Entity

Time filter

Source Type

Amsterdam, NY, United States

Gallagher D.,Columbia University | Gallagher D.,New York Obesity Nutrition Research Center | DeLegge M.,Medical University of South Carolina
Journal of Parenteral and Enteral Nutrition | Year: 2011

The study of body composition is a rapidly evolving science. In today's environment, there is a great deal of interest in assessing body composition, especially in the obese subject, as a guide to clinical and nutrition interventions. There are some strikingly different compartments of body composition between the obese and the lean patient. We do have the ability to measure body composition accurately, although these techniques can be labor intensive and expensive. The recognition of patients with sarcopenic obesity has identified a potential high-risk patient population. These body composition abnormalities may have even greater importance in the intensive care patient. Copyright © 2011 American Society for Parenteral and Enteral Nutrition. Source


Gibson C.D.,New York Obesity Nutrition Research Center | Karmally W.,Columbia University | Mcmahon D.J.,Columbia University | Wardlaw S.L.,Columbia University | Korner J.,Columbia University
Diabetes, Obesity and Metabolism | Year: 2012

Aim: Dopaminergic hypofunction and hyperprolactinaemia have been implicated in the pathogenesis of obesity and glucose intolerance. The aim of this pilot study was to determine the efficacy of cabergoline, a dopamine receptor agonist, on body weight and glucose tolerance in obese non-diabetic persons with normal plasma prolactin levels. Methods: This 16-week double blind, placebo-controlled pilot study randomized non-diabetic obese adults (body mass index 30-42 kg/m2) to placebo or cabergoline (0.25 mg twice weekly for 4 weeks followed by 0.5 mg twice weekly for the next 12 weeks). Of 40 subjects enrolled, 29 completed 16 weeks: 16 randomized to placebo and 13 to cabergoline. All subjects were counselled on a 500 kcal/day calorie deficit diet. A 75-g oral glucose tolerance test was performed at baseline and at 16 weeks. Results: As expected, prolactin levels decreased after cabergoline (p < 0.001). Weight loss was similar after placebo compared with cabergoline treatment: 1.0 vs. 1.2% body weight, respectively. Fasting glucose levels did not differ between groups after treatment, however, 90-min postprandial glucose and insulin decreased in the cabergoline group only (p = 0.029). HOMA-IR (homeostasis model of assessment) increased by 40% after placebo and 1.5% after cabergoline treatment. Conclusions: This pilot study suggests that cabergoline therapy may improve glucose tolerance independent of weight loss, however, a larger, longer term study of dopamine receptor agonist therapy in obese individuals is warranted to confirm this finding. © 2011 Blackwell Publishing Ltd. Source


Geliebter A.,New York Obesity Nutrition Research Center | Geliebter A.,Columbia University | Geliebter A.,Touro College
Appetite | Year: 2013

Several neuroimaging studies are presented, which derive from prior work on gastric distension. Using a nonsurgical approach, we inserted gastric balloons into rats, which led to a marked decrease in food intake that normalized at 8 weeks. Body weight, however, remained below controls, which encouraged pursuit of studies in humans. A gastric balloon was inserted in obese and lean subjects, and filled through a tube that led behind the subject with water to 0, 200, 400, 600, 800 mL, on different days prior to ingestion of a liquid meal. As gastric volume increased, intake decreased by about 40%. Stomach capacity was then investigated using a gastric balloon, by assessing subjective (maximal tolerance) and objective measures (gastric compliance). Obese individuals had a much larger stomach capacity than lean by both measures. Next, in a 2-month study, an indwelling gastric balloon was inflated to 400 mL for 1 month and deflated for 1 month in counterbalanced order. Body weight was reduced during the month when the balloon was inflated within the 2nd and 3rd week. The subsequent study involved fMRI in response to gastric distension of 0, 250, and 500 mL while the subject was in a scanner. Ratings of fullness, but not discomfort, increased at 500 mL. Amygdala and insula activation were associated with gastric distension. The amygdala, as part of the limbic system, is involved in emotion and reward, and the insula in interoception. The right amygdala activation was inversely related to BMI, consistent with greater gastric capacity at a higher BMI. The next fMRI study in obese and lean subjects used visual and auditory stimuli of high energy dense (ED) and low ED foods. Increased activation was observed in the midbrain, putamen, posterior cingulate gyrus, hippocampus, and superior temporal gyrus in the obese vs. lean group in response to high vs. low ED food cues. Several of these areas lie within the mesolimbic reward pathway, and greater activation to high ED foods in the obese, suggests they have increased reward-driven eating behavior. Lastly, an fMRI study using the same stimuli was conducted pre and post-gastric bypass surgery. There were postsurgical reductions in neural activity in mesolimbic areas including the prefrontal cortex, and to a greater degree for high ED than low ED cues, reflecting more normalized responses. Through the use of various methodologies, the stomach's influence on food intake, sensations of fullness, and brain activation is presented with suggestions for future research. © 2013 Elsevier Ltd. All rights reserved. Source


