Insulin sensitivity and brain reward activation in overweight Hispanic girls: a pilot study

Abstract

Background: Insulin resistance is a link between obesity and the associated disease risk. In addition to its role as an energy regulatory signal to the hypothalamus, insulin also modulates food reward.

Objective: To examine the relationship of insulin sensitivity (SI) and fasting insulin with cerebral activation in response to food and non-food cues in children.

Methods: Twelve overweight Hispanic girls (age: 8-11) participated in two study visits, a frequently sampled intravenous glucose tolerance test and a functional neuroimaging session (GE HDxt 3.0Tesla) with visual stimulation tasks. Blocks of images (high calorie [HC], low calorie [LC] and non-food [NF]) were presented in randomized order.

Results: Comparing HC with NF, SI was inversely associated with activation in the anterior cingulate (r(2) = 0.65; P < 0.05), the insula (r(2) = 0.69; P < 0.05), the orbitofrontal cortex (r(2) = 0.74; P < 0.05), and the frontal and rolandic operculum (r(2) = 0.76; P < 0.001). Associations remained significant after adjustment for body mass index. Association of fasting insulin and cerebral activation disappeared after adjustment for waist circumference.

Conclusion: In addition to weight loss, insulin sensitivity may pose an important target to regulate neural responses to food cues in the prevention of excessive weight gain.

Keywords: Brain reward; childhood obesity; functional imaging; insulin sensitivity.

Figure 1

A, B Association of insulin sensitivity (SI), insula activation (parameter estimates, PE) (Figure 1A: r² = 0.69; p < 0.005) and left anterior cingulate activation (Figure 1B: r² = 0.65; p < 0.005), contrasting cerebral activation in response to high calorie visual stimuli > non-food visual stimuli.

Figure 1

A, B Association of insulin sensitivity (SI), insula activation (parameter estimates, PE) (Figure 1A: r² = 0.69; p < 0.005) and left anterior cingulate activation (Figure 1B: r² = 0.65; p < 0.005), contrasting cerebral activation in response to high calorie visual stimuli > non-food visual stimuli.

Figure 2

A, B Association of insulin sensitivity (SI), putamen activation (parameter estimates, PE) (Figure 2A: r² = 0.74; p < 0.005) and insula activation (Figure 2B: r² = 0.66; p < 0.005), contrasting cerebral activation in response to high calorie visual stimuli > low calorie visual stimuli.

Figure 2

A, B Association of insulin sensitivity (SI), putamen activation (parameter estimates, PE) (Figure 2A: r² = 0.74; p < 0.005) and insula activation (Figure 2B: r² = 0.66; p < 0.005), contrasting cerebral activation in response to high calorie visual stimuli > low calorie visual stimuli.

Figure 3

A, B Association of fasting insulin concentrations, caudate activation (parameter estimates, PE) (Figure 3A: r² = 0.70; p < 0.005) and insula activation (Figure 3B: r² = 0.69; p < 0.005), contrasting cerebral activation in response to high calorie visual stimuli > non-food visual stimuli.

Figure 3

A, B Association of fasting insulin concentrations, caudate activation (parameter estimates, PE) (Figure 3A: r² = 0.70; p < 0.005) and insula activation (Figure 3B: r² = 0.69; p < 0.005), contrasting cerebral activation in response to high calorie visual stimuli > non-food visual stimuli.