Thinking about Eating Food Activates Visual Cortex with Reduced Bilateral Cerebellar Activation in Females with Anorexia Nervosa: An fMRI Study

Background: Women with anorexia nervosa (AN) have aberrant cognitions about food and altered activity in prefrontal cortical and somatosensory regions to food images. However, differential effects on the brain when thinking about eating food between healthy women and those with AN is unknown. Methods: Functional magnetic resonance imaging (fMRI) examined neural activation when 42 women thought about eating the food shown in images: 18 with AN (11 RAN, 7 BPAN) and 24 age-matched controls (HC). Results: Group contrasts between HC and AN revealed reduced activation in AN in the bilateral cerebellar vermis, and increased activation in the right visual cortex. Preliminary comparisons between AN subtypes and healthy controls suggest differences in cortical and limbic regions. Conclusions: These preliminary data suggest that thinking about eating food shown in images increases visual and prefrontal cortical neural responses in females with AN, which may underlie cognitive biases towards food stimuli and ruminations about controlling food intake. Future studies are needed to explicitly test how thinking about eating activates restraint cognitions, specifically in those with restricting vs. binge-purging AN subtypes

Differential activation of the frontal pole to high vs low calorie foods: The neural basis of food preference in Anorexia Nervosa?

Neuroimaging studies in anorexia nervosa (AN) suggest that altered food reward processing may result from dysfunction in both limbic reward and cortical control centers of the brain. This fMRI study aimed to index the neural correlates of food reward in a subsample of individuals with restrictive AN: twelve currently ill, fourteen recovered individuals and sixteen healthy controls. Participants were shown pictures of high and low-calorie foods and asked to evaluate how much they wanted to eat each one following a four hour fast. Whole-brain task-activated analysis was followed by psychophysiological interaction analysis (PPI) of the amygdala and caudate. In the AN group, we observed a differential pattern of activation in the lateral frontal pole: increasing following presentation of high-calorie stimuli and decreasing in during presentation of low-calorie food pictures, the opposite of which was seen in the healthy control (HC) group. In addition, decreased activation to food pictures was observed in somatosensory regions in the AN group. PPI analyses suggested hypo-connectivity in reward pathways, and between the caudate and both somatosensory and visual processing regions in the AN group. No significant between-group differences were observed between the recovered group and the currently ill and healthy controls in the PPI analysis. Taken together, these findings further our understanding of the neural processes which may underpin the avoidance of high-calorie foods in those with AN and might exacerbate the development of compulsive weight-loss behavior, despite emaciation

Comparative study of the effects of electrical stimulation in the nucleus accumbens, the mediodorsal thalamic nucleus and the bed nucleus of the stria terminalis in rats with schedule-induced polydipsia

In the schedule-induced polydipsia model, hungry rats receiving a food pellet every minute will display excessive drinking behaviour (compulsive behaviour). We aimed 1) to evaluate if electrical stimulation in the nucleus accumbens (N ACC), the mediodorsal thalamic nucleus (MD) or the bed nucleus of the stria terminalis (BST) can decrease water intake in the schedule-induced polydipsia model; 2) to compare water intake between these groups for different stimulation amplitudes; and 3) to compare the effect of low frequency (2 Hz) with high frequency (100 Hz) stimulation. Rats were randomly divided into four groups: electrode implanted in the 1) N ACC (n = 7), 2) MD (n = 8), 3) BST (n = 8), or 4) a sham-operated control group (n = 7). Postoperatively, each rat of group 1, 2 and 3 was randomly tested in the model using pulses with a frequency of 2 Hz and 100 Hz, each at an amplitude of 0.1, 0.2, 0.3, 0.4 and 0.5 mA, or without stimulation. Group 4 was tested 11 times without stimulation. Each day the rats were tested in random order. High-frequency electrical stimulation in all three brain areas decreased water intake significantly at an amplitude of 0.2 mA or higher, however, without differences between the brain areas. Based on these results, we expect a decrease in compulsions in patients suffering from treatment-resistant obsessive-compulsive disorder during electrical stimulation in the N ACC, the MD and the BST. However, we foresee no difference in energy consumption to decrease symptoms during electrical stimulation between these brain areas. (C) 2008 Elsevier B.V. All rights reserved

The Aspergillus niger D-xylulose kinase gene is co-expressed with genes encoding arabinan degrading enzymes, and is essential for growth on D-xylose and L-arabinose

The Aspergillus nigerd-xylulose kinase encoding gene has been cloned by complementation of a strain deficient in d-xylulose kinase activity. Expression of xkiA was observed in the presence of l-arabinose, l-arabitol and d-xylose. Expression of xkiA is not mediated by XLNR, the xylose-dependent positively-acting xylanolytic regulator. Although the expression of xkiA is subject to carbon catabolite repression, the wide domain regulator CREA is not directly involved. The A. nigerd-xylulose kinase was purified to homogeneity, and the molecular mass determined using electrospray ionization mass spectrometry agreed with the calculated molecular mass of 62816.6 Da. The activity of XKIA is highly specific for d-xylulose. Kinetic parameters were determined as Km(d-xylulose) = 0.76 mm and Km(ATP) = 0.061 mm. Increased transcript levels of the genes encoding arabinan and xylan degrading enzymes, observed in the xylulose kinase deficient strain, correlate with increased accumulation of l-arabitol and xylitol, respectively. This result supports the suggestion that l-arabitol may be the specific low molecular mass inducer of the genes involved in arabinan degradation. It also suggests a possible role for xylitol in the induction of xylanolytic genes. Conversely, overproduction of XKIA did not reduce the size of the intracellular arabitol and xylitol pools, and therefore had no effect on expression of genes encoding xylan and arabinan degrading enzymes nor on the activity of the enzymes of the catabolic pathway

The Aspergillus niger D-xylulose kinase gene is co-expressed with genes encoding arabinan degrading enzymes, and is essential for growth on D-xylose and L-arabinose

The Aspergillus nigerd-xylulose kinase encoding gene has been cloned by complementation of a strain deficient in d-xylulose kinase activity. Expression of xkiA was observed in the presence of l-arabinose, l-arabitol and d-xylose. Expression of xkiA is not mediated by XLNR, the xylose-dependent positively-acting xylanolytic regulator. Although the expression of xkiA is subject to carbon catabolite repression, the wide domain regulator CREA is not directly involved. The A. nigerd-xylulose kinase was purified to homogeneity, and the molecular mass determined using electrospray ionization mass spectrometry agreed with the calculated molecular mass of 62816.6 Da. The activity of XKIA is highly specific for d-xylulose. Kinetic parameters were determined as Km(d-xylulose) = 0.76 mm and Km(ATP) = 0.061 mm. Increased transcript levels of the genes encoding arabinan and xylan degrading enzymes, observed in the xylulose kinase deficient strain, correlate with increased accumulation of l-arabitol and xylitol, respectively. This result supports the suggestion that l-arabitol may be the specific low molecular mass inducer of the genes involved in arabinan degradation. It also suggests a possible role for xylitol in the induction of xylanolytic genes. Conversely, overproduction of XKIA did not reduce the size of the intracellular arabitol and xylitol pools, and therefore had no effect on expression of genes encoding xylan and arabinan degrading enzymes nor on the activity of the enzymes of the catabolic pathway