Acosta, Andrés

AbstractObjectiveSatiety, defined as the duration of the sensation of fullness, is usually measured by validated visual analog scales (VAS) for appetite. Gastric function plays a key role in food intake regulation. However, the association between gastric emptying (GE) and VAS appetite is unknown.MethodsIn this cross‐sectional study, 134 participants (mean [SEM] age = 39 [0.8] years, mean [SEM] BMI = 38 [0.5] kg/m2, 67% females) completed simultaneous measurements of GE and VAS appetite. After a 320‐kcal meal, GE was measured by scintigraphy and appetite by validated 100‐mm VAS for 240 minutes. Satiation was defined as calories consumed to terminate meal and was measured by an ad libitum meal. GE, VAS, and ad libitum meal tests were measured on the same day. Percent of meal retention in the stomach, VAS area under curve (AUC0‐240 min), and overall appetite score (OAS) were calculated. Pearson correlation (ρ) determined the association of GE with VAS appetite and satiation. Appetite components were also analyzed by quartiles based on GE120 min.ResultsGE120 min was correlated with sensation of VAS hungerAUC(0‐240 min) (ρ = 0.24, p = 0.004), fullnessAUC(0‐240 min) (ρ = 0.16, p = 0.05), and OASAUC(0‐240 min) (ρ = 0.20, p = 0.02). Patients with rapid GE120 min had a mean increase in VAS hungerAUC(0‐240 min) by 32 mm/min (15.62%, p = 0.03) compared with normal/slow GE120 min.ConclusionsGE is associated with the sensations of appetite, and rapid GE is associated with increased appetite, which may contribute to weight gain.

AbstractWith the recent urbanization and globalization, the adult obesity rate has been increasing, which was paralleled with a dramatic surge in the incidence and prevalence of nonalcoholic fatty liver disease (NAFLD). NAFLD poses a growing threat to human health as it represents the most common cause of chronic liver disease in developed countries. It encompasses a wide spectrum of conditions starting from a build-up of fat in hepatocytes (steatosis), to developing inflammation (steatohepatitis), and reaching up to cirrhosis. It is also associated with higher rates of cardiovascular mortalities. Therefore, proper timely treatment is essential and weight loss remains the cornerstone in the treatment of obesity-related liver diseases. When diet, exercise, and lifestyle changes are not successful, the current recommendation for weight loss includes antiobesity medications and bariatric endoscopic and surgical interventions. These interventions have shown to result in significant weight loss and improve liver steatosis and fibrosis. In the current literature review, we highlight the expected outcomes and side effects of the currently existing options to have a weight-centric NAFLD approach.

Abstract Obesity is a multifactorial disease with a variable and underwhelming weight loss response to current treatment approaches. Precision medicine proposes a new paradigm to improve disease classification based on the premise of human heterogeneity, with the ultimate goal of maximizing treatment effectiveness, tolerability, and safety. Recent advances in high-throughput biochemical assays have contributed to the partial characterization of obesity's pathophysiology, as well as to the understanding of the role that intrinsic and environmental factors, and their interaction, play in its development and progression. These data have led to the development of biological markers that either are being or will be incorporated into strategies to develop personalized lines of treatment for obesity. There are currently many ongoing initiatives aimed at this; however, much needs to be resolved before precision obesity medicine becomes common practice. This review aims to provide a perspective on the currently available data of high-throughput technologies to treat obesity.

Sensory and motor functions of the stomach, including gastric emptying and accommodation, have significant effects on energy consumption and appetite. Obesity is characterized by energy imbalance; altered gastric functions, such as rapid gastric emptying and large fasting gastric volume in obesity, may result in increased food intake prior to reaching usual fullness and increased appetite. Thus, many different interventions for obesity, including different diets, anti-obesity medications, bariatric endoscopy, and surgery, alter gastric functions and gastrointestinal motility. In this review, we focus on the role of the gastric and intestinal functions in food intake, pathophysiology of obesity, and obesity management.

ObjectiveLittle is known about the predictors of response to obesity interventions.MethodsIn 450 participants with obesity, body composition, resting energy expenditure, satiety, satiation, eating behavior, affect, and physical activity were measured by validated studies and questionnaires. These variables were used to classify obesity phenotypes. Subsequently, in a 12‐month, pragmatic, real‐world trial performed in a weight management center, 312 patients were randomly assigned to phenotype‐guided treatment or non‐phenotype‐guided treatment with antiobesity medications: phentermine, phentermine/topiramate, bupropion/naltrexone, lorcaserin, and liraglutide. The primary outcome was weight loss at 12 months.ResultsFour phenotypes of obesity were identified in 383 of 450 participants (85%): hungry brain (abnormal satiation), emotional hunger (hedonic eating), hungry gut (abnormal satiety), and slow burn (decreased metabolic rate). In 15% of participants, no phenotype was identified. Two or more phenotypes were identified in 27% of patients. In the pragmatic clinical trial, the phenotype‐guided approach was associated with 1.75‐fold greater weight loss after 12 months with mean weight loss of 15.9% compared with 9.0% in the non‐phenotype‐guided group (difference −6.9% [95% CI −9.4% to −4.5%], P < 0.001), and the proportion of patients who lost >10% at 12 months was 79% in the phenotype‐guided group compared with 34% with non‐phenotype‐guided treatment group.ConclusionsBiological and behavioral phenotypes elucidate human obesity heterogeneity and can be targeted pharmacologically to enhance weight loss.

