes mellitus in mice. In the present study, we isolated rat ob cDNA and examined the tissue distribution of the ob gene expression in rats. We also studied the gene expression in genetically obese Zucker fatty (fa/fa) rats. The rat ob gene product, a 167 amino acid protein with a putative signal sequence, was 96 and 83% homologous to the mouse and human ob proteins, respectively. Northern blot analysis using the rat ob cDNA probe identified a single mRNA species of 4.5 kb in size in the adipose tissue, while no significant amount of ob mRNA was present in other tissues in rats. The ob gene was expressed in the adipose tissue with region specificities. The rank order of the ob mRNA level in the adipose tissue was epididymal, retroperitoneal, and pericardial white adipose tissue > mesenteric and subcutaneous white adipose tissue > or = interscapular brown adipose tissue. The ob gene expression occurred in mature adipocytes rather than in stromalvascular cells isolated from the rat adipose tissue. Expression of the ob gene was markedly augmented in all the adipose tissue examined in Zucker fatty (fa/fa) rats at the stage of established obesity. The present study leads to the better understanding of the physiologic and pathophysiologic roles of the ob gene.

Adipose Tissue↗

PubMed2004

Visceral obesity without insulin resistance in late-onset obesity rats.

We describe a line of transgenic rats in which the males develop a unique autosomal dominant, late-onset obesity (LOB) phenotype. LOB males gradually accumulate fat specifically in visceral, but not peripheral, fat depots despite a normal intake of a low fat diet. LOB females normally develop only mild obesity with advanced age. However, the phenotype can be induced rapidly in young females by ovariectomy and prevented by estrogen replacement. LOB males are highly sensitive to dietary fat. Young, nonobese LOB males gain more weight on a 30% fat diet and lose more weight when treated with the lipase inhibitor, Orlistat, than their nontransgenic littermates. Remarkably, despite severe visceral obesity, LOB rats have normal fasting blood glucose, insulin, and corticosterone; show normal or increased insulin sensitivity in glucose and insulin tolerance tests; have increased plasma adiponectin levels; and display a heightened response to treatment with rosiglitazone. Their visceral adiposity reflects a specific increase in visceral adipocyte number, not size. Analysis of the transgene in LOB rats revealed a deletion in the gene encoding the S26 subunit of the mitochondrial ribosome that results in the production of a truncated protein, which we show to be imported into mitochondria. However, the transgene integrant is complex, so whether this is the sole molecular disruption underlying this phenotype remains to be established. Nevertheless, LOB rats provide a valuable new model of late-onset, male-preponderant, visceral-specific obesity, clearly dissociated from insulin resistance.

Absorption↗

PubMed2003

Obesity, regional fat distribution, and syndrome X in obese black versus white adolescents: race differential in diabetogenic and atherogenic risk factors.

The incidence of type 2 diabetes mellitus in children is increasing with the increasing prevalence of obesity, particularly in African-American children. We hypothesized that African-American obese adolescents are more insulin resistant than their white peers, but have lower insulin secretion, thus increasing their risk of type 2 diabetes mellitus. The present study investigated insulin sensitivity and secretion, visceral adiposity (VAT), and cardiovascular disease (CVD) risk profile in black obese adolescents (BOA) vs. white obese adolescents (WOA). Twenty-four BOA and 26 WOA underwent a hyperinsulinemic-euglycemic clamp to assess insulin sensitivity, a hyperglycemic clamp to determine insulin secretion, dual energy x-ray absorptiometry for body composition and computed tomography scan at L4-L5 to measure VAT and sc abdominal adipose tissue. Fasting lipid and automated blood pressure measurements were obtained. The WOA and BOA groups were divided into low VAT and high VAT groups. BOA compared with WOA of similar body mass index and percent body fat had less visceral adiposity, lower hepatic glucose production, and lower lipid levels. Visceral adiposity was associated with lower insulin sensitivity in both groups [low vs. high VAT; BOA, 2.9 +/- 0.4 vs. 1.7 +/- 0.2 micromol/kg x min per pmol/liter (P = 0.016); WOA, 2.6 +/- 0.5 vs. 1.5 +/- 0.1 (P = 0.032)]. However, this was compensated by higher insulin secretion in whites (low VAT, 934.8 +/- 121.8; high VAT, 1590.6 +/- 232.8 pmol/liter; P = 0.037), but not in blacks (low VAT, 1398.9 +/- 214.0; high VAT, 1423.7 +/- 108.7 pmol/liter). Glucose disposition index (insulin sensitivity x first phase insulin) was lower in high VAT vs. low VAT BOA, but not in WOA. In each racial group, high VAT groups had elevation of systolic and diastolic blood pressure, but dyslipidemia was worse in WOA with high VAT. In conclusion, a given level of body mass index confers different metabolic risks for WOA vs. BOA. Although differences in fat patterning may help explain the more atherogenic risk profile in whites, the cause of the more diabetogenic insulin sensitivity/secretion profile in blacks remains unknown and needs to be investigated further.

