Changes in NPY staining in the arcuate nucleus during and after food restriction in lactating rats

This study investigated the effects of food restriction on Neuropeptide Y (NPY) staining in the arcuate nucleus of lactating rats to evaluate a role for NPY in the maintenance of lactational diestrus in food restricted rats. NPY staining was compared on days 15, 20 and 25 of lactation between animals fed ad libitum (AL) and animals food restricted on days 8-14 postpartum (FR). To determine the contribution of nursing underfed pups to any differences observed, litters were switched daily between an additional AL and FR group from day 15 postpartum and dams were sacrificed on day 20 postpartum. Twenty four hrs. prior to sacrifice animals received 1$\mu$g of colchicine icv. Animals were perfused and their brains were processed for NPY immunocytochemistry. FR dams had a higher number of NPY stained cells in the arcuate nucleus on day 15 of lactation than AL dams, and this effect persisted for five days after refeeding (p $<$.05). Increases in NPY staining in food restricted rats were unrelated to the nutritional status of their litters. Finally, data revealed that dams that remained in lactational diestrus on day 25, tended to have more NPY-stained cells in the arcuate nucleus than dams that had shown an estrous smear (p =.08). These results indicate that food restriction affects NPY immunoreactivity in the arcuate nucleus and the time course of these changes suggest that NPY may play a role in prolonging lactational diestrus

Food restriction attenuates the hormonal and neuronal responses to the positive feedback effects of estradiol to prolong lactational diestrus in rats

Food restriction prolongs lactational infertility in rats. The experiments presented in this thesis were done to investigate the possibility that this effect is due to an attenuated response to the positive feedback effects of estradiol (E2) that stimulate the surge in luteinizing hormone (LH) release. Furthermore, the hypothesis that the hypothalamus is one site affected by food restriction in attenuating E2 induced LH surges was examined. The first series of experiments examined the ability of E2 to induce LH surges in both ad lib fed and food restricted dams at different times of lactation. Results were that on day 20 postpartum (pp) ad lib fed dams showed LH surges after E2 treatment, but food restricted dams did not. Ovariectomy (OVX) or RU486 treatment restored the ability of E2 to induce LH surges in food restricted dams, and chronic progesterone (P) reduced E2-induced LH surges in ad lib fed OVX dams. The second series of experiments showed that food restricted dams had less Fos-like immunoreactive (FOS-ir) cells in the anteroventral preoptic area (AVPV) than ad lib fed dams on day 20 pp. These effects were reflected in a reduced ability of E2 to induce P receptor (PR) immunoreactivity, but not in the number of E2 receptors (ERÌ) in the AVPV. As with the LH surge, the effects of food restriction on E2 induction of PRs were mediated by P. Results suggest that the lactational diestrus is prolonged by a decrease in sensitivity to E2 in the AVPV, and this effect is mediated by the high levels of P in food restricted dams

Session 2-3-G: Starving to Gamble: Hunger and gambling-related craving interact to heighten persistent play among problem gamblers

Describes how hunger and gambling-related cravings relate to problem gambling

Chopped Arms &#x26; Big Macs: ERP Correlates of Viewing and Imagining Aversive and Food Photos

OBJECTIVES&#xd;&#xa;We investigated the Event-Related Potential (ERP) correlates of perceived and imagined food photos and their relation to the perception and imagery of unpleasant emotional photos. Our aim was to determine whether similar or different patterns of neural activity were associated with viewing and imagining food photos versus emotional photos. &#xd;&#xa;&#xd;&#xa;METHODS &#xd;&#xa;Nine volunteers with prescreened normal mood and anxiety levels wore a 32 channel Cap with embedded electrodes (10/20 international system) connected to a high-density low-noise Neuroscan EEG system. Participants were tested during two different blocks: a hunger block (containing 25 neutral and food photos) and an emotional block (containing 3 sets of 20 neutral, unpleasant and pleasant photos). The photos were selected from the International Affective Picture System (Lang, Bradley, &#x26; Cuthbert, 1999). In both blocks, each trial began with a blank screen followed by presentation of a centered fixation point, displayed for 1 second. A photo was displayed for 3 seconds followed by a 1-second blank mask. For the next 3 seconds, participants were asked to form a mental image of the photo they had just viewed and then rate its vividness (i.e., the self-reported imagery intensity, D&#x2019;Angiulli &#x26; Reeves, 2002) on a 5-point rating scale (1 = no image, 5 = very vivid). &#xd;&#xa;&#xd;&#xa;RESULTS&#xd;&#xa;Grand averages of ERPs recorded during perception of unpleasant and food photos revealed an early negative deflection (150-250 milliseconds post-stimulus) in the anterior areas (Centro-Frontal electrodes) followed by a late positive waveform (850-950 milliseconds post-stimulus) in the posterior areas (Parietal and Occipital electrodes). A similar pattern was observed for the ERPs recorded during the imagery of unpleasant photos, except that it was observed across the entire scalp and at significantly lower amplitudes. For food imagery, we found a negative deflection (450-550 milliseconds post-stimuli) followed by a late positive waveform for all anterior and posterior areas. Importantly, unpleasant imagery was rated as less vivid than food imagery. &#xd;&#xa;&#xd;&#xa;CONCLUSION &#xd;&#xa;These results suggest that unpleasant and food photos involve similar top-down EEG activation patterns during perception, but not during imagery. Indeed, the vividness data strongly suggest that the negative deflection may indicate suppression of unpleasant imagery. Our findings may have important application for desensitization and conditioning in the treatment of eating disorders.&#xd;&#xa

Clarifying the ghrelin system’s ability to regulate feeding behaviours despite enigmatic spatial separation of the GHSR and its endogenous ligand

Ghrelin is a hormone predominantly produced in and secreted from the stomach. Ghrelin is involved in many physiological processes including feeding, the stress response, and in modulating learning, memory and motivational processes. Ghrelin does this by binding to its receptor, the growth hormone secretagogue receptor (GHSR), a receptor found in relatively high concentrations in hypothalamic and mesolimbic brain regions. While the feeding and metabolic effects of ghrelin can be explained by the effects of this hormone on regions of the brain that have a more permeable blood brain barrier (BBB), ghrelin produced within the periphery demonstrates a limited ability to reach extrahypothalamic regions where GHSRs are expressed. Therefore, one of the most pressing unanswered questions plaguing ghrelin research is how GHSRs, distributed in brain regions protected by the BBB, are activated despite ghrelin’s predominant peripheral production and poor ability to transverse the BBB. This manuscript will describe how peripheral ghrelin activates central GHSRs to encourage feeding, and how central ghrelin synthesis and ghrelin independent activation of GHSRs may also contribute to the modulation of feeding behaviours

Palatable Food Dampens the Long-Term Behavioral and Endocrine Effects of Juvenile Stressor Exposure but May Also Provoke Metabolic Syndrome in Rats

The juvenile period is marked by a reorganization and growth of important brain regions including structures associating with reward seeking behaviors such as the nucleus accumbens (NA) and prefrontal cortex (PFC). These changes are impacted by stressors during the juvenile period and may lead to a predisposition to stress induced psychopathology and abnormal development of brain reward systems. Like in humans, adult rodents engage certain coping mechanisms such as increases in the consumption of calorie-rich palatable foods to reduce stress, but this behavior can lead to obesity and metabolic disorders. In this study, we examined whether stressors during the juvenile period led to increased caloric intake when a palatable diet was accessible, and whether this diet attenuated adult stress responses. In addition, we examined if the stress buffering effects produced by the palatable diet were also accompanied by an offset propensity towards obesity, and by alterations in mRNA expression of dopamine (DA) receptors in the NA and PFC in adulthood. To this end, juvenile male Wistar rats underwent episodic stressor exposure (forced swim, elevated platform stress and restraint) on postnatal days (PD) 27-29 and received access to regular chow or daily limited access to a palatable diet until adulthood. At the age of 2 months, rats were tested on a social interaction test that screens for anxiety-like behaviors and their endocrine responses to an acute stressor. Animals were sacrificed, and their brains processed to detect differences in DA receptor subtype expression in the PFC and NA using qPCR. Results showed that rats that were stressed during the juvenile period displayed higher social anxiety and a sensitized corticosterone response as adults and these effects were attenuated by access to the palatable diet. Nevertheless, rats that experienced juvenile stress and consumed a palatable diet showed greater adiposity in adulthood. Interestingly, the same group displayed greater mRNA expression of DA receptors at the NA. This suggests that access to a palatable diet mitigates the behavioral and endocrine effects of juvenile stressor exposure in adulthood, but at the cost of metabolic imbalances and a sensitized dopaminergic system

Vessel Shrinkage as a Sign of Atherosclerosis Progression in Type 2 Diabetes : A Serial Intravascular Ultrasound Analysis

OBJECTIVE—The aim of this study was to determine the natural history of vascular remodeling of atherosclerotic plaques in patients with type 2 diabetes and the predictors of vessel shrinkage

Angiographically borderline left main coronary artery lesions: correlation of transthoracic doppler echocardiography and intravascular ultrasound: a pilot study

<p>Abstract</p> <p>Background</p> <p>the clinical decision making could be difficult in patients with borderline lesions (visually assessed stenosis severity of 30 to 50%) of the left main coronary artery (LM). The aim of the study was to evaluate the relationship between transthoracic Doppler (TTDE) peak diastolic flow velocity (PDV) and intravascular ultrasound (IVUS) measurements in the assessment of angiographically borderline LM lesions.</p> <p>Methods</p> <p>27 patients (mean age 64 ± 8 years, 21 males) with borderline LM stenosis referred for IVUS examination were included in the study. We performed standard IVUS with minimal lumen area (MLA) and plaque burden (PB) measurement and routine quantitative coronary angiography (QCA) with diameter stenosis (%DS) and area stenosis (%AS) assessment in all. During TTDE, resting PDV was measured in the LM.</p> <p>Results</p> <p>interpretable Doppler signal could be obtained in 24 patients (88% feasibility); therefore these patients entered the final analysis. MLA was 7.1 ± 2.7 mm². TTDE measured PDV correlated significantly with IVUS-derived MLA (r = -0.46, p < 0.05) and plaque burden (r = 0.51, p < 0.05). Using a velocity cut-off of 112 cm/sec TTDE showed a 92% sensitivity and 62% specificity to identify IVUS-significant (MLA < 6 mm²) LM stenosis.</p> <p>Conclusion</p> <p>In angiographically borderline LM disease, resting PDV from transthoracic echocardiography is increased in presence of increased plaque burden by IVUS. TTDE evaluation might be a useful adjunct to other invasive and non-invasive methods in the assessment of borderline LM lesions. Further, large scale studies are needed to establish the exact cut-off value of PDV for routine clinical application.</p

Stress and obesity: The ghrelin connection

Ghrelin is a hormone associated with feeding and energy balance. Not surprisingly, this hormone is secreted in response to acute stressors and it is chronically elevated after exposure to chronic stress in tandem with a number of metabolic changes aimed at attaining homeostatic balance. In the present review, we propose that ghrelin plays a key role in these stress-induced homeostatic processes. Ghrelin targets the hypothalamus and brain stem nuclei that are part of the sympathetic nervous system to increase appetite and energy expenditure and promote the use of carbohydrates as a source of fuel at the same time as sparing fat. Ghrelin also targets mesolimbic brain regions such as the ventral segmental area and the hippocampus to modulate reward processes, to protect against damage associated with chronic stress, as well as to potentially increase resilience to stress. In all, these data support the notion that ghrelin, similar to corticosterone, is a critical metabolic hormone that is essential for the stress response