OBJECTIVE: A new measure of body image, named the body image assessment for obesity (BIA-O) was developed and tested for reliability and validity in a sample of 1209 adult men and women. Separate BIA-O procedures were developed for men and women. Current, ideal and reasonable body image estimates of Caucasian and AfricanAmerican men and women were compared. METHOD: Figural stimuli of males and females were developed for body sizes ranging from very thin to very obese in 18 increments. Participants selected ®gures that represented estimates of current, ideal and reasonable (a body size that could be maintained over time) body size. Some participants (n 641) also completed two measures of body dissatisfaction in a test of the validity of the BIA-O as a measure of body dissatisfaction. A sample of 77 participants was administered the BIA-O on two occasions to test the test ± retest reliability of the BIA-O. RESULTS: The reliability of the BIA-O was supported by test ± retest reliability coef®cients which ranged from 0.65 to 0.93. Concurrent validity of the discrepancy between current and ideal and current and reasonable body size estimates was supported by positive correlations with two measures of body dissatisfaction. The BIA-O body size estimates of Caucasians and African-Americans, controlled for age and BMI, were compared. As BMI increased, Caucasian men and women were found to select larger current body size estimates in comparison to African-Americans. DISCUSSION: The reliability and validity of the BIA-O were supported. Greater body size dissatisfaction in obese Caucasians, relative to African-Americans of the same size, may be a function of biased estimates of current body size.

Cholecystokinin (CCK) decreases meal size through activation of CCK-A receptors on vagal afferents. We tested the hypothesis that the selective CCK-A agonist GI181771X induces weight loss in obese patients. Patients with body mass index > or = 30 or > or = 27 kg/m2 with concomitant risk factors were randomized to 24-week, double-blind treatment with different GI181771X doses or matching placebo together with a hypocaloric diet. The primary efficacy end point was the absolute change in body weight. To monitor pancreatic and gallbladder effects, patients underwent abdominal ultrasound and magnetic resonance imaging before and after treatment. We randomized 701 patients to double-blind treatment. GI181771X did not reduce body weight and had no effect on waist circumference or other cardiometabolic risk markers. Gastrointestinal side effects were more common with GI181771X than with placebo treatment, whereas hepatobiliary or pancreatic abnormalities did not occur. CCK-A by itself does not have a central role in long-term energy balance.

Objective: To compare changes in weight in obese patients who received long-acting octreotide (octreotide LAR) at one of three dose levels (20, 40, or 60 mg) or placebo over 6 months and to identify the lowest dose of octreotide LAR that safely achieved optimal weight loss. Design: Randomized, double-blind, placebo-controlled trial of octreotide LAR at three dose levels. Patients: A total of 172 adults (28 men and 144 women) with at least moderate obesity (body mass index (BMI) range 30-65 kg/m 2 ) and evidence of insulin hypersecretion were enrolled. Patients were predominantly either Caucasian (50.0%) or African American (45.3%). The mean age (38711 year), weight (110.7723 kg), and BMI (39.876.5 kg/m 2 ) were similar across the four treatment groups. Measurements: Efficacy measures included weight, BMI, fasting serum glucose; triglycerides; percentage of total body fat and abdominal fat as measured by dual-energy X-ray absorptiometry; skin fold thickness; waist-to-hip circumference; leptin; percentage of carbohydrates, fat, and protein ingested; nutritional evaluation (including dietary analysis -3-day food record); quality of life (QoL; using the Impact of Weight on Quality of Life-Litet); Beck Depression Inventory; and Carbohydrate Craving Questionnaire. Safety measures included medical history, vital signs, physical examinations, hematology, blood chemistries, thyroid function tests, hemoglobin A1c, gallbladder ultrasound, electrocardiograms, and adverse events. Results: After 6 months of treatment, patients receiving 40 or 60 mg of octreotide LAR experienced statistically significant weight loss compared to baseline, with mean differences from placebo in percent weight change of À1.98 and À1.87%, respectively. This finding was accompanied by statistically significant mean decreases in BMI compared to baseline, that is, a mean decrease of 0.73 and 0.79 kg/m 2 for the 40 and 60 mg treatment arms, respectively. The observed weight loss was progressive during the 6-month treatment in the two higher dose groups. The lowest dose to reach statistical significance in weight loss after 6 months' treatment was 40 mg. Post hoc analysis revealed a 3.5-3.8% weight loss at month 6 in the two higher dose groups among Caucasian patients having insulin secretion greater than the median of the cohort, defined as CIR gp (corrected insulin response at the glucose peak) X1.43. There were no statistically significant changes in QoL scores, body fat, leptin concentration, Beck Depression Inventory, or macronutrient intake. Mean changes of blood glucose AUC 0-180 min during an oral glucose tolerance test in patients taking octreotide LAR were 39-40 mg/dl h higher than those on placebo. A total of 7-21% of the patients taking octreotide LAR reached a 5% or greater decrease in body weight from Baseline, compared to 11% for the placebo group. This was not statistically significant. The most common adverse events included diarrhea, headache, cholelithiasis, nausea, and abdominal pain. Conclusion: Octreotide LAR given at 40 or 60 mg r...

