53 research outputs found

    Galanin in the PVN increases nutrient intake and changes peripheral honnone levels in the rat

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    Abstract In self-selection feeding paradigms, rats display differential patterns of nutrient (protein, carbohydrate or fat) intake. Factors known to influence this selection include brain peptides as well as circadian parameters. In this series of experiments we investigated the role of PVN galanin in nutrient intake during the early and late dark periods in the rat. Rats were allowed to select between three isocaloric diets enriched in protein, carbohydrate or fat. Following a 2-week adaptation period, the animals' 24-h intake was monitored for 4 weeks. Galanin was injected into the PVN and food intake was measured 1, 2 and 24 h post-injection. Galanin significantly increased the 1 h total food intake but it failed to increase the intake of any particular nutrient. Galanin had no effect 2 or 24 h post-injection. Analysis of the data grouped by preference based on the rats 24 h baseline selection patterns over the 4-week period revealed that galanin seem to increase the preferred nutrient. That is, galanin preferentially increased the intake of the carbohydrate-or fatrich diet in animals with high (over 40% of the total food intake) 24-h baselines in this particular nutrient. Finally, analysis of the plasma hormone levels after paraventricular galanin administration revealed a significant increase in noradrenaline levels, a small reduction in plasma insulin with no effects on adrenaline, glucose or corticosterone. The data revealed that galanin in the PVN influences both food intake and metabolic functioning. PVN galanin significantly increases sympathetic outflow and seems to stimulate the intake of the individual rat's preferred macronutrient

    Overfeeding, Autonomic Regulation and Metabolic Consequences

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    The autonomic nervous system plays an important role in the regulation of body processes in health and disease. Overfeeding and obesity (a disproportional increase of the fat mass of the body) are often accompanied by alterations in both sympathetic and parasympathetic autonomic functions. The overfeeding-induced changes in autonomic outflow occur with typical symptoms such as adiposity and hyperinsulinemia. There might be a causal relationship between autonomic disturbances and the consequences of overfeeding and obesity. Therefore studies were designed to investigate autonomic functioning in experimentally and genetically hyperphagic rats. Special emphasis was given to the processes that are involved in the regulation of peripheral energy substrate homeostasis. The data revealed that overfeeding is accompanied by increased parasympathetic outflow. Typical indices of vagal activity (such as the cephalic insulin release during food ingestion) were increased in all our rat models for hyperphagia. Overfeeding was also accompanied by increased sympathetic tone, reflected by enhanced baseline plasma norepinephrine (NE) levels in both VMH-lesioned animals and rats rendered obese by hyperalimentation. Plasma levels of NE during exercise were, however, reduced in these two groups of animals. This diminished increase in the exercise-induced NE outflow could be normalized by prior food deprivation. It was concluded from these experiments that overfeeding is associated with increased parasympathetic and sympathetic tone. In models for hyperphagia that display a continuously elevated nutrient intake such as the VMH-lesioned and the overfed rat, this increased sympathetic tone was accompanied by a diminished NE response to exercise. This attenuated outflow of NE was directly related to the size of the fat reserves, indicating that the feedback mechanism from the periphery to the central nervous system is altered in the overfed state.

    Metabolic consequences of chronic sleep restriction in rats:Changes in body weight regulation and energy expenditure

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    Epidemiological studies have shown an association between short or disrupted sleep and an increased risk to develop obesity. In animal studies, however, sleep restriction leads to an attenuation of weight gain that cannot be explained by changes in energy intake. In the present study, we assessed whether the attenuated weight gain under conditions of restricted sleep is a consequence of an overall increase in energy expenditure. Adult male rats were subjected to a schedule of chronic sleep restriction (SR) for 8 days with a 4 h window of unrestricted rest per day. Electroencephalogram and electromyogram recordings were performed to quantify the effect of the sleep restriction schedule on sleep-wake patterns. In a separate experiment, we measured sleep restriction-induced changes in body weight, food intake, and regulatory hormones such as glucose, insulin, leptin and corticosterone. To investigate whether a change in energy expenditure underlies the attenuation of weight gain, energy expenditure was measured by the doubly labeled water method from day 5 until day 8 of the SR protocol. Results show a clear attenuation of weight gain during sleep restriction but no change in food intake. Baseline plasma glucose, insulin and leptin levels are decreased after sleep restriction which presumably reflects the nutritional status of the rats. The daily energy expenditure during SR was significantly increased compared to control rats. Together, we conclude that the attenuation of body weight gain in sleep restricted rats is explained by an overall increase in energy expenditure together with an unaltered energy intake. Published by Elsevier Inc

    Evaluation of a lifestyle intervention program in primary care on physical and mental health and quality of life of cancer survivors:A pilot study

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    Introduction: Cancer survivors often suffer from fatigue and (mental) health impairments. Despite evidence for effectiveness, lifestyle interventions are seldom applied in their aftercare. The aim of this study was to assess feasibility of a lifestyle intervention program on physical and mental wellbeing and quality of life (QoL) of cancer survivors, and to get a first impression of effectiveness, by means of a pilot study. Methods: Nine subjects were enrolled in a 12-month lifestyle intervention pilot study without a control group, conducted in a Dutch primary care centre. The intervention consisted of individual and group lifestyle training focusing on diet, exercise and mind-body interaction. The main outcomes were physical and mental health and QoL. Results: All 9 subjects completed the 12-month lifestyle intervention program. We found a large positive effect on fatigue (r = −0.9), stress (r = −0.8) and anxiety (r = −0.9). With respect to quality of life, large improvements in vitality (r = 0.7), role limitations due to physical health (r = −0.7), role limitations due to emotional problems (r = −0.8) and personal health experience (r = 0.8) were found. Subjects’ arm strength increased (r = 0.9), but there were no significant changes in other physical parameters, depressive symptoms, social optimism and autonomy. Contradictory results were found for pain. Conclusion: Implementation of this lifestyle intervention program seems feasible in this small uncontrolled pilot study. The reduced QoL that is typical for cancer survivors was positively influenced by this program. Most prominent results were retrieved for fatigue and mental functioning, whereas little effects were found for physical health
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