bluuebunny/crossref_metadata_2025 huggingface dataset:
The Social Self, Body Dissatisfaction, and Binge Eating in Obese Females
Authors: Grilo Carlos M. , Wiljley Denise E. , Jones Adele , Brownell Kelly D. , Rodin Judith
Published: September 2012

We examined the relationship of the social self to body dissatisfaction and to binge eating in two clinical samples of obese females. In the first study, with 32 nonbingeing obese females, social self measures of Public Self‐Consciousness and Social Anxiety were positively correlated with body dissatisfaction. Self‐esteem was negatively correlated with body dissatisfaction. In the second study, 11 obese binge eaters were compared with 11 matched nonbingeing obese females. Binge eaters were characterized by significantly higher levels of social anxiety and body dissatisfaction than the obese nonbingeing controls. These findings support the hypothesized links of social self concerns to body dissatisfaction and to binge eating in obese females.
Influence of Opioids in Hypothalamic Nuclei on Cold Thermogenesis of Lean and Obese LA/N‐cp Rats
Authors: Rodd Donald W. , Loomis Joseph L. , Farrell Peter A.
Published: September 2012

An overactive endogenous opioid peptide system (EOP) in the hypothalamus of the obese rats could contribute to a subnormal metabolic response to cold stress. Specific mu, delta, kappa opioid receptor antagonists and naloxone were infused into cannulaes aimed at the paraventricular nucleus (PVN) of awake freely moving obese (LA/N‐cp corpulent) and lean littermate rats. Metabolic responses were measured by indirect calorimetry during thermoneutrality (30°C) and at 10°C for 60 minutes each. When expressed relative to metabolic body size (kg−.75) obese rats had lower values (obese = 21.1 ± 1.9 vs. lean = 27.9 ± 2.7 ml·kg−.75.min, mean ± s.d., p<0.05) at 10°C during saline infusion. EOP antagonist infusions at 30°C had no effect on metabolic rate for either lean or obese animals. Mu (23.5 ± 3.4 ml·kg.‐75· min) and delta (23.0 ± 2.0) antagonism and naloxone (25.0 ± 2.3) significantly increased the metabolic response to cold in obese but not lean rats. These data suggest that certain subtypes of EOP receptors in or near PVN are overactive in obese rats. This overactive state may inappropriately inhibit the thermogenic response to cold stress in obesity.
Estimates of the Prevalence of Obesity in Canadian Children
Authors: Limbert Joanne , Crawford Susan M. , McCargar Linda J.
Published: September 2012

Childhood obesity is becoming a topic of great concern due to the rising prevalence of this condition in North America. Studies conducted in the United States have indicated that the prevalence of obesity has increased dramatically over the past few decades. The purpose of this study was to estimate the prevalence of obesity in Canadian children between the ages of 5 and 12 years by examining data from two national and two regional surveys. The 85th percentiles of each of four anthropometric indices derived from large normative populations were used as diagnostic criteria for obesity. As expected, the resulting prevalences varied according to the criteria used.

A significant increase in childhood obesity between the 1981 to 1988 national surveys was observed when the three indices which used skinfolds were applied. Weight‐for‐height percentiles did not indicate an increase in obesity in these samples. Regional samples showed a less than expected prevalence of obesity among the middle‐class children and a higher than expected rate among the inner city boys. It can be concluded that there is a need for a defined criteria for identifying obesity in children in order to avoid confusion resulting from the wide variation in estimates of prevalence resulting from different standards and measurements. Using adiposity‐based criteria for obesity it was clearly evident that the prevalence of obesity has increased in Canadian children.
Baseline Predictors of Success When Comparing Two Treatments
Authors: Roback Paul J. , Goldstein David J. , Rampey Alvin H. , Wilson Michael G.
Published: September 2012

