Leptin in the Anterior Piriform Cortex Affects Food Intake in Rats

Leptin administered intracerebroventricularly (ICV) or intrahypothalamically inhibits food intake (FI), however, to our knowledge the effects of leptin administration have only been examined in one extrahypothalamic site (dorsal raphe nucleus). Our objectives were t. (1) determine the FI effects of leptin administration into the anterior piriform cortex (APC), an area linked to the control of FI in amino acid (AA) deficiency, (2) examine leptin action during short term anorexia that develops in response to AA deficiency. Bilateral injections of leptin (0.25 μ) into the APC suppressed FI of a balanced diet between 6 and 12 h by 36% (p < 0.01) and over the first 12 and 24 h by 15% (p < 0.05). Bilateral administration of leptin (0.1 μg) inhibited FI between 12 and 24 h by approximately 48% (p < 0.05) on a threonine-imbalanced diet without significantly affecting FI on a threonine-corrected diet. The increase of plasma leptin concentrations in response to feeding a threonine-basal diet was greater than that following an AA imbalanced diet, suggesting that suppression of FI by an AA imbalanced diet is not mediated by an increase of leptin. Our results suggest that (1) administration of leptin into a brain area outside the hypothalamus suppresses FI, and (2) leptin is unlikely to play a selective role in the short term anorectic response to AA deficiency. These data are consistent with the hypothesis that endogenous leptin can act within the APC to modulate FI.     

Effect of lead exposure on patterns of food intake in weanling rats

The reduction in growth resulting from lead (Pb) exposure in weanling rats is consistent with a lowering of the biological set-point for food intake. In this study the effects of lead on the patterns of food intake were examined. For 10 days (from ages 26 to 36 days), female rats were provided with drinking water containing 250 ppm lead as the acetate (n = 6) or equivalent acetate as sodium acetate (n = 6). A computerized system was used to monitor daily food intake at 5-min intervals over 10 successive 23-h periods (each period consisting of 12 h dark, 11 h light). Control rats consumed approximately 75% to 85% of their food intake during the dark phase. Exposure to lead resulted in decreased body weight, tail length, and cumulative food intake. Decreased food intake associated with lead during the first 6 days of exposure was due to a decrease in the size of each meal during the dark phase, which reflected a decrease in the duration of each meal. These results suggest that lead, at least initially, was affecting food-satiety signals to produce a premature termination of food intake during a meal. After 6 days, the lead-exposed rats appear to have adjusted their meal size and meal duration to approximately control values. However, this compensation appears to have occurred at the expense of the daily (nocturnal) number of meals, which decreased slightly (although not significantly) in lead-exposed animals. Thus, the total daily intake of food in lead-treated animals remained depressed relative to control animals.     

利用黄鼬控制害鼠的研究Ⅰ.黄鼬控制害鼠能力初探

目的 研究黄鼬控制害鼠的能力。方法 人工饲养，定时喂食，观察。结果 黄鼬在有选择的条件下，仅取食动物类食物，在动物类食物中嗜食鼠类，日食量达体重的20%左右，不同季节的活动时间有一定的差异。结论 利用黄鼬可控制特定环境中的害鼠，用人工饲养的方法。观察，分析黄鼬的食性，食量及生活习性。以探讨黄鼬控制害鼠的能力。可为进一步利用黄鼬控制害鼠提供资料。     

Control of food consumption by learned cues: a forebrain-hypothalamic network

Motivation plays an important role in the control of food intake. This review will focus on recent findings using a neural systems analysis of a behavioral model for learned motivational control of eating. In this model, environmental cues that acquire motivational properties through Pavlovian conditioning can subsequently override satiety and promote eating in sated rats. Evidence will be presented that a brain network formed by the amygdala, lateral hypothalamus, and medial prefrontal cortex mediates this phenomenon of conditioned potentiation of feeding. The animal model may be informative for understanding control of eating in humans including maladaptive influences that contribute to overeating.     

Prader–Willi syndrome: From genetics to behaviour,with special focus on appetite treatments

Prader–Willi syndrome (PWS) is a neurodevelopmental disorder resulting from a deletion in the expression of the paternally derived alleles in the region of 15q11–q13. PWS has a prevalence rate of 1:10,000–1:30,000 and is characterized by marked endocrine abnormalities including growth hormone deficiency and raised ghrelin levels.The hyperphagic phenotype in PWS is established over a number of phases and is exacerbated by impaired satiety, low energy expenditure and intellectual difficulties including obsessive–compulsive disorder and/or autistic behaviours. Clinical management in PWS typically includes familial/carer restriction and close supervision of food intake. If the supervision of food is left unmanaged, morbid obesity eventuates, central to the risk of cardiorespiratory disorder. None of the current appetite management/intervention strategies for PWS include pharmacological treatment, though recent research shows some promise.We review the established aberrant genetics and the endocrine and neuronal attributes which may determine disturbed regulatory processes in PWS. Focusing on clinical trials for appetite behaviours in PWS, we define the effectiveness of pharmacological treatments with a view to initiating and focusing research towards possible targets for modulating appetite in PWS.     

Zucker obese rats are insensitive to the CRH-increasing effect of oleoyl-estrone

Adult female Zucker lean and obese rats were treated for 14 days with 3.5 nm/kg oleoyl-estrone (OE) in liposomes (Merlin-2) through continuous i.v. injection with osmotic minipumps. Rat wt. and food intake were measured daily. On days 0, 3, 6, 10, and 14, groups of rats were killed and their hypothalamic nuclei [lateral preoptic (LPO), median preoptic (MPO), paraventricular (PVN), ventromedial (VMH), and arcuate (ARC)] were dissected, homogenized, and used for the measurement of corticosterone-releasing hormone (CRH) by radioimmunoassay. The OE treatment decreased food intake by 67.4% in lean and 62.6% in obese rats (means for 14 days). Body wt. decreased steadily in lean and obese rats, the gap between controls and treated rats becoming 11.5% of initial body wt. in the lean and 12.4% in the obese. The levels of CRH in the ARC nucleus were at least 10-fold higher than in the other nuclei. No changes in CRH were observed in any of the nuclei of obese rats, with levels up to day 6 similar to those of lean rats. In the lean rats, the LPO and ARC nuclei showed peaks on day 10, while the MPO showed no changes and the PVN and VMH nuclei showed a progressive increase, to a maximum at the end of the study (day 14). This contrasted with the peak of plasma adrenocorticotropic hormone (ACTH) and corticosterone (day 6 in lean and day 14 in obese rats). There was a definite lack of correlation between the plasma levels of these two hormones and the levels of CRH in the hