Dataset Information

Oxytocin Administration Increases Proactive Control in Men with Overweight or Obesity: A Randomized, Double-Blind, Placebo-Controlled Crossover Study.

ABSTRACT:

Objective

Preclinical and clinical evidence suggests that oxytocin administration decreases food intake and weight. The mechanisms underlying the anorexigenic effects of oxytocin in humans are unknown but critical to study to consider oxytocin as a neurohormonal weight loss treatment. Complementing ongoing research into metabolic and food motivation mechanisms of oxytocin, this study hypothesized that in humans, oxytocin improves cognitive control over behavior.

Methods

In a randomized, double-blind, placebo-controlled crossover study of 24-IU single-dose intranasal oxytocin, 10 men with overweight or obesity completed a stop-signal task assessing ability and strategy to suppress behavioral impulses, in which they performed a choice-reaction task (go task) but had to withhold their response when prompted (stop task). It was hypothesized that oxytocin would improve suppression of behavioral impulses.

Results

After receiving oxytocin, compared with placebo, participants showed increased reaction times in the go task (mean [M] = 936 milliseconds vs. 833 millseconds; P = 0.012; 95% CI: 29 to 178) and displayed fewer stop errors (M = 36.41% vs. 41.15%; P = 0.049; 95% CI: -9.43% to -0.03%).

Conclusions

Oxytocin triggers increased proactive control over behavior. Future studies need to further characterize the impact of oxytocin on cognitive control and investigate its potential role in the anorexigenic effects of oxytocin in human obesity.

SUBMITTER: Plessow F

PROVIDER: S-EPMC8695366 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Prader-Willi syndrome (PWS) is a rare, complex multisystem genetic disorder which includes hypothalamic dysfunction, hyperphagia, cognitive and behavioral problems, increased anxiety, and compulsive behaviors. Individuals with PWS have a deficit of oxytocin producing neurons in the paraventricular nucleus of the hypothalamus. Oxytocin plays a role in regulation of feeding behaviors, social interactions, and emotional reactivity, which are all issues that significantly affect the quality of life for individuals with this syndrome. We performed a double-blind, placebo-controlled, crossover study in 24 children with PWS at three academic institutions using 5 days of intranasal oxytocin (IN-OT) or 5 days of intranasal placebo spray, followed by a 4 week washout period, and then patients returned for 5 days of treatment with the alternate source. Questionnaires, including the Aberrant Behavior Checklist, Social Responsiveness Scale, Repetitive Behavior Scale - Revised, and the Hyperphagia Questionnaire, as well as Clinical Global Impression scales were administered. Blood testing for sodium, potassium, and glucose levels on days 2, 4, and 6, and a 24?hr diet recall. All scales factor improvement from Day 3 to Day 6 favored oxytocin over placebo. No single factor showed a statistically significant difference (P?<?0.05) between groups at Day 6. The drug effect appeared to be diminished at Day 14. There was no evidence of a difference between oxytocin and placebo in safety lab parameters, 60?min post dose vital signs, weight, or diet parameters. The results from this study suggest that low dose intranasal oxytocin is safe for individuals with PWS and may result in reduction in appetite drive, and improvements in socialization, anxiety, and repetitive behaviors. Further, long-term studies with a larger population of participants are necessary to confirm these findings. The results of this study are encouraging that oxytocin may be a safe and effective treatment for many of the issues that negatively impact individuals with PWS.

Project description:BackgroundPrior evidence suggests that capsinoids ingestion may increase resting energy expenditure (EE) and fat oxidation (FATox), yet whether they can modulate those parameters during exercise conditions remains poorly understood. We hypothesized that dihydrocapsiate (DHC) ingestion would increase EE and specifically FATox during an acute bout of aerobic exercise at FATmax intensity (the intensity that elicits maximal fat oxidation during exercise [MFO]) in men with overweight/obesity. Since FATmax and MFO during aerobic exercise appear to be indicators of metabolic flexibility, whether DHC has an impact on FATox in this type of population is of clinical interest.MethodsA total of 24 sedentary men (age = 40.2 ± 9.2 years-old; body mass index = 31.6 ± 4.5 kg/m2 [n = 11 overweight, n = 13 obese]) participated in this randomized, triple-blinded, placebo-controlled, crossover trial (registered under ClinicalTrials.gov Identifier no. NCT05156697). On the first day, participants underwent a submaximal exercise test on a cycle ergometer to determine their MFO and FATmax intensity during exercise. After 72 hours had elapsed, the participants returned on 2 further days (≥ 72 hours apart) and performed a 60 min steady-state exercise bout (i.e. cycling at their FATmax, constant intensity) after ingesting either 12 mg of DHC or placebo; these conditions were randomized. Respiratory gas exchange was monitored by indirect calorimetry. Serum marker concentrations (i.e. glucose, triglycerides, non-esterified fatty acids (NEFAs), skin temperature, thermal perception, heart rate, and perceived fatigue) were assessed.ResultsThere were no significant differences (P > 0.05) between DHC and placebo conditions in the EE and FATox during exercise. Similarly, no significant changes were observed in glucose, triglycerides, or NEFAs serum levels, neither in the skin temperature nor thermal perception across conditions. Heart rate and perceived fatigue did not differ between conditions.ConclusionsDHC supplementation does not affect energy metabolism during exercise in men with overweight/obesity.

Project description:BACKGROUND:Oxytocin (OXT), shown to decrease food intake in animal models and men, is a promising novel treatment for obesity. We have shown that in men with overweight and obesity, intranasal (IN) OXT reduced the functional magnetic resonance imaging (fMRI) blood oxygenation level-dependent signal in the ventral tegmental area (VTA), the origin of the mesolimbic dopaminergic reward system, in response to high-calorie food vs. nonfood images. Here, we employed functional connectivity fMRI analysis, which measures the synchrony in activation between neural systems in a context-dependent manner. We hypothesized that OXT would attenuate the functional connectivity of the VTA with key food motivation brain areas only when participants viewed high-calorie food stimuli. METHODS:This randomized, double-blind, and placebo-controlled crossover study of 24 IU IN OXT included ten men with overweight or obesity (mean?±?SEM BMI: 28.9?±?0.8?kg/m2). Following drug administration, subjects completed an fMRI food motivation paradigm including images of high and low-calorie foods, nonfood objects, and fixation stimuli. A psychophysiological interaction analysis was performed with the VTA as seed region. RESULTS:Following OXT administration, compared with placebo, participants exhibited significantly attenuated functional connectivity between the VTA and the insula, oral somatosensory cortex, amygdala, hippocampus, operculum, and middle temporal gyrus in response to viewing high-calorie foods (Z???3.1, cluster-corrected, p?<?0.05). There was no difference in functional connectivity between VTA and these brain areas when comparing OXT and placebo for low-calorie food, nonfood, and fixation images. CONCLUSION:In men with overweight and obesity, OXT attenuates the functional connectivity between the VTA and food motivation brain regions in response to high-calorie visual food images. These findings could partially explain the observed anorexigenic effect of OXT, providing insight into the mechanism through which OXT ameliorates food cue-induced reward anticipation in patients with obesity. Additional studies are ongoing to further delineate the anorexigenic effect of OXT in obesity.