Attentional impulsivity in binge eating disorder modulates response inhibition performance and frontal brain networks.

BACKGROUND: A subgroup of overweight and obese people is characterized by binge eating disorder (BED). Increased impulsivity has been suggested to cause binge eating and subsequent weight gain. In the current study, neuronal correlates of increased impulsivity in binge eating disorder during behavioral response inhibition were investigated. METHODS: Magnetic brain activity and behavioral responses of 37 overweight and obese individuals with and without diagnosed BED were recorded while performing a food-related visual go-nogo task. Trait impulsivity was assessed with the Barratt Impulsiveness Scale (BIS-11). RESULTS: Specifically, increased attentional impulsiveness (a subscale of the BIS-11) in BED was related to decreased response inhibition performance and hypoactivity in the prefrontal control network, which was activated when response inhibition was required. Furthermore, participants with BED showed a trend for a food-specific inhibition performance decline. This was possibly related to the absence of a food-specific activity increase in the prefrontal control network in BED, as observed in the control group. In addition, an increase in activity related to the actual button press during prepotent responses and alterations in visual processing were observed. CONCLUSIONS: Our results suggest an attentional impulsiveness-related attenuation in response inhibition performance in individuals with BED. This might have been related to increased reward responsiveness and limited resources to activate the prefrontal control network involved in response inhibition. Our results substantiate the importance of neuronal markers for investigating prevention and treatment of obesity, especially in specific subgroups at risk such as BED.

Working memory-related brain activity is associated with outcome of lifestyle intervention.

OBJECTIVE: Lifestyle interventions including reduction of caloric intake are still the most pursued option to treat obesity. However, their outcome in terms of weight loss strongly differs between participants. In our study, we hypothesized that initial differences in brain activation in a food specific memory task are associated with weight change during a lifestyle intervention. DESIGN AND METHODS: Magnetic brain activity was recorded during a one-back visual memory task with food and nonfood pictures in 33 overweight and obese subjects before they underwent a lifestyle intervention. The intervention lasted 6 months and aimed for a reduction in daily caloric intake by 400 kcal. Body mass index (BMI) was determined before and after the intervention. RESULTS: Differences between outer tertiles representing people who increased their BMI by 1.4% ± 1.1% (non-responders) and who reduced their BMI by -6.9% ± 2.6% (responders) are reported. Neuronal activity was related to BMI change in sensor and source space. Non-responders showed higher activation in right inferior frontal and left occipital visual areas, whereas responders showed increased activation in right temporal areas including hippocampus and fusiform gyrus. CONCLUSIONS: Differences in the cerebral response during a food specific memory task indicate an altered cognitive control over food intake. These differences might determine the ability to eat less and successfully lose weight.

Nasal insulin changes peripheral insulin sensitivity simultaneously with altered activity in homeostatic and reward-related human brain regions.

AIMS/HYPOTHESIS: Impaired insulin sensitivity is a major factor leading to type 2 diabetes. Animal studies suggest that the brain is involved in the regulation of insulin sensitivity. We investigated whether insulin action in the human brain regulates peripheral insulin sensitivity and examined which brain areas are involved. METHODS: Insulin and placebo were given intranasally. Plasma glucose, insulin and C-peptide were measured in 103 participants at 0, 30 and 60 min. A subgroup (n = 12) was also studied with functional MRI, and blood sampling at 0, 30 and 120 min. For each time-point, the HOMA of insulin resistance (HOMA-IR) was calculated as an inverse estimate of peripheral insulin sensitivity. RESULTS: Plasma insulin increased and subsequently decreased. This excursion was accompanied by slightly decreased plasma glucose, resulting in an initially increased HOMA-IR. At 1 h after insulin spray, the HOMA-IR subsequently decreased and remained lower up to 120 min. An increase in hypothalamic activity was observed, which correlated with the increased HOMA-IR at 30 min post-spray. Activity in the putamen, right insula and orbitofrontal cortex correlated with the decreased HOMA-IR at 120 min post-spray. CONCLUSIONS/INTERPRETATION: Central insulin action in specific brain areas, including the hypothalamus, may time-dependently regulate peripheral insulin sensitivity. This introduces a potential novel mechanism for the regulation of peripheral insulin sensitivity and underlines the importance of cerebral insulin action for the whole organism.

High cerebral insulin sensitivity is associated with loss of body fat during lifestyle intervention.

AIMS/HYPOTHESIS: Loss of weight and body fat are major targets in lifestyle interventions to prevent diabetes. In the brain, insulin modulates eating behaviour and weight control, resulting in a negative energy balance. This study aimed to test whether cerebral insulin sensitivity facilitates reduction of body weight and body fat by lifestyle intervention in humans. METHODS: The study was performed as an additional arm of the TUebingen Lifestyle Intervention Program (TULIP). In 28 non-diabetic individuals (14 female/14 male; mean ± SE age 42 ± 2 years; mean ± SE BMI 29.9 ± 0.8 kg/m²), we measured cerebrocortical insulin sensitivity by using magnetoencephalography before lifestyle intervention. Total and visceral fat were measured by using MRI at baseline and after 9 months and 2 years of lifestyle intervention. RESULTS: Insulin-stimulated cerebrocortical theta activity at baseline correlated with a reduction in total adipose tissue (r = -0.59, p = 0.014) and visceral adipose tissue (r = -0.76, p = 0.001) after 9 months of lifestyle intervention, accompanied by a statistical trend for reduction in body weight change (r = -0.37, p = 0.069). Similar results were obtained after 2 years. CONCLUSIONS/INTERPRETATION: Our results suggest that high insulin sensitivity of the human brain facilitates loss of body weight and body fat during lifestyle intervention.