Adipose Tissue↗

PubMed2004

Plasma ghrelin concentrations are decreased in insulin-resistant obese adults relative to equally obese insulin-sensitive controls.

Ghrelin, an orexigenic hormone that may play a role in body weight regulation, is reduced in states of obesity. Because obesity is associated with insulin resistance and compensatory hyperinsulinemia, we determined whether these metabolic characteristics were independently associated with suppressed ghrelin concentrations. To investigate this hypothesis, using steady-state plasma glucose concentrations, we identified 20 insulin-resistant (IR) and 20 insulin-sensitive (IS) individuals who were equally obese. The mean body mass indexes were 32.5 +/- 0.4 and 32.0 +/- 0.4 kg/m(2) for the IR and IS groups, respectively. Fasting insulin concentrations were 19.5 and 7.4 micro U/ml (P < 0.001), respectively. Ghrelin concentrations were suppressed in the IR group (252 +/- 19 pg/ml) relative to the IS group (412 +/- 35 pg/ml; P < 0.001). Ghrelin correlated inversely with both insulin resistance (r = -0.64; P < 0.001) and fasting insulin concentration (r = -0.58; P < 0.001). Multivariate analysis confirmed that both insulin resistance and hyperinsulinemia independently predicted low ghrelin concentrations. Our results demonstrate that in obese individuals, insulin resistance and hyperinsulinemia are inversely associated with ghrelin concentrations. Thus, insulin resistance or related metabolic abnormalities may constitute part of a feedback mechanism by which body weight is regulated in humans.

Blood Glucose↗

PubMed2000

Serum soluble tumor necrosis factor-alpha receptor 2 is elevated in obesity but is not related to insulin sensitivity: a study in identical twins discordant for obesity.

Tumor necrosis factor-alpha (TNFalpha) and its soluble receptor 2 (TNFR2) are expressed in adipose tissue and are possibly involved in the pathogenesis of insulin resistance. Information about serum levels of TNFR2 in human obesity, especially the possible role of genetic factors and body fat distribution, is scanty. We measured serum TNFalpha and soluble TNFR2 concentrations in 23 identical twin pairs who had an average 18-kg intrapair difference in body weight. The mean TNFalpha concentration was 44.1 ng/L in obese and 34.2 ng/L in lean cotwins (P = 0.051). The respective values for TNFR2 were 1,989 and 1,840 ng/L (P = 0.004). The intrapair difference in TNFR2 level correlated positively (r-value always > or = 0.56; P < or = 0.01) with intrapair differences in body mass index, percent body fat, and abdominal sc fat area (assessed by magnetic resonance imaging), but not with differences in visceral fat area, glucose or insulin areas under the curve, or insulin sensitivity index in the oral glucose tolerance test. The intraclass correlation for TNFR2 was 0.67, and the genetic variation in circulating TNFR2 level was almost 6-fold higher than the variation due to obesity. We conclude that the soluble TNFR2 concentration is determined by both genetic factors and adiposity, especially sc fat. Measurement of circulating TNFR2 does not seem to be useful in identifying obese individuals who are insulin resistant.

Aged↗

PubMed2006

Outcome and complications of gastric bypass in super-super obesity versus morbid obesity.

BACKGROUND: Roux-en-Y gastric bypass (RYGBP) reduces the co-morbidities of obesity. Patients with super-super obesity (BMI>or=60) present additional technical and medical challenges. This study compares the results in super-super-obese patients with patients with a BMI of <60 over a 5.5-year period. METHODS: Retrospective analysis was performed of the 504 patients who underwent open RYGBP from January 1999 through June 2004. Patients were divided into 2 groups: Group A (444 patients) had a BMI <60, and Group B (60 patients) had a BMI>or=60, and also had a greater percentage of males. The groups were otherwise similar in demographics and co-morbidities. RESULTS: Concomitant ventral herniorrhaphy was performed in 23 patients (5%) in Group A and in 3 patients (5%) in Group B. Concomitant cholecystectomy was done in 11.2% in Group A and 10% in Group B. Group A patients had an incidence of leaks of 1.3%, and there were no leaks in Group B. Wound infection rate for Group A was 5% vs 1.7 % in Group B (NS). Mortality for both groups was similar. The stricture rate for Group A was 0.9% compared with 1.7 % for Group B. After 1 year, excess weight lost was 41.7% in Group A and 38.3% in Group B. The development of anemia was not statistically different (8.3% vs 11.0 %). Incidence of postoperative gallbladder disease and incisional hernia was similar. CONCLUSIONS: Super-super-obese patients should not be excluded from RYGBP because of a perceived increased risk based upon BMI.

Adolescent↗

PubMed1989

Plasma glucagon response to intravenous alanine in obese and non-obese subjects.

To investigate glucagon (IRG) and insulin (IRI) responses to alanine infusion in obesity and to assess the effect of body weight reduction with respect to hormonal balance, we compared six obese subjects with nine normal weight controls. None of the subjects were diabetic by OGTT criteria. Plasma IRI and IRG were measured following IV alanine at a rate of 0.1 g/kg over a period of 2 min. Our obese subjects had an increase in IRG response to alanine, which was due to decreased suppression of alpha-cell function due to insulin resistance. Weight reduction via calorie restriction reduced insulin demand, resulting in reduced plasma IRI by restoring beta-cell function, and the IRG response was paradoxically decreased as compared with that before weight loss. It is conceivable that improvements in insulin sensitivity after body weight reduction may re-establish the normalization of pancreatic beta-cell function and the insulin-induced inhibition of IRG secretion. Our obese subjects were characterized by decreased IRG secretion which was reflected in a change in body weight reduction.

Alanine↗

PubMed2006

Obesity and obesity-related illnesses in borderline patients.

The purpose of this study was to examine the prevalence, risk factors, and consequences of obesity in borderline patients 6 years after an index admission for psychiatric reasons. Two hundred and sixty-four borderline patients who met Revised Diagnostic Interview for Borderlines (DIB-R; Zanarini, Gunderson, Frankenburg, & Chauncy, 1989) and Diagnostic and Statistical Manual of Mental Disorders (3rd ed. ref.) (DSM-III-R; APA, 1987) criteria for BPD were interviewed concerning their body mass index (BMI) and related medical problems. Seventy-four of the 264 borderline patients at 6-year follow up were obese, having a BMI > or = 30 kg/m2. They were significantly more likely than the nonobese patients to report suffering from diabetes, hypertension, osteoarthritis, chronic back pain, carpal tunnel syndrome, urinary incontinence, gastroesophageal reflux disorder, gallstones, and asthma. Four significant risk factors were found: chronic PTSD, lack of exercise, a family history of obesity, and a recent history of psychotropic polypharmacy. These results suggest that obesity is common among heavily treated borderline patients and is associated with a number of chronic medical disorders.

Adult↗

PubMed1994

Anti-obesity effect of CL 316,243, a highly specific beta 3-adrenoceptor agonist, in mice with monosodium-L-glutamate-induced obesity.

