bluuebunny/crossref_metadata_2025_split huggingface dataset:
Body Size Preferences and Desired Weight of Patients Who Have Received Obesity Surgery and of Comparison Adults
Authors: Rand Colleen S. W. , Macgregor AlexM. C. 
Published: September 2012

AbstractPatients who had received obesity surgery (n=144) and comparison adults (n=72) selected the most attractive male and female size and the samesex size they most wanted to look like from an array of 15 outline drawings. Subjects also reported their height, and current and desired weights (transformed into body mass index units [BMI]). There was a remarkable consensus on the sizes considered most attractive: Two male sizes were chosen by 78% of all subjects, and two female sizes by 83%. The hypothesis that adults who had obesity surgery would idealize thin sizes and, therefore, select thinner sizes and lower weights than comparison adults was not supported. Not only did patients and comparison adults selecte the same desired size, but women patients desired significantly larger BMIs than comparison women. There was a large range of desired BMIs associated with each desired size; the correlation between desired BMI and desired size was significant for women but not for men. It was speculated that subjects' desired size reflected cultural norms while subjects' desired BMI was a function of their current weight. Health professionals working in weight loss and/or physical fitness areas need to help clients understand weight‐size relationships so that clients can have both realistic weight and realistic size goals.
Absence of Linkage Between Human Obesity and the Mouse Agouti Homologous Region (20q11.2) or Other Markers Spanning Chromosome 20q
Authors: Xu Weizhen , Reed Danielle R. , Ding Yuan , Price R. Aden 
Published: September 2012

AbstractXU, WEIZHEN, DANIELLE R REED, YUAN DING AND R ARLEN PRICE. Absence of linkage between human obesity and the mouse agouti homologous region (20q11.2) or other markers spanning chromosome 20q. Obes Res.Mutant alleles of the agouti gene cause obesity in the mouse and the homologous gene in humans has been mapped to chromosome 20q11.2. An allelic variant of the agouti gene could account for obesity in humans and we tested this hypothesis by genotyping 210 sibling pairs from 45 families segregating an obesity phenotype. Using sibling pair linear regression analysis, evidence for linkage between obesity and markers flanking the agouti locus and other markers spanning chromosome 20q was assessed. We found no correlation between identity‐by‐descent at these markers and obesity differences within pairs. In the mouse, obesity caused by mutations of the agouti gene develops later in life, so a subset of families with adult‐onset obesity were also tested for linkage, with negative results. Although it is not possible to exclude alleles of the agouti gene as a contributor to obesity in humans, the absence of positive linkage in this study suggests that either the agouti gene has small effects or the allele frequency is low.
Serotonin, Eating Behavior, and Fat Intake
Authors: Blundell John E. , Lawton Clare L. , Halford Jason CG 
Published: September 2012

AbstractThere is an intimate relationship between nutritional intake (eating) and serotonin activity. Experimental manipulations (mainly neuropharmacological) of serotonin influence the pattern of eating behavior, subjective feelings of appetite motivation, and the response to nutritional challenges. Similarly, nutritional manipulations (food restriction, dieting, or altered nutrient supply) change the sensitivity of the serotonin network.Traditionally, serotonin has been linked to the macronutrient carbohydrate via the intermediary step of plasma amino acid ratios. However, it has also been demonstrated that 5‐HT drugs will reduce energy intake and reverse body weight gain in rats exposed to weight increasing high fat diets. 5‐HT drugs can also reduce food intake and block weight gain of rats on a high fat cafeteria diet. Some diet selection studies in rats indicate that the most prominent reduction of macronutrient intake is for fat. These data indicate that 5‐HT activity can bring about a reduction in fat consumption. In turn, different types of dietary fat can alter brain 5‐HT activity.In human studies the methodology of food choice experiments has often precluded the detection of an effect of 5‐HT manipulation on fat intake. However, there is evidence that in obese and lean subjects some 5‐HT drugs can readily reduce the intake of high fat foods. Data also suggest that 5‐HT activation can lead to a selective avoidance of fat in the diet. These effects of 5‐HT on the intake of dietary fat may involve a pre‐absorptive mechanism and there is evidence that 5‐HT is linked to cholecystokinin and enterostatin. These proposals have theoretical and practical implications and suggest possible strategies to intensify or advance fat‐induced satiety signals.
Combined Drug Treatment of Obesity
Authors: Atkinson Richard L. , Blank Roy C. , Loper Judy F. , Schumacher Donald , Lutes Richard A. 
Published: September 2012

AbstractPharmacological treatment of obesity has been neglected as a viable therapeutic option for many years. Recent long term studies with combinations of obesity drugs gives promise that drugs may play a role in weight maintenance, which classically has been the most difficult aspect of treating obesity. Currently available obesity drugs include centrally acting adrenergic agents and serotonin agonists. Drugs still in development include a lipase inhibitor that produces fat malabsorption, a combined adrenergic‐serotonergic reuptake inhibitor, various gut‐central nervous system peptides, and a number of beta‐3 agonists. Any of these obesity drugs given alone produces modest weight loss, and for most, weight loss continues for as long as medication is given. The most successful drug regimens to date are combinations of phentermine and fenfluramine or of ephedrine, caffeine, and/or aspirin. The former combination produces reduction in body weight and complications of obesity for 2 to almost 4 years in clinical trials to date. More research is needed to document long term efficacy and particularly the long term safety of these and other combinations.
Apolipoprotein A‐IV: A Circulating Satiety Signal Produced by the Small Intestine
Authors: Tso Patrick , Chen Qi , Fujimoto Kazuma , Fukagawa Koji , Sakata Toshiie 
Published: September 2012

How fat feeding, especially lipoproteins and apolipoproteins, may affect food intake is unclear. Apolipoprotein A‐IV (apo A‐IV) is a protein associated with chylomicrons, and its synthesis by the small intestine is markedly stimulated following ingestion of fat. We explored the anorectic effect of chylous lymph on feeding behavior. Intestinal lymph samples collected during lipid infusion intraduode‐nally when administered intravenously markedly suppressed food intake in fasting rats. To determine if the suppressor was lipid or apo A‐IV, fasting rats were infused intravenously with a 2% Intralipid emulsion, but it did not suppress food intake. These data suggest that the factor in chylous lymph that suppresses food intake is probably apo A‐IV. To test this, apo A‐IV in chylous lymph was removed by immunoprecipitation, and the chylous lymph with apo A‐TV removed lost its anorectic effect. Next, we infused purified apo A‐IV intravenously in fasted rat, and it inhibited food intake in a dose‐dependent manner. We therefore conclude that increased apo A‐IV in chylous lymph is a factor involved in anorexia after fat feeding.Infusion of 0.5 μg of apo A‐IV into the third ventricle failed to suppress food intake. Higher doses (1|Xg or higher) of apo A‐IV infused into the third ventricle inhibited food intake in a dose‐dependent manner. To further test the hypothesis that apo A‐IV is an important factor controlling food intake, we administered goat anti‐rat apo A‐IV serum into the third ventricle of rats that were allowed food and water ad libitum. In all rats tested, this treatment resulted in enhanced food intake. In conclusion, we propose that apo A‐IV may act centrally to control food intake.
Glucose‐Responsive Neurons In the Brainstem
Authors: Adachi Akira , Kobashi Motoi , Funahashi Makoto 
Published: September 2012

Area Postrema: The influence on feeding behavior caused by ablation of the area postrema (AP) in rodents indicates the participation of this structure in the control of ingestion. Two types of glucose responsive neurons were identified in the AP: one is characterized by increasing the discharge rate in response to glucose (glucoreceptor type) and the other by decreasing the discharge rates in response to glucose (glucose sensitive type). These glucose responsive neurons may participate in glycemic homeostasis.Nucleus of Solitary Tract: The glucose responsive neurons exist within the caudal portion of nucleus of the solitary tract (NTS), a relay station in visceral afferents. Two types similar to the AP were also recognized. It is confirmed that hepatic glucose sensitive afferents terminate on some of the glucose sensitive neurons. This convergence may serve as a fail‐safe mechanism. In addition, the NTS involving complex neural networks of excitatory and inhibitory interneurons may be concerned with integration of glycemic information.Dorsal Motor Nucleus of Vagus: Some neurons within the dorsal motor nucleus of the vagus (DMV) were identified as the glucose responsive ones. Both types were also recognized. It is confirmed by antidromic activation that these glucose responsive DMV neurons send their axons toward the gastric or coeliac branch that innervates either the stomach, intestine or pancreas. Some of the DMV neurons may subserve an enteroceptor function by themselves. They may also play a role in the brainstem neural control of glycemic homeostasis as the failsafe mechanism.
The Effect of Protoporphyrinogen Oxidase Inhibitors on Microsomal and Mitochondrial Cytochromes
Authors: Krijt Jan , Maruna Pavel , Petrovicky Pavel , Janousek Vaclav 
Published: September 2012

Neurological dysfunction is a characteristic feature of acute porphyrias, unexplained until now. One of the possible explanations is a deficiency of heme in the central nervous system, caused by a block in porphyrin biosynthesis. To test this possibility, the content of brain mitochondrial cytochrome a3 was determined after intracerebroventricular administration of the protoporphyrinogen oxidase‐inhibiting herbicide fomesafen. It was established in in vitro experiments that fomesafen is a potent inhibitor of brain mitochondrial protoporphyrinogen oxidase (PROTOOX). Addition of 10−6 M fomesafen to incubation mixture decreased PROTOOX from 1.02 nmol/mg/h (controls) to 0.42 nmol/mg/h. 10−5M of fomesafen decreased this activity to 0.27 nmol/mg/h.In in vivo experiments, 5 μ1 of fomesafen solution containing 0.2 M fomesafen/I was administered to male rats by intracerebroventricular injection. The content of brain mitochondrial cytochrome a3 was determined 72 hours later. A slight decrease of the a3 content was observed (control rats 0.25 nmol/mg protein, treated rats 0.22 nmol/mg). Brain cytochrome P450 activities were below detection limits in both control and treated groups.In a separate experiment, male ICR mice were fed 1000 ppm of the protoporphyrinogen oxidase‐inhibiting herbicide oxadiazon in the diet for 10 days. Liver microsomal cytochrome P450 content was decreased and liver porphyrins increased. An increase of porphyrin content was also observed in the testes of oxadiazon‐fed mice, but testicular cytochrome a3 content was unchanged. The results indicate that, contrary to liver microsomal cytochromes P450, the mitochondrial cytochromes are not susceptible to changes in heme biosynthesis.
The Human Obesity Gene Map: The 1996 Update
Authors: Pérusse Louis , Chagnon Yvon C. , Dionne France T. , Bouchard Claude 
Published: September 2012

AbstractAn update of the human obesity gene map up to October 1996 is presented. Evidence from Mendelian disorders exhibiting obesity as a clinical feature, single‐gene mutation rodent models, quantitative trait loci uncovered in crossbreeding experiments with mouse, rat, and pig models, association and case‐control studies with candidate genes, and linkage studies with genes and other markers is reviewed. All chromosomal locations of the animal loci are converted into human genome locations based on syntenic relationships between the genomes. A complete listing of all these loci reveals that only 4 of the 24 human chromosomes are not yet represented, i.e., 9, 18, 21, and Y. Several chromosome arms are characterized by the presence of several putative loci. The following arms include at least three such loci: 1p, 1q, 3p, 4q, 6p, 7q, 8p, 8q, 11p, 11q, 15q, 20q, and Xq. Studies with negative association and linkage results are also reviewed.
Gender Differences in the Response of Plasma Leptin Concentrations to Weight Loss in Obese Older Individuals
Authors: Nicklas Barbara J. , Katzel Leslie I. , Ryan Alice S. , Dennis Karen E. , Goldberg Andrew P. 
Published: September 2012

AbstractPlasma leptin concentration is directly related to the degree of obesity and is higher in women than in men of the same body mass index (BMI). We hypothesized that fasting plasma leptin concentrations and the response of leptin to weight loss would differ in older men and women of a similar fat mass. Plasma leptin concentrations (radioimmunoassay) and fat mass (DXA) were measured in 47 older, obese (BMI=30 ± 4 kg/m2) women and 23 older, obese (BMI=31 ± 3 kg/m2) men after a 2 to 4 week period of weight and dietary stabilization, and then in 22 of the women and 18 of the men after a 6‐month weight loss intervention (250–350 kcal/d deficit). Leptin correlated with fat mass in men and women (r=0.75 and r=0.77, respectively; p values<0.0001), but women had 3‐fold higher leptin levels for a given fat mass than men (p=0.01). In response to the 6‐month hypocaloric diet, men and women lost a similar percentage of fat mass (−13% and −16%, respectively), but the relative decline in circulating leptin was greater in women than men (‐45% and −21%, respectively; p<0.0001). In addition, when leptin was normalized for fat mass using the ratio method, the decrease in leptin per kilogram of fat mass was greater in women than men (‐0.37 ± 0.34 vs. −0.04 ± 0.06 ng/mL/kg; p<0.01).After weight loss, the change in leptin concentrations correlated positively with the change in fat mass in men (r=0.60; p<0.01), but not in women (r=0.31; p=0.17). Furthermore, the loss in fat mass correlated negatively with baseline leptin levels in women (r=‐0.47; p<0.05), but not in men (r=0.03, p=NS). These results indicate that the decline in leptin concentration with weight loss correlates with the loss in fat mass in men; but, in women, other factors affect the decrease in leptin concentration. This suggests that the role of leptin in the regulation of obesity is gender‐specific and may account for gender differences in response to hypocaloric treatment and maintenance of lost weight.
Relationships Between Changes in Body Composition and Changes in Cardiovascular Risk Factors: The SOS Intervention Study
Authors: Siöström C. David , Lissner Lauren , Siostrom Lars 
Published: September 2012

AbstractSJÖSTRÖM, C DAVID, LAUREN LISSNER, LARS SJÖSTROM. Relationships between changes in body composition and changes in cardiovascular risk factors: The SOS Intervention Study.Relationships between 2‐year changes in body composition (estimated from computed tomography‐validated anthropometry based on sagittal trunk diameter, weight, and height), adipose tissue (AT) distribution, and cardiovascular risk factors (blood pressure, lipids, glucose, insulin, uric acid) were examined in 842 treated adults with severe obesity with weight changes from −95. 5 to +30. 6 kg. Although the change (Δ) of visceral AT mass (expressed in % total AT) for a given change in body mass index (ΔBMI) was 6‐fold larger in men than in women, Δwaist and Δwaist/hip were similar in both sexes. In men, risk factor changes were similarly related to Awaist, Abodyweight, and ΔBMI, whereas in women, Δbodyweight seemed to be the single independent variable with the highest explanatory power. In multivariate regressions adjusted for ΔBMI and baseline conditions, Δvisceral AT mass was more strongly associated with risk factor changes than were Δwaist and ‡waist/hip. When using a three‐compartment model (lean body mass, subcutaneous and visceral AT masses) plus neck and thigh girths (indicators of subcutaneous AT distribution), risk factor changes were related both to ‡subcutaneous and ‡visceral AT masses but not to Δlean body mass. In agreement with cross‐sectional findings, Δneck was positively and Δthigh was negatively related to some risk factor changes. Thus, the use of waist as a single risk factor indicator seems less effective for epidemiological studies than the simple anthropometric measures presented here, which are able to separate the effects of visceral AT mass, subcutaneous AT mass, and subcutaneous AT distribution on metabolic parameters under both cross‐sectional and longitudinal conditions.
Feeding Response to Mercaptoacetate in Osborne‐Mendel and S5B/PL Rats
Authors: Singer Lori K. , York David A. , Bray George A. 
Published: September 2012

AbstractSINGER, LORI K, DAVID A YORK, GEORGE A BRAY. Feeding response to mercaptoacetate in Osborne‐Mendel and S5B/PL Rats.The purpose of this experiment was to determine if Osborne‐Mendel (OM) rats, which are susceptible to dietary‐induced obesity, and S5B/PL (S5B) rats, which are resistant to dietary‐induced obesity, differ in their feeding responses to mercaptoacetate (MA), which blocks fatty acid oxidation, or 2‐deoxy‐D‐glucose (2DG), which blocks glucose utilization. 2DG (100 mg/kg or 200 mg/ kg) increased food intake in both strains of rats on a high‐fat diet (56% energy from fat). Mercaptoacetate (600 umol/kg) increased food intake in OM but not S5B rats on a high‐fat diet. When maintained on a low‐fat diet (10% energy from fat), MA (400 umol/kg or 600 umol/kg) stimulated food intake in OM rats, whereas S5B rats increased food intake only after the highest dose of MA (600 umol/kg). MA stimulated carbohydrate and protein intake in OM rats maintained on a macro‐nutrient selection diet, whereas S5B rats maintained on this diet did not significantly increase intake of any mac‐ronutrient after MA. These results demonstrate that OM and S5B rats have a similar food intake response to 2DG but a dissimilar response to MA. The variable response to MA in these strains may be due to a difference in peripheral or central signaling systems related to fatty acid oxidation or a difference in metabolic environments between the strains, which in turn affects the feeding response to MA. These studies suggest that a difference in control of fatty acid oxidation may account for the difference in susceptibility to obesity when eating a high‐fat diet.
Effect of Aging on Norepinephrine and Phenylephrine Stimulated Lactate Production by White Adipocytes
Authors: Faintrenie G. , Géloën A. 
Published: September 2012

We have recently demonstrated that adipose tissue can produce lactate independently of lipolysis in insulin‐resistant rats and that lactate production depends on aj‐adrenergic stimulation. In this study, we have investigated the influence of aging on norepinephrine‐and‐phenylephrine‐stimulated lactate production and glycerol production. We showed that basal and norepinephrine stimulated lactate production were significantly increased in adipocytes isolated from old vs. young rats (0.165 ± 0.006 vs. 0.055 ± 0.008 for basal and 0.576 ± 0.026 vs. 0.277 ± 0.019 umol lactate/106 cell/15 minutes for norepinephrine‐stimulated lactate production, respectively, p<0.05). The sensitivity of lactate production to norepinephrine stimulation in adipocytes isolated from old rats was significantly decreased (EC50=523 ± 63.7 vs. 46.7 ± 6.34 nM, respectively, p><0.05). Maximal lactate production obtained with norepinephrine and phenylephrine was not significantly different in either group (0.576 ± 0.026 vs. 0.520 ± 0.036 in old and 0.277 ± 0.019 vs. 0.275 ± 0.017 umol/106 cell/15 minutes in young rats, respectively, ns). Lactate production by adipocytes isolated from old rats were significantly less sensitive to phenylephrine stimulation compared with young (EC50=3.67 ± 1.16 vs. 0.07 ± 0.01 nM, respectively, p<0.05) indicating that the effects of aging on norepinephrine and phenylephrine stimulation were probably induced by a decreased number of α1‐adrenoceptors.The mechanism by which aging increases adipocyte responsiveness of lactate production has not yet been elucidated.
Acute Administration of Phenylpropanolamine Fails to Affect Resting Energy Expenditure in Men of Normal Weight
Authors: Rushing Paul A. , Winders Suzan E. , Watson Sheree L. , Klesges Robert C. 
Published: September 2012

AbstractRUSHING, PA, SE WINDERS, SL WATSON, RC KLESGES. Acute administration of phenylpropanolamine fails to affect resting energy expenditure in men of normal weight.Studies have consistently found that dieters using over‐the‐counter weight control products containing phenylpropanolamine (PPA) are more successful at losing weight than those who do not. To explore the possibility that drug‐induced metabolic changes contribute to weight loss associated with this compound, this study investigated the effects of PPA on resting metabolic rate in 20 healthy men of normal weight between the ages of 18 and 29. After the arrival of the subjects to the laboratory, blood pressure was taken and resting energy expenditure (REE) and respiratory quotient (RQ) were assessed for 20 minutes (Baseline) via indirect calorimetry. Half of the subjects were then given 75 mg of immediate‐release PPA (administered orally via a gelatin capsule), while the other half received placebo. Immediately after drug administration, metabolic rate was measured for an additional 95 minutes (During Drug). After this assessment, blood pressure was again measured. Although significant increases in both systolic and diastolic blood pressure were observed after PPA administration, the drug had no effect on REE or RQ. These results, consistent with that previously reported in mildly overweight women, further establish that it is unlikely that drug‐induced metabolic changes contribute to PPA‐induced weight loss in humans.