Abstract Background Spontaneous hyperinflation is reported to the Food and Drug Administration as a complication of intragastric balloons. It is postulated that orogastric contamination of the intragastric balloon may cause this phenomenon. We sought to investigate the effects of intentional balloon contamination with gastric contents on intragastric balloon diameter and contents, whether methylene blue plays a role in preventing spontaneous hyperinflation, and review the available literature on spontaneous hyperinflation. Methods Four pairs of balloons with different combinations of sterile saline, contaminants, and methylene blue were incubated in a 37° Celsius water bath for 6 months to simulate physiological conditions with serial measurements of balloon diameter. Our findings were compared against a systematic review across multiple databases to summarize the available literature. Results Balloon mean diameter decreased from 33.5 cm ± 0.53 cm to 28.5 cm ± 0.46 cm (p < 0.0001). No significant differences were seen with the methylene blue group. Only 11 cases were found reported in the literature. Conclusions Despite contaminating intragastric balloons with gastric aspirates, hyperinflation did not occur, and other factors may be in play to account for this phenomenon, when observed. Rates of hyperinflation remain under-reported in the literature. Further controlled experiments are needed.

Obesity is a chronic, multifactorial disease associated with a large number of comorbidities. The clinical management of obesity involves a stepwise integrated approach, beginning with behavioral and lifestyle modification, followed by antiobesity medications, endobariatric procedures, and bariatric surgery. Weight gain and subsequent obesity are common side effects of medications, such as prednisone or antipsychotics. In this era of precision medicine, it is essential to identify patients at the highest risk of weight gain as a result of medication use. Pharmacogenomics could play an important role in obesity management by optimizing use of antiobesity medications as well as minimizing adverse weight gain. This review aims to provide a comprehensive analysis of the current literature on the role of pharmacogenomics in obesity and medication‐induced weight gain. In summary, there are more robust studies of medication associated with weight gain and pharmacogenomics, and more studies are needed to understand the role of pharmacogenomics in antiobesity medications.

Buffet meal intake was inversely related to the ability to resist the urge to overeat. Factors associated with ingestive behavior significantly correlated with satiety and gastric accommodation. Gastric capacity during fasting is associated with calorie intake to the point of comfortable fullness; factors associated with ingestive behavior are associated with satiety and gastric accommodation.

AbstractBackgroundRapid gastric emptying, increased food intake, and alterations in gastrointestinal hormones are associated with obesity. The effect of regular physical activity (PA) on food intake, gastric emptying (GE), gastric accommodation, and gastrointestinal (GI) hormones in adults with obesity remains unclear. Our aim was to compare, at time of presentation, weight trends, eating behavior, GE, and GI hormone levels among individuals with obesity who engage in regular PA compared to those who do not.MethodsIn 270 participants with obesity, we performed validated measurements of GI phenotypes: GE of solids and liquids, gastric volume (GV) during fasting and after consumption of 200 mL Ensure®, satiety by kcal intake (T‐kcal) during a buffet meal, satiation (volume to fullness [VTF] and maximal tolerated volume [MTV]) of a liquid nutrient, and plasma levels of fasting and postprandial GLP‐1, PYY, CCK, and ghrelin. Physical Activity Stages of Change Questionnaire was used to assess whether participants were regularly PA or not.Key resultsPA was associated with lower BMI (Δ 2.01 kg/m2, P = .001) and body weight (Δ 4.42 kg, P = .0278). GE of solids (T‐50% Δ 7.54 min, P = .021) and liquids (T‐50% Δ 2.99 min, P = .029%) was significantly more rapid in physically active participants. PA was also associated with relatively higher postprandial ghrelin AUC (Δ 10.4 pg/mL, P = .015). There was no significant difference in postprandial satiation, satiety, GV, or other GI hormones (CCK, PYY, or GLP‐1) between groups.Conclusions & InferencesPhysical activity is associated with lower BMI, but faster GE and higher postprandial ghrelin levels, two factors that are also associated with obesity.

Abstract Purpose Obesity is associated with alterations in appetite, gastrointestinal hormone levels and excessive fat mass. We previously published a double-blind, placebo-controlled, randomized, 16-week trial on effects of once-daily glucagon-like peptide-1 (GLP-1) analog, liraglutide on weight, satiation, and gastric functions in obese volunteers. The aim of this substudy is to compare to placebo the effects of liraglutide on appetite, taste preference, regional body fat stores, and anthropometric measurements. Methods Forty obese adults received standard instruction for weight management, monthly behavioral intervention utilizing motivational interviews, and 16-week treatment of once-daily liraglutide (escalated to 3 mg SQ daily). At baseline and 16 weeks, the following were measured: appetite and taste preferences rated every 30 min for 5 h after ingesting 300 mL Ensure®; maximal tolerated volume (MTV) with a nutrient drink test; fasting and postprandial bioactive GLP-1 (7–36) and peptide YY (PYY) levels; total and regional body fat with dual-energy X-ray absorptiometry, and waist and hip circumference. Results Thirty-five participants (17 liraglutide; 18 placebo) completed the trial. Compared to placebo group, liraglutide group had significant reductions in MTV; prospective food consumption score; desire to eat something sweet, salty, savory or fatty; and an increase in perceived fullness. Postprandial plasma levels of GLP-1 decreased and PYY levels increased with liraglutide relative to baseline. Significant reductions in total body, trunk, and upper and lower body fat without reduction in lean body mass were observed. Conclusion Liraglutide 3 mg SQ modulates appetite, taste preference, gut hormones, and regional body fat stores in adults with obesity without reduction in lean body mass.