Journal of Nutrition Ingestive Behavior and Neurosciences

Iron-Deficiency Sensitizes Mice to Acute Pain Stimuli and Formalin-Induced Nociception [Ingestive Behavior and Neurosciences]

Dowling, P., Klinker, F., Amaya, F., Paulus, W., Liebetanz, D. — Tue, 20 Oct 2009 10:01:51 PDT

Iron deficiency has been described as a risk factor in secondary restless legs syndrome (RLS), although it has not been investigated whether iron deficiency induces sensory symptoms in RLS patients. In this study, we established a mouse model of iron deficiency by administering a purified iron-deficient (ID) diet (<8 mg/kg iron) or nonpurified standard diet [normal diet (ND)] (<179 mg/kg iron) to male C57Bl/6 mice from postnatal d 28 for 1, 4, or 15 wk. The level of iron deficiency was assessed by the plasma iron concentration. After varying durations of iron deficiency, both acute and chronic sensory components of pain were measured using hot-plate and formalin tests, which preferentially assess A- and C-fibers, respectively. Based on hot-plate reaction time, ID mice had a lower acute pain threshold than the ND mice after 4 and 15 wk but not after 1 wk. In addition, ID mice had an increased chronic pain response compared with the ND mice only in the late phase of the formalin-test after 1, 4, and 15 wk of iron deficiency. This increased pain response was accompanied by an elevated expression of c-Fos immunoreactive cells at the ipsilateral dorsal horn, suggesting that iron deficiency indirectly increases cell activity at the spinal cord level. These results demonstrate that iron deficiency increases acute and chronic pain responses in mice and may cause similar alterations to the acute pain threshold and sensitivity to C-fiber–mediated chronic pain in ID RLS patients.

Satiation Due to Equally Palatable Sweet and Savory Meals Does Not Differ in Normal Weight Young Adults [Ingestive Behavior and Neurosciences]

Griffioen-Roose, S., Mars, M., Finlayson, G., Blundell, J. E., de Graaf, C. — Tue, 20 Oct 2009 10:01:51 PDT

Sensory properties are greatly involved in the process of satiation. Regarding the nature of sensory signals, an important distinction can be made between sweet and savory taste. It is unclear, however, whether sweet and savory differ in their influence on satiation. Our objective was to investigate the difference between a sweet and savory taste on satiation, independent of palatability, texture, energy density, and macronutrient composition. A crossover design was used, consisting of 3 test conditions in which 2 tastes (sweet and savory) were compared. Sixty-four healthy, nonsmoking, unrestrained participants (18 males and 46 females), with a mean age of 22.3 ± 2.4 y and a mean BMI of 21.6 ± 1.7 kg/m², enrolled. Rice was used as a test meal served in either a sweet or savory version. The meals were similar in palatability, texture, energy density, and macronutrient composition. Ad libitum intake, eating rate, and changes in pleasantness and appetite during the meals were measured. Ad libitum intake did not differ between the 2 meals; participants ate a mean of 314 ± 144 g of the sweet meal and 333 ± 159 g of the savory meal. Eating rate (sweet, 38 ± 14 g/min; savory, 37 ± 14 g/min) and changes in pleasantness and appetite during the meals were similar. Homogeneous meals with a sweet or savory taste, similar in palatability, texture, energy density, and macronutrient composition, do not differ in their influence on satiation in normal weight young adults.

Green Tea (-)-Epigallocatechin-3-Gallate Inhibits {beta}-Amyloid-Induced Cognitive Dysfunction through Modification of Secretase Activity via Inhibition of ERK and NF-{kappa}B Pathways in Mice [Ingestive Behavior and Neurosciences]

Fri, 18 Sep 2009 10:01:30 PDT

Alzheimer's disease (AD) is characterized by the extracellular deposition of β-amyloid peptide (Aβ) in cerebral plaques. Aβ is derived from the β-amyloid precursor protein (APP) by the enzymes -, β- and -secretase. Compounds that enhance -secretase, but inhibit β- or -secretase activity, have therapeutic potential in the treatment of AD. Green tea, or its major polyphenolic compound, has been shown to have neuroprotective effects. In this study, we investigated the possible effects of (-)-epigallocatechin-3-gallate (EGCG) on memory dysfunction caused by Aβ through the change of Aβ-induced secretase activities. Mice were pretreated with EGCG (1.5 or 3 mg/kg body weight in drinking water) for 3 wk before intracerebroventricular administration of 0.5 µg Aβ_1–42. EGCG dose-dependently reduced the Aβ_1–42-induced memory dysfunction, which was evaluated using passive avoidance and water maze tests. Aβ_1–42 induced a decrease in brain -secretase and increases in both brain β- and -secretase activities, which were reduced by EGCG. In the cortex and the hippocampus, expression of the metabolic products of the β- and -secretases from APP, C99, and Aβ also were dose-dependently suppressed by EGCG. Paralleled with the suppression of β- and -secretases by EGCG, we found that EGCG inhibited the activation of extracellular signal-regulated kinase and nuclear transcription factor-B in the Aβ_1–42-injected mouse brains. In addition, EGCG inhibited Aβ_1–42-induced apoptotic neuronal cell death in the brain. To further test the ability of EGCG to affect memory, EGCG (3 mg/kg body weight) was administered in drinking water for 1 wk to genetically developed preseniline 2 (PS2) mutant AD mice. Compared with untreated mutant PS2 AD mice, treatment with EGCG enhanced memory function and brain -secretase activity but reduced brain β- and -secretase activities as well as Aβ levels. Moreover, EGCG inhibited the fibrillization of Aβ in vitro with a half maximal inhibitory concentration of 7.5 mg/L. These studies suggest that EGCG may be a beneficial agent in the prevention of development or progression of AD.

Undernourished Children Have Different Temperaments Than Better-Nourished Children in Rural Bangladesh [Ingestive Behavior and Neurosciences]

Baker-Henningham, H., Hamadani, J. D., Huda, S. N., Grantham-McGregor, S. M. — Thu, 20 Aug 2009 10:02:31 PDT

Undernutrition in early childhood is associated with poor cognitive development and some changes in behavior. However, there is little information on their temperament. Our objective in this study was to determine whether undernourished children aged 6–24 mo had different temperament traits than better-nourished children. Two hundred and twelve undernourished children (weight for age < –2 Z-scores) attending community nutrition centers in 20 villages in rural Bangladesh and 108 better-nourished children (weight-for-age ≥ –2 Z-scores) matched for age, sex, and village participated in the study. Temperament was assessed through an interviewer-administered maternal questionnaire consisting of 7 subscales: manageability, activity, emotionality, sociability, attention, soothability, and fear. After adjusting for significant covariates, the undernourished children were less sociable [regression coefficient (B) = –0.96; 95% CI = –0.04, –1.88], less attentive (B = –0.94; 95% CI = –0.19, –1.69), more fearful (B = 1.43; 95% CI = 2.44, 0.42), and had more negative emotionality (B = –1.08; 95% CI = 0.006, –2.16). In conclusion, these undernourished children had comprehensive differences in temperament traits, which may increase their risk of developing behavioral and mental health problems in later childhood.