Since few medications are equally effective in all patients, physicians can maximize the risk/benefit ratio of therapy for their patients by limiting exposure based on baseline predictors of success. Traditional procedures typically evaluate the response of patients receiving the same treatment regimen without evaluating a comparator. However, when treatments are compared, such as in clinical trials, traditional procedures of identifying predictors must be modified to analyze the treatment effect on the primary outcome variable. We focus on clinical and statistical considerations that arise when developing baseline predictors through models which consider treatment differences. To illustrate an application of this method, we used data from 1,026 patients completing at least 6 months of double‐blind therapy in clinical trials comparing fluoxetine (N=522) with placebo (N=504) for weight loss. Stepwise regression procedures were used to identify baseline variables which were predictive of a beneficial fluoxetine treatment effect on last‐visit‐carried‐forward (LVCF) weight change. In this example, age, smoking activity, and uric acid concentration were the best baseline predictors of long‐term treatment effect relative to LVCF weight change. Patients were more likely to achieve long‐term benefit with fluoxetine if they were older, and/or were nonsmokers, and/or had high concentrations of uric acid at baseline. These predictors, developed through models keying on treatment effect, can be used to identify patients who are more likely to accrue benefits with active therapy beyond those expected with placebo therapy, thus enriching the treatment population so that a higher proportion of treated patients are successful.
Metabolic Differences in Response to a High‐Fat vs. a High‐Carbohydrate Diet
Authors: Bandini Linda G. , Schoeller Dale A. , Dietz William H.
Published: September 2012

Energy expenditure was measured in a group of 7 subjects who received two isocaloric isonitrogenous diets for a period of 9–21 days with a 4–10‐day break between diets. Diet 1 was a high‐fat diet (83.5 ± 3.6% of total energy). Diet 2 was a high carbohydrate diet (83.1 ± 3.7% of total energy). Resting and postprandial resting metabolic rate were measured by open circuit indirect calorimetry 2–4 times during each metabolic period. Total energy expenditure (TEE) was measured by the doubly labeled water method over an 8–13‐day period. The respiratory quotient was measured 2–4 hours after a meal during each metabolic period for the calculation of total energy expenditure by the doubly labeled water method. Levels of total T3 (TT3), T3 uptake, free thyroid index and T4 were measured at the end of each metabolic period. No significant changes in resting metabolic rate (RMR) were apparent on the two diets (1567 ± 426 kcal/d high‐fat diet and 1503 ± 412 kcal/d high‐carbohydrate diet n=7, p<0.15). Total energy expenditure measured in 5 subjects was significantly higher during the high‐carbohydrate phase of the diet (2443 ± 422 vs. 2078 ± 482 kcal/d p<0.05). Activity estimated from TEE/RMR was greater on the high‐carbohydrate diet but only approached statistical significance (p<0.06). Total T3 was significantly lower and free thyroid index and T3 uptake were significantly higher at the end of the high fat diet in comparison to the high‐carbohydrate diet.

These data suggest that individual tolerance to a high‐fat diet varies considerably and may significantly lower TEE by changing levels of physical activity. The explanation for changes in thyroid hormone levels independent of changes in metabolic rate remains unclear.
The Male Obese Wistar Diabetic Fatty Rat Is a New Model of Extreme Insulin Resistance
Authors: Greene Stephanie F. , Johnson Patricia R. , Eiffert Kristin C. , Greenwood MRC , Stern Judith S.
Published: September 2012

The male obese Wistar Diabetic Fatty (WDF) rat is a genetic model of obesity and non‐insulin dependent diabetes (NIDDM). The obese Zucker rat shares the same gene for obesity on a different genetic background but is not diabetic. This study evaluated the degree of insulin resistance in both obese strains by examining the binding and post binding effects of muscle insulin receptors in obese, rats exhibiting hyperinsulinemia and/or hyperglycemia. Insulin receptor binding and affinity and tyrosine kinase activity were measured in skeletal muscle from male WDF fa/fa (obese) and Fa/? (lean) and Zucker fa/fa (obese) and Fa/Fa (homozygous lean) rats. Rats were fed a high sucrose (68% of total Kcal) or Purina stock diet for 14 weeks. At 27 weeks of age, adipose depots were removed for adipose cellularity analysis and the biceps femoris muscle was removed for measurement of insulin binding and insulin‐stimulated receptor kinase activity. Plasma glucose (13.9 vs. 8.4 mM) and insulin levels (14,754 vs. 7440 pmoI/L) were significantly higher in WDF obese than in Zucker obese rats. Insulin receptor number and affinity and TK activity were unaffected by diet. Insulin receptor number was significantly reduced in obese WDF rats (2.778 ± 0.617 pmol/mg protein), compared to obese Zucker rats (4.441 ± 0.913 pmol/mg potein). Both obese strains exhibited down regulation of the insulin receptor compared to their lean controls. Maximal tyrosine kinase (TK) activity was significantly reduced in obese WDF rats (505 ± 82 fmol/min/mg protein) compared to obese Zucker rats (1907 ± 610 fmol/min/mg protein). Only obese WDF rats displayed a decrease in TK activity per receptor. These observations establish the obese WDF rat as an excellent model for exploring mechanisms of extreme insulin resistance, particularly post‐receptor tyrosine kinase‐associated defects, in non‐insulin dependent diabetes.
Use of Glycated Hemoglobin to Assess Glycemic Control in Wistar Diabetic Fatty Rats and Zucker Fatty Rats
Authors: Albright Ann L. , Johnson Patricia R. , Greene Stephanie , Stern Judith S.
Published: September 2012