Geliebter A.,New York Obesity Nutrition Research Center
Appetite | Year: 2013

Several neuroimaging studies are presented, which derive from prior work on gastric distension. Using a nonsurgical approach, we inserted gastric balloons into rats, which led to a marked decrease in food intake that normalized at 8 weeks. Body weight, however, remained below controls, which encouraged pursuit of studies in humans. A gastric balloon was inserted in obese and lean subjects, and filled through a tube that led behind the subject with water to 0, 200, 400, 600, 800 mL, on different days prior to ingestion of a liquid meal. As gastric volume increased, intake decreased by about 40%. Stomach capacity was then investigated using a gastric balloon, by assessing subjective (maximal tolerance) and objective measures (gastric compliance). Obese individuals had a much larger stomach capacity than lean by both measures. Next, in a 2-month study, an indwelling gastric balloon was inflated to 400 mL for 1 month and deflated for 1 month in counterbalanced order. Body weight was reduced during the month when the balloon was inflated within the 2nd and 3rd week. The subsequent study involved fMRI in response to gastric distension of 0, 250, and 500 mL while the subject was in a scanner. Ratings of fullness, but not discomfort, increased at 500 mL. Amygdala and insula activation were associated with gastric distension. The amygdala, as part of the limbic system, is involved in emotion and reward, and the insula in interoception. The right amygdala activation was inversely related to BMI, consistent with greater gastric capacity at a higher BMI. The next fMRI study in obese and lean subjects used visual and auditory stimuli of high energy dense (ED) and low ED foods. Increased activation was observed in the midbrain, putamen, posterior cingulate gyrus, hippocampus, and superior temporal gyrus in the obese vs. lean group in response to high vs. low ED food cues. Several of these areas lie within the mesolimbic reward pathway, and greater activation to high ED foods in the obese, suggests they have increased reward-driven eating behavior. Lastly, an fMRI study using the same stimuli was conducted pre and post-gastric bypass surgery. There were postsurgical reductions in neural activity in mesolimbic areas including the prefrontal cortex, and to a greater degree for high ED than low ED cues, reflecting more normalized responses. Through the use of various methodologies, the stomach's influence on food intake, sensations of fullness, and brain activation is presented with suggestions for future research. Copyright © 2013 Elsevier Ltd. All rights reserved. Source


O'Keeffe M.,New York Obesity Nutrition Research Center | St-Onge M.-P.,Columbia University
International Journal of Obesity | Year: 2013

Humans have an innate requirement for sleep that is intrinsically governed by circadian and endocrine systems. More recently, reduced sleep duration has gained significant attention for its possible contribution to metabolic dysfunction. Significant evidence suggests that reduced sleep duration may elevate the risk for impaired glucose functioning, insulin resistance and type 2 diabetes. However, to date, few studies have determined the implications of reduced sleep duration with regard to glucose control during pregnancy. With the high prevalence of overweight and obesity in women of reproductive age, the occurrence of gestational diabetes mellitus (GDM) is increasing. GDM results in elevated risk of maternal and fetal complications, as well as increased risk of type 2 diabetes postpartum. Infants born to women with GDM also carry a life-long risk of obesity and type 2 diabetes. The impact of reduced sleep on glucose management during pregnancy has not yet been fully assessed and a paucity of literature currently exits. Herein, we review the association between reduced sleep and impaired carbohydrate metabolism and propose how reduced sleep during pregnancy may result in further dysfunction of the carbohydrate axis. A particular focus will be given to sleep-disordered breathing, as well as GDM-complicated pregnancies. Putative mechanisms of action by which reduced sleep may adversely affect maternal and infant outcomes are also discussed. Finally, we will outline important research questions that need to be addressed. © 2013 Macmillan Publishers Limited. Source

Discover hidden collaborations