Oatmeal improves appetite control and increases satiety. The effects may be attributed to the viscosity and hydration properties of its β-glucan content.

The objective of this study was to identify mechanisms through which valproic acid (VPA) causes weight gain. Healthy participants (N = 52) were randomized to VPA or placebo in a double-blind study. Energy intake (EI) was measured in the laboratory at lunch and dinner, and physical activity (PA) was measured with accelerometry. Glucose levels and hormones [Peptide YY(3-36), glucagon-like peptide-1 (GLP-1), leptin, ghrelin, insulin] that regulate EI were measured. Assessments occurred at baseline and week 3. Change from baseline was evaluated with mixed models (alpha = 0.05). Weight significantly increased in the VPA group (+0.49 kg), but not the placebo group. The VPA group increased fast food fats cravings and decreased glucose levels compared with placebo. Change in weight, EI and PA did not differ by group. Within group analyses indicated that the VPA group increased PA, hunger, binge eating, depression and GLP-1. VPA-associated weight gain is not likely due to changes in PA or the gut hormones studied. Although EI did not increase when measured after 3 weeks of treatment, VPA decreased glucose levels and increased motivation to eat; hence, EI might have increased in the short-term. Research testing VPA on short-term (1 week) EI, metabolism, and substrate partitioning is warranted.

OBJECTIVE: To determine the relationship between two common apoA-IV variants (Thr 347 ?Ser; Gln 360 ?His), and body mass index (BMI) and percentage body fat. DESIGN: Cross-sectional study. SUBJECTS: Eight-hundred and forty-eight subjects screened for participation in ongoing clinical studies. MEASUREMENTS: ApoA-IV genotype, body mass index, waist-to-hip ratio and percentage body fat by bioelectric impedance. RESULTS: Participants had an average age of 41 AE 12 y and an average BMI of 28.2 AE 5.5 kgam 2 . Individuals homozygous for the Ser 347 allele had higher BMI (32.3 AE 6.6 vs 28.6 AE 5.3 kgam 2 ; P`0.01) and percentage body fat (36.9 AE 7.8 vs 31.0 AE 9.6%; P`0.05) compared with individuals homozygous for Thr 347 . In contrast, the presence of at least one copy of the His 360 allele was associated with lower BMI (27.2 AE 5.0 vs 28.4 AE 5.6 kgam 2 ; P`0.05) and percentage body fat (28.6 AE 8.2 vs 30.7 AE 9.1%; P`0.05). The genotype effects persisted after normalization of the data for the potential confounding effects of gender, age and race. When grouped by BMI percentile, the frequency of the Ser 347 aSer 347 genotype increased while the frequency of the His 360 allele decreased with increasing BMI. CONCLUSIONS: These data suggest a role for apoA-IV in fat storage or mobilization and that genetic variations in the apoA-IV gene may play a role in the development of obesity.

The metabolic controls of eating are embedded in a neural system that permits an interaction with the environment. The result is an integrated adaptive response that coordinates the internal milieu with the prevailing environment. Securing adequate amounts of fat and optimizing its storage and use has an evolutionary basis. By generating neuronal and endocrine feedback signals, behavior and metabolism could then adapt to fluctuations in food availability. However, in modern society, foods that appeal to the palate are neither in shortage nor are they difficult to procure. These foods can activate brain reward circuitry beyond their evolved 'survival advantage' limits. Many foods high in fat invoke an undeniably pleasurable sensation and could excessively stimulate the brain's reward pathways leading to overeating. However, the high appeal and potential for being eaten in excess notwithstanding, fat has the added distinction of inducing powerful signals in the gut that are transduced to the brain and result in the regulation of appetite. Fatty acids are sensed by G-protein-coupled receptors on enteroendocrine cells which trigger the release of peptides involved in appetite regulation. Lipid sensing may also occur through the fatty acid translocase, CD-36, on enterocytes. Additionally, fat can activate dopaminergic systems affecting reward, to promote an inhibition over eating. Prolonging the presence of fats in the gastrointestinal lumen permits the activation of signaling mechanisms. Thylakoids, found within the chloroplasts of plants, are flattened disc-like membranous vesicles in which the light-dependent reactions of photosynthesis occur. By interacting with lipids and delaying fat digestion, thylakoid membranes promote the release of peptides involved in appetite regulation and may influence the reward system. This review explores gut lipid sensing and signaling in the context of appetite regulation. The effects of thylakoid membranes on eating behavior are also reviewed.