The Wistar Diabetic Fatty rat (WDF fafa) is a con‐genic strain of the Wistar Kyoto rat. Studies using blood glucose reveal that only fatty male (not female) WDF rats spontaneously develop hyperglycemia when fed a stock diet Blood glucose values have not provided consistent results for evaluation of glycemic status in fatty male WDF rats. Zucker fatty (fafa) rats, while sharing the fa gene and the development of hyperinsulinemia and hyperlipemia, do not spontaneously become hyperglycemic. In order to examine strain differences and the effects of age on long‐term average glycemic status in WDF and Zucker rats, glycated hemoglobin (GHb) was analyzed. Glycated hemoglobin was measured in male lean and obese WDF and Zucker rats at 2,3,6, and 12 months of age. Nonfasted plasma glucose was measured in male lean and obese WDF rats at 2, 3, 6, and 12 months of age and in lean and obese Zucker rats at 3, 6, and 12 months of age. Plasma insulin was measured in lean and obese WDF and Zucker rats at 3, 6, and 12 months of age. Obese WDF rats had significantly elevated GHb compared to lean controls at 3, 6, and 12 months of age. Glycated hemoglobin was substantially above the normal range (3.8‐6.5%) at 3 months of age (14.1%). Glycated hemoglobin significantly declined in the obese WDF rats between 6 and 12 months of age. Nonfasted plasma glucose was significantly elevated in the obese WDF rats at 3 months (14.1 ± 2.1 mM/L) and 6 months of age (16.2 ± 2.3 mM/L) compared to lean controls. At 12 months of age there was no difference in plasma glucose between obese and lean WDF rats. Obese and lean Zucker rats had similar levels of GHb and plasma glucose at all ages. In conclusion, GHb provides more integrated data for classifying disease status of WDF rats and evaluation of potential long‐term complications associated with hyperglycemia.
Chronic Calorie Restriction Alters Glycogen Metabolism in Rhesus Monkeys
Authors: Ortmeyer Heidi K. , Bodkin Noni L. , Hansen Barbara C.
Published: September 2012

Chronic caloric restriction (CR) prevents the development of obesity and maintains health, slows aging processes, and prevents or substantially delays the development of non‐insulin‐dependent diabetes. Because changes in energy metabolism could be involved in all of these positive effects of CR, we examined glycogen synthase (GS) and glycogen phosphorylase (GP) activities and glucose 6‐phosphate (G6P) and glycogen concentrations in skeletal muscle samples before and during a euglycemic hyperinsulinemic clamp in 6 older aged monkeys in which CR had been continued for 10.4 ± 2.1 years.

Basal GS activity (fractional velocity and independent) was significantly higher in the CR monkeys than has been previously shown in normal, hyperinsulinemic and diabetic monkeys. The normal effect of insulin to activate GS was absent in the CR group due to the paradoxical finding in some of these monkeys of a reduction in GS activity by insulin. Insulin also had the unexpected effect of increasing the independent activity of GP above basal activity (p<0.05). There was an inverse relationship between the change (insulin‐stimulated minus basal) in GS fractional velocity and GP activity ratio (r=‐0.91, p<0.005). The basal independent activities of GS and GP were also inversely correlated (r=‐0.79, p<0.05). The insulin‐stimulated concentration of G6P tended to be higher than the basal concentration (p<0.06) and was significantly higher than that previously shown in normal monkeys (p<0.05).

We suggest that long‐term calorie restriction (1) results in alterations in glycogen metabolism that may be important to the anti‐diabetogenic and anti‐aging effects of CR and (2) unmasks early defects which may indicate the likelihood of ultimately developing obesity and diabetes.
Higher Calorie Content Preserves Myocardial Electrical Activity During Very‐Low‐Calorie Dieting
Authors: Greenway Frank L. , Rauw William J. , Atkinson Richard L.
Published: September 2012

We investigated the effect of calorie and protein content of very‐low‐calorie diets for weight loss upon myocardial electrical activity. Patients were followed on very low calorie diets for up to 20 weeks. Study No. 1 had 16 obese patients (4 men and 12 women). Study No. 2 had 113 obese women. Both study groups were consecutive samples with patients who had BMI >30. In Study No. 1 patients were given 400 kcaVd with 50 gm of protein and 45 gm of carbohydrates over 12 weeks. In Study No. 2 patients were given either Metabolic Nutrition Program™ (MNP™) which contained 600 kcal/d with 70 gm protein and 70 gm carbohydrates, or Optifast‐70® which contained 420 kcaVd with 70 gm protein and 32 gm carbohydrates, for up to 20 weeks. Electrocardiograms were obtained at baseline and during the third month in Study No. 1, and monthly in Study No. 2. The sum of the voltage in leads I+II+III and the length of the QT interval were derived from the electrocardiograms. In Study No. 1 the QRS voltage decreased from 2.77 ± .18 mv to 2.45 ± .17 mv (p<.02). Patients lost 18.1 kg ± 4 kg and the QT interval remained unchanged. In Study No. 2 at 20 weeks the QRS voltage decreased on Optifast‐70® (p<001) in comparison to MNP™, in which the QRS voltage remained unchanged. Patients on Optifast‐70® lost 17.5 ± .53 kg, patients on MNP™ lost 18.5 ± .66 kg and the QT interval in both groups remained unchanged. The formula diets tested of less than 600 kcaVd were associated with a decrease in electrocardiographic voltage>.
Obesity in Minority Populations: An Epidemiologic Assessment
Authors: Kumunyika Shiriki K.
Published: September 2012

This article reviews issues relating to the prevalence, health implications, and prevention and treatment perspectives of obesity in U.S racial and ethnic minority groups. The growing interest in obesity in minority populations reflects an awareness of the high prevalence of obesity among black, Hispanic, Asian and Pacific Islander and Native Americans as well as a generally increased interest in minority health. In addition, the fact that some aspects of obesity among minorities differ from those in whites suggests that new insights may be gained from studying obesity in diverse populations. However, there are many methodological problems to be overcome, including some that arise from the way minority groups are defined. Under the assumption that all obesity results from a period of sustained positive energy balance at the individual level, an epidemiologic explanation for the excess of obesity in minorities at the population level seems readily apparent. A surplus of obesity‐promoting forces and a deficit of obesity‐inhibiting forces, caused by secular changes in food availability and physical activity, accompany the early phases of modernization and economic advancement. The high prevalence of obesity in minority populations can be viewed as a function of the slope and timing of these secular changes. Genetic predisposition, cultural attitudes, and exposure to maternal obesity and diabetes in utero may be potentiating factors. In this context, interventions targeting individuals would seem inevitably to put racial and ethnic minority groups on the path toward the same weight control crisis now observed in the majority white population. This suggests that the underlying causes of the societal energy balance problem must be addressed at the population level in order for effective clinical approaches to be developed for minority populations with a high obesity prevalence.
Obesity Research and Medical Journalism
Authors: Bray George A.
Published: September 2012

With publication of the first number of volume 3 of OBESITY RESEARCH, the time is ripe to review where we have been and where we are going. There are now two widely accepted journals covering the field of obesity. It was not always so. Until 20 years ago only one journal had appeared with the word “obesity” in its title, and its publication was short lived (Table 1). The growth of medical journalism in this field over the past 20 years, as in other fields, is a reflection of the growth of scientific manpower and knowledge which had its beginnings in the scientific revolution more than 300 years ago. The frustration engendered by this steady and rapid growth of scientific journals has been reflected in the quotations from many scholars. Below are a few of these.
Pregnancy Weight Retention in Morbid Obesity
Authors: Hunt Steven C. , Daines Maria Matthews , Adams TedD. , Heath EdwardM. , Williams Roger R.
Published: September 2012

HUNT, STEVEN C, MARIA M DAINES, TED D ADAMS, EDWARD M HEATH AND ROGER R WILLIAMS. Pregnancy weight retention in morbid obesity. Obes Res. 1995;3:121–130.

Recent hypotheses suggest that for women who develop morbid obesity, increases in weight associated with pregnancy may represent a significant contribution to their obesity status. The effects of multiple pregnancies on weight gain were studied in 96 morbidly obese women (<13.6 kg over ideal weight at ages 20–24 or before an earlier first pregnancy and currently >44.5 kg over ideal weight) and 115 random control women from the Utah population. Self‐reported weights for each pregnancy included: prepregnancy, greatest during pregnancy, and 6 weeks following delivery, which were validated against available hospital records. Mean number of pregnancies in each group were similar (4.2 and 4.3), ranging from 1 to 9. Mean current age was 46 and mean weight gain since ages 20–24 was 46.0 kg in the morbidly obese and 14.1 kg in controls. Regression of current weight on total number of pregnancies, adjusting for weight at ages 20–24, showed a 1.3 kg/pregnancy increase in current weight (p=0.03) with no difference between groups (p=0.6). Weight gain subsequent to the last pregnancy was not related to the number of pregnancies (p=0.2). Morbidly obese women gained more weight during pregnancy than controls only for the first pregnancy. Gains were similar for all other pregnancies. Morbidly obese women had smaller weight losses after delivery than the controls, but these differences were not significant. For the first pregnancy, morbidly obese women had a net weight retention that was 4.0 kg greater than the controls at 6 weeks post‐partum and an average of 1.6 kg/pregnancy greater retention for the remaining pregnancies. Pregnancy weight gains for each pregnancy subsequent to the first pregnancy were constant. These findings suggest: 1) women who develop morbid obesity have slightly less weight loss after delivery and greater between‐pregnancy weight gains than controls; 2) the number of pregnancies does not affect the amount of weight gained after the last pregnancy; and 3) while multiparity may augment weight gain in morbidly obese women, it is probably not a primary factor in the later development of morbid obesity.
Both Maternal Over‐ and Undernutrition During Gestation Increase the Adiposity of Young Adult Progeny in Rats
Authors: Fiorotto Marta L , Davis Teresa A. , Schoknecht Patricia , Mersmann Harry J. , Pond Wilson G.
Published: September 2012

FIOROTTO, MARTA L, TERESA A DAVIS, PATRICIA SCHOKNECHT, HARRY J MERSMANN AND WILSON G POND. Both maternal over‐ and undernutrition during gestation increase the adiposity of young adult progeny in rats. ObesRes. 1995;3:131–141.

We examined the influence of maternal diet during gestation on the growth and body composition of the progeny. On day 1 of gestation, rat dams were assigned to one of four feeding regimens: free access to standard rodent chow throughout gestation (AL); 20 g feed/day (prebreeding intake) throughout gestation (PB); 10 g feed/day from day 1 to day 14, then ad libitum from day 15 to parturition (RAL); 10 g feed/day from day 1 to 14, then 20 g/day to parturition (RPB). Progeny were fed ad libitum on standard chow diet from 3 to 12 weeks of age; food intake and weight gain were measured over this time. Body composition was measured at 12 weeks. The PB regimen restricted maternal food intake during the third trimester only; the RAL regimen restricted intake by 50% for two trimesters and produced hyperphagia in the third; the RPB regimen restricted intake by 50% for two trimesters, then intake (per unit body weight) was similar to that of AL dams during the third trimester. Litter size and progeny birth, weaning, and 12‐week body weights were similar among the four groups. At 12 weeks of age, PB progeny had the highest body fat (per kg fat‐free mass), despite similar feed intake during the 9‐week postweaning period. The increased fat was proportionally distributed among intra‐abdominal and subcutaneous depots. Progeny of RAL, AL, and RPB dams had similar amounts of body fat, but in RAL progeny more fat was present in intra‐abdominal depots. The weights of fat‐free mass, gastrointestinal tract and hindlimb skeletal muscles were unaffected by maternal diet Restriction of maternal feed intake during the third week of gestation had subtle effects on the body composition of young adult progeny that could not be explained on the basis of differences in postweaning voluntary feed intake.
Trafficking of Dietary Fat in Lean Rats
Authors: Bessesen Daniel H. , Rupp Connie L. , Eckel Robert H.
Published: September 2012

BESSESEN, DANIEL H, CONNIE L RUPP AND ROBERT H ECKEL. Trafficking of dietary fat in lean rats. Obes Res. 1995;3:191–203.

Despite increasing interest in the role that fuel partitioning plays in determining body composition, the relative importance of oxidative versus storage pathways in the clearance of dietary fat remains unclear. A widely held view is that the primary destination of chylomicron triglyceride fatty acids (TGFA) is adipose tissue, and the primary source of lipid fuel for skeletal muscle is non‐esterified fatty acids (NEFA). An alternate view is that muscle, not adipose tissue, is the primary site of TGFA clearance. This view is supported by estimates of the total lipoprotein lipase content of muscle and adipose tissue. To directly study the partitioning of dietary fat between oxidation and storage, 14C‐labeled oleic acid was fed to Sprague Dawley rats and its metabolic fate followed over 30 days. Two hours after ingestion, more than 3.5 times as much label was found in skeletal muscle tissue (2.42 ± 0.45 nmols) and CO2 (0.25 ± 0.01 nmols) than was found in adipose tissue (0.71 ± 0.14 nmols). Intramuscular triglyceride was the lipid class most extensively labeled. After skeletal muscle, liver was the next most important site of TGFA clearance. Surprisingly a substantial quantity of label remained associated with the GI tract even 24 hours after ingestion. Between 2 and 10 days following ingestion there was a net decline in the C content of muscle, liver and GI tract, associated with a net rise in the 14C content of adipose tissue. These findings demonstrate: 1) the importance of skeletal muscle and liver in whole organism TGFA clearance, 2) the importance of intramuscular partitioning of lipid fuels between direct oxidation and storage as TG, 3) the potentially important role of the GI tract in the delivery of dietary fat to the circulation 10–24 hours following ingestion, and 4) the stability of adipose tissue as a storage site. The complex nature of the tissue‐specific clearance of TGFA over time is perhaps better described by the term ‘trafficking’ than by the more commonly used term “partitioning.” Future studies of TGFA clearance combined with sampling of relevant tissues over time will provide insight into the specific roles that abnormalities in liver, muscle and adipose tissue TGFA metabolism play in the development of hypertriglyceridemic disorders and states of increased or reduced body weight.
Blockade of the Glucocorticoid Receptor with RU 486: Effects In Vitro and In Vivo on Human Adipose Tissue Lipoprotein Lipase Activity
Authors: Ottosson Malin , Mårin Per , Karason Kristjan , Elander Anna , Björntorp Per
Published: September 2012

Cortisol is known to induce lipoprotein lipase (LPL) activity in human adipose tissue in vitro and in vivo such as in Cushing's syndrome. The significance of the glucocorticoid receptor (GR) for this induction was evaluated in the present study. The synthetic steroid molecule RU 486, a potent glucocorticoid antagonist, was used as a tool to block the GR, in vitro and in vivo. In addition to LPL activity, glucose tolerance, blood pressure and plasma lipids, all variables influenced by Cortisol, were studied in order to evaluate the peripheral antiglucocorticoid activity of RU 486 in vivo, in man. Addition of both Cortisol and RU 486 to incubations of human adipose tissue pieces significantly inhibited the increase in LPL activity that could be induced by Cortisol alone (p<0.01). In a ten‐fold molarity excess RU 486 totally abolished Cortisol action (p<0.01). With Cortisol and RU 486 in equimolar concentrations the RU 486 blockade was probably incomplete and LPL activity induced (p<0.05). The results imply that the stimulating effect of Cortisol on LPL activity in human adipose tissue is mediated via the GR. Administration of 400 mg RU 486 at 2200 hours on two consecutive days to healthy men caused a significant rise in serum Cortisol levels measured at 0800 hours (p<0.05). The mean LPL activity in the subcutaneous abdominal adipose tissue remained unchanged. The mean level of serum triglycerides decreased significantly (p<0.01) and there was a negative correlation between change in LPL activity and change in triglyceride levels (r=‐0.73, p<0.05). Glucose tolerance and blood pressure were not affected. In conclusion, a total blockade of the GR with RU 486 can be achieved in human adipose tissue in vitro. The blockade abolishes the stimulating effect of Cortisol on LPL activity suggesting that the stimulation is GR dependent. In vivo, with the dose used, the negative pituitary feedback regulation probably compensates for the blockade, at least during the morning hours, thus obviating any peripheral effect of blockade of the GR.
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

Patients 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

XU, 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

There 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

Pharmacological 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.
Mechanism of Increase in Basal Lipolysis of Enlarged Adipocytes in Obese Animals
Authors: Tsujita Takahiro , Morimoto Chie , Okuda Hiromichi
Published: September 2012

Sonication of rat fat cells caused an increase in lipolysis in the absence of lipolytic hormones (basal lipolysis) and loss of epinephrine responsiveness. Sonication of endogenous lipid droplets from fat cells also induced an increase in lipolysis in the presence of HSL. Addition of phosphatidylcholine to the sonicated lipid droplets reduced the hydrolysis of triglyceride by HSL. These results suggest that the active HSL is already present in the fat cell even in the absence of lipolytic hormone, and phosphatidylcholine on the surface of endogenous lipid droplets causes inhibition toward lipolytic action of HSL. The decrease in the surface phosphatidylcholine concentration in endogenous lipid droplets was proved to cause the increase in basal lipolysis. It is demonstrated that basal lipolysis was elevated in the enlarged fat cells of obese rats by reduction of surface phosphatidylcholine concentration of the endogenous lipid droplets.
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.
Low Ambient Temperature and Neuroendocrine Response to Hypoglycemia in Men
Authors: Jeẑová Daniela , Juránková Elena , Kvetn̂anský Richard , Kaciuba‐Uscilko Hanna , Nazar Krystyna , Vigdŝ Milan
Published: September 2012

Nutritional factors, such as an excess or a deficiency of glucose, play an important role in neuroendocrine regulations. Hormonal and metabolic responses to hypoglycemia were examined in healthy non‐obese volunteers under conditions of low ambient temperature. Hypoglycemia was induced by intravenous injection of insulin in two randomized trials performed at room temperature and at 4°C. At room temperature, the typical neuroendocrine response to hypoglycemia was established. The increases of ACTH, β‐endorphin, growth hormone and Cortisol in response to insulin hypoglycemia failed to be modified by low ambient temperature. Acute cold exposure significantly reduced epinephrine and totally inhibited prolactin response to insulin‐induced hypoglycemia. In spite of significant changes in epinephrine response to hypoglycemia at low ambient temperature, no striking differences in plasma glucose levels compared to those measured at room temperature were observed. However, under conditions of low temperature the reestablishment of normoglycemia was delayed. No changes in free fatty acids were found under our experimental conditions. The presented data show that low ambient temperature exerts selective effects on some neuroendocrine and metabolic parameters.
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.
Histaminergic Control of Mucosal Repair in the Small Intestine
Authors: Fujimoto Kazuma , Gotoh Yudai , Ogata Shin‐Ichi , Tsunada Seiji , Ohyatna Takashi , Ootani Akifumi , Okamoto Kazuyo , Sakata Toshiie
Published: September 2012

The aim of the present paper was to summarize histamine‐mediated repair of rat intestinal mucosa. To evaluate intestinal repair, we examined lipid transport (an index of intestinal mucosal function) after 15 minutes occlusion of the superior mesenteric artery. Rats were pretreated with α‐fluoromethylhistidine (a suicide inhibitor of histidine decarboxylase, a synthesizing enzyme of histamine), H1‐receptor antagonist (chlorpheniramine maleate), H2‐antagonist (cimetidine), or H3‐antagonist (thioperamide) before ischemia‐reperfusion (I/R). Lipid transport to rat mesenteric lymph decreased significantly 24 hours after I/R in all groups tested compared to sham‐treated rats. Lipid transport was restored 48 hours after I/R in the vehicle‐pretreated control group. Lipid transport was not restored to the control level 48 hours after I/R in rats pretreated with H1‐antagonist and a suicide inhibitor of histidine decarboxylase. In contrast, intestinal function was restored to the control level 48 hours after I/R in rats pretreated with H2‐ and H3‐antagonists. These results support our previous findings that newly formed histamine after I/R plays an important role in mucosal recovery through H1‐receptors.
The Function of 5‐HT3 Receptors on Colonic Transit in Rats
Authors: Haga Keiichiro , Asano Kiyoshi , Fukuda Takemi , Kobayakawa Toshihiro
Published: September 2012

The function of serotonin (5‐HT)3 receptors on colonic transit was investigated in unanesthetized rats. The colonic transit was accelerated by 5‐HT (10 mg/kg, s.c.), 2‐methyl‐5‐HT (30 mg/kg, s.c.), neostigmine (0.03‐0.1 mg/kg, s.c.), corticotropin releasing factor (CRF; 1 μg intracerebroventricular administration) and restraint stress (for 45 minutes). A potent and selective 5‐HT3 receptor antagonist, aza‐setron {(±)‐N‐(1‐azabicyclo[2.2.2]oct‐3‐yl)‐6‐chloro‐4‐methyl‐3‐oxo‐3,4‐dihydro‐2H‐1,4‐benzoxazine‐8‐carboxamide monohydrochloride; 0.01–10 mg/kg, p.o.} inhibited the 5‐HT‐, CRF‐ and stress‐accelerated colonic transit in a dose‐dependent manner. Ondansetron (10 mg/kg, p.o.) and granisetron (1 mg/kg, p.o.) also inhibited the stress‐accelerated colonic transit, but azasetron was more effective than these two drugs. Atropine methylbromide (0.1 mg/kg, s.c.) and tetrodotoxin (0.01 mg/kg, s.c.) inhibited the accelerated colonic transit under stress conditions, but methysergide (10 mg/kg, s.c.), SDZ205‐557 (10 mg/kg, s.c.), domperidone (30 mg/kg, p.o.), trimebutine (300 mg/kg, p.o.), and metoclopramide (30 mg/kg, p.o.) did not. Azasetron (10 μg) administered intracerebroventricularly did not inhibit the stress‐induced acceleration. These results suggest that endogenous 5‐HT which is released through stress accelerates the colonic transit via the 5‐HT3 receptors and finally a cholinergic mechanism. It is considered that azasetron inhibits colonic transit particularly under stress conditions through the blockade of the peripheral 5‐HT3 receptors. Azasetron may improve bowel function in stress‐related colonic dysfunction like irritable bowel syndrome.
Weight Loss During 12 Weeks' Ad Libitum Carbohydrate‐Rich Diet in Overweight and Normal‐Weight Subjects at a Danish Work Site
Authors: Siggaard Regitze , Raben Anne , Astrup Arne
Published: September 2012

The effect of 12 weeks' ad libitum carbohydrate‐rich, low‐fat diet on total body weight, lean body mass, and fat mass was studied in a group of healthy subjects at a Danish work‐site (I) (n=50, BMI = 28.4 ± 0.7 kg/m2). Sixteen subjects served as controls (C) (BMI = 27.0 ± 1.0 kg/m2). After 12 weeks the I subjects had decreased their fat intake from 39.0 ± 1.1 energy‐% (E%) to 28.0 ± 1.2 E% and increased their carbohydrate intake from 46.0 ± 1.1 E% to 56.4 ± 1.1 E% (p < 0.05 vs. C). Moreover, a significant loss of body weight (4.2 ± 0.4 kg) and fat mass (4.4 ± 0.6 kg) was observed in I (p < 0.05 vs. C). The weight loss in I was not regained at 24 and 52 weeks' follow‐up (82% of I participating) compared to baseline. The cost per kg lost weight amounted to $14.7/person. In conclusion, instructions at a work site in ad libitum intake of a carbohydrate‐rich, low‐fat diet resulted in a significant loss of body weight and fat mass in overweight and normal‐weight subjects.