The effects of CL 316,243, a highly specific beta 3-adrenoceptor agonist (relative selectivities of 0, 1 and 100,000 for beta 1-, beta 2- and beta 3-receptors, respectively), were evaluated in mice with monosodium L-glutamate (MSG)-induced obesity as well as in control mice injected with physiological saline instead of MSG. Both MSG- and saline-treated mice were divided into three groups and at 8 weeks of age received either CL 316,243 (0.1 or 1.0 mg/kg) or distilled water through a gastric tube for 2 weeks. CL 316,243 not only reduced white adipose tissue mass but also activated brown adipose tissue and systemic metabolism, and hence reduced body mass without affecting food intake. Furthermore, CL 316,243 decreased hyperglycemia and hypertriglyceridemia in MSG-treated mice. However, at the higher dose, CL 316,243 also increased liver triglyceride in MSG-treated mice. These observations suggest that CL 316,243 exerts an anti-obesity effect in mice with MSG-induced obesity and consequently may prove efficacious in the treatment of human obesity.

Adrenergic beta-Agonists↗

PubMedDate not supplied

[Circadian rhythm of blood pressure and obesity--blood pressure variation and obesity].

INTRODUCTION: The association between obesity and arterial hypertension has been established in a great number of studies. Our objective was to investigate whether circadian rhythm of blood pressure is disturbed among obese people. MATERIAL AND METHODS: In this cros-sectional, randomized study, Schiller BR-102 device was used for ambulatory blood pressure monitoring. One hundred and twenty outpatients were divided into three randomized groups: obese body mass index 30 kg/m2 (52 patients), overweight (28 patients), with body mass index 25.0-29.9 kg/m2 and normal weight (control group) (48 patients), with body mass index 18.5-24.9 kg/m2. In all patients we investigated the following blood pressure parameters: average blood pressure (total, day-time and night-time), maximal blood pressure and dipping or non-dipping blood pressure pattern during night (for systolic and diastolic blood pressure, respectively). RESULTS: In body mass index beyond 30 kg/m2 only systolic blood pressure parameters were significantly higher--average blood pressure--during daytime (P = 0.034) and during night (P = 0.014); maximal blood pressure (P = 0.001). In body mass index beyond 30 kg/m2, absence of normal blood pressure during night was significantly more often registered (P = 0.007). DISCUSSION AND CONCLUSION: The non-dipping blood pressure pattern and increase of systolic blood pressure only reveal hyperactivation of sympathetic nervous system as a leading patophysiological mechanism causing arterial hypertension in obese patients.

Blood Pressure↗

PubMed1995

Impaired insulin-induced platelet antiaggregating effect in obesity and in obese NIDDM patients.

To investigate the effects of insulin on platelets in obesity and in non-insulin-dependent diabetes mellitus (NIDDM)--classic insulin-resistant states--we determined ADP-induced platelet aggregation and platelet cGMP (guanosine 3',5'-cyclic monophosphate) content in platelet-rich plasma obtained from nine obese subjects and nine age-matched healthy volunteers and from eight NIDDM obese patients and nine age-matched healthy volunteers after a 3-min incubation with human recombinant insulin (0, 240, 480, 960, and 1,920 pmol/l). Platelet aggregation was evaluated using different ADP doses to measure the ADP concentration determined on the basis of a dose-response curve necessary to elicit a maximal aggregation of 50% (ED50). Insulin induced a dose-dependent decrease of platelet aggregation to ADP (P = 0.0001) in healthy subjects. A significant effect was evident starting from an insulin concentration of 240 pmol/l. On the contrary, in insulin-resistant subjects, insulin reduced platelet sensitivity to ADP only at a concentration of 1,920 pmol/l. When ADP ED50 values obtained in platelet-rich plasma incubated with insulin were expressed in percentage of the ADP ED50 values obtained in platelet-rich plasma without insulin, considered as 100%, we observed that ADP ED50 with 1,920 pmol/l insulin was 153.6 +/- 13.2% in the younger healthy subject group (P = 0.004), 150.0 +/- 3.8% in the older healthy subject group (P = 0.0001), 116.1 +/- 6.1% in obese subjects (P = 0.031), and 120.0 +/- 8.6% in NIDDM patients (P = 0.05). In healthy subjects, insulin induced a dose-dependent increase of platelet cGMP (P = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