Gastrointestinal-projecting neurones in the dorsal motor nucleus of the vagus exhibit direct and viscerotopically organized sensitivity to orexin

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65136/1/jphysiol.2002.029546.pd

Family time, parental behaviour model and the initiation of smoking and alcohol use by ten-year-old children: an epidemiological study in Kaunas, Lithuania

BACKGROUND: Family is considered to be the first and the most important child development and socialization bond. Nevertheless, parental behaviour model importance for the children, as well as family time for shared activity amount influence upon the child's health-related behaviour habit development has not been yet thoroughly examined. The aim of this paper is to indicate the advanced health-hazardous behaviour modelling possibilities in the families, as well as time spent for joint family activities, and to examine the importance of time spent for joint family activities for the smoking and alcohol use habit initiation among children. METHODS: This research was carried out in Kaunas, Lithuania, during the school year 2004–2005. The research population consisted of 369 fifth-grade schoolchildren (211 (57.2%) boys and 158 (42.8%) girls) and 565 parents: 323 (57.2%) mothers and 242 (48.2%) fathers. The response rate was 80.7% for children; 96.1% and 90.6% for mothers and fathers correspondingly. RESULTS: Eating a meal together was the most frequent joint family activity, whereas visiting friends or relatives together, going for a walk, or playing sports were the most infrequent joint family activities. More than two thirds (81.5%) of parents (248 (77.0%) mothers and 207 (85.9%) fathers (p < 0.05)) reported frequenting alcohol furnished parties at least once a month. About half of the surveyed fathers (50.6%) together with one fifth of the mothers (19.9%) (p < 0.001) were smokers. More frequently than girls, boys reported having tried smoking (6.6% and 23.0% respectively; p < 0.001) as well as alcohol (31.16% and 40.1% respectively; p < 0.05). Child alcohol use was associated both with paternal alcohol use, and with the time, spent in joint family activities. For instance, boys were more prone to try alcohol, if their fathers frequented alcohol furnished parties, whereas girls were more prone to try alcohol, if family members spent less time together. CONCLUSION: Joint family activity time deficit together with frequent parental examples of smoking and alcohol use underlie the development of alcohol and smoking addictions in children to some extent. The above-mentioned issues are suggested to be widely addressed in the comprehensive family health education programs

Sex differences in basal hypothalamic anorectic and orexigenic gene expression and the effect of quantitative and qualitative food restriction

Abstract Background Research into energy balance and growth has infrequently considered genetic sex, yet there is sexual dimorphism for growth across the animal kingdom. We test the hypothesis that in the chicken, there is a sex difference in arcuate nucleus neuropeptide gene expression, since previous research indicates hypothalamic AGRP expression is correlated with growth potential and that males grow faster than females. Because growth has been heavily selected in some chicken lines, food restriction is necessary to improve reproductive performance and welfare, but this increases hunger. Dietary dilution has been proposed to ameliorate this undesirable effect. We aimed to distinguish the effects of gut fullness from nutritional feedback on hypothalamic gene expression and its interaction with sex. Methods Twelve-week-old male and female fast-growing chickens were either released from restriction and fed ad libitum or a restricted diet plus 15% w/w ispaghula husk, a non-nutritive bulking agent, for 2 days. A control group remained on quantitative restriction. Hypothalamic arcuate nucleus neuropeptides were measured using real-time PCR. To confirm observed sex differences, the experiment was repeated using only ad libitum and restricted fed fast-growing chickens and in a genetically distinct breed of ad libitum fed male and female chickens. Linear mixed models (Genstat 18) were used for statistical analysis with transformation where appropriate. Results There were pronounced sex differences: expression of the orexigenic genes AGRP (P < 0.001) and NPY (P < 0.002) was higher in males of the fast-growing strain. In genetically distinct chickens, males had higher AGRP mRNA (P = 0.002) expression than females, suggesting sex difference was not restricted to a fast-growing strain. AGRP (P < 0.001) expression was significantly decreased in ad libitum fed birds but was high and indistinguishable between birds on a quantitative versus qualitative restricted diet. Inversely, gene expression of the anorectic genes POMC and CART was significantly higher in ad libitum fed birds but no consistent sex differences were observed. Conclusion Expression of orexigenic peptides in the avian hypothalamus are significantly different between sexes. This could be useful starting point of investigating further if AGRP is an indicator of growth potential. Results also demonstrate that gut fill alone does not reduce orexigenic gene expression

Obesity Takes Its Toll on Visceral Pain: High-Fat Diet Induces Toll-Like Receptor 4- Dependent Visceral Hypersensitivity

Exposure to high-fat diet induces both, peripheral and central alterations in TLR4 expression. Moreover, functional TLR4 is required for the development of high-fat diet-induced obesity. Recently, central alterations in TLR4 expression have been associated with the modulation of visceral pain. However, it remains unknown whether there is a functional interaction between the role of TLR4 in diet-induced obesity and in visceral pain. In the present study we investigated the impact of long-term exposure to high-fat diet on visceral pain perception and on the levels of TLR4 and Cd11b (a microglial cell marker) protein expression in the prefrontal cortex (PFC) and hippocampus. Peripheral alterations in TLR4 were assessed following the stimulation of spleenocytes with the TLR4-agonist LPS. Finally, we evaluated the effect of blocking TLR4 on visceral nociception, by administering TAK-242, a selective TLR4-antagonist. Our results demonstrated that exposure to high-fat diet induced visceral hypersensitivity. In parallel, enhanced TLR4 expression and microglia activation were found in brain areas related to visceral pain, the PFC and the hippocampus. Likewise, peripheral TLR4 activity was increased following long-term exposure to high-fat diet, resulting in an increased level of pro-inflammatory cytokines. Finally, TLR4 blockage counteracted the hyperalgesic phenotype present in mice fed on high-fat diet. Our data reveal a role for TLR4 in visceral pain modulation in a model of diet-induced obesity, and point to TLR4 as a potential therapeutic target for the development of drugs to treat visceral hypersensitivity present in pathologies associated to fat diet consumption

Obesity prevalence from a European perspective: a systematic review

<p>Abstract</p> <p>Background</p> <p>Obesity has been recognised as an important contributing factor in the development of various diseases, but comparative data on this condition are limited. We therefore aimed to identify and discuss current epidemiological data on the prevalence of obesity in European countries.</p> <p>Methods</p> <p>We identified relevant published studies by means of a MEDLINE search (1990–2008) supplemented by information obtained from regulatory agencies. We only included surveys that used direct measures of weight and height and were representative of each country's overall population.</p> <p>Results</p> <p>In Europe, the prevalence of obesity (body mass index ≥ 30 kg/m²) in men ranged from 4.0% to 28.3% and in women from 6.2% to 36.5%. We observed considerable geographic variation, with prevalence rates in Central, Eastern, and Southern Europe being higher than those in Western and Northern Europe.</p> <p>Conclusion</p> <p>In Europe, obesity has reached epidemic proportions. The data presented in our review emphasise the need for effective therapeutic and preventive strategies.</p

Role of protein kinase c in modulation of excitability of Ca1 pyramidal neurons in the rat

Biochemical and in situ hybridization studies demonstrated that the levels of protein kinase C variants were significantly increased in the hippocampus of the experimental models of epilepsy in rats. In addition it has been demonstrated that protein kinase C plays an important role in modulating synaptic transmission in the hippocampus. We examined the effects of activating of protein kinase C on the excitability of CA1 pyramidal neurons and synaptic transmission, using whole-cell current-clamp and extracellular field potential recording techniques. Indolactam V (1 M) a novel protein kinase C activator, increased the excitability of CA1 neurons acting at both pre- and post-synaptic sites. Indolactam V, acting postsynaptically, significantly reduced the threshold for initiation of action potential from 42 3.8 mV to 51 3.1 mV and selectively inhibited the slow afterhyperpolarizing potential. Indolactam V also altered the neuronal firing properties in response to prolonged depolarizing pulse by eliminating the spike frequency accommodation. Our data indicate that indolactam V potentiated both amplitudes of Shaffer-collateral stimulation evoked excitatory postsynaptic currents and disynaptically evoked inhibitory evoked postsynaptic currents. However, the potentiation of inhibitory evoked postsynaptic currents amplitudes was not observed after blockade of NMDA and AMPA/kainate currents suggesting it was due to excitatory activity driving inhibitory neurons. The results indicate that the potentiation of pharmacologically isolated excitatory postsynaptic currents (215% of control) and amplitudes of population spikes (290% of control) was due to action of indolactam V presynaptically since the agonist reduced the paired-pulse ratio and the potentiating effect was not blocked by dialyzing the postsynaptic neuron through the recording electrode with a specific protein kinase C inactivator calphostin C. These findings suggest that protein kinase C increases the amplitude of epileptiform activity by causing potentiation of excitatory synaptic transmission, increasing the excitability of postsynaptic neurons and reducing negative feed back provided by slow afterhyperpolarizing potential. Published by Elsevier Ltd on behalf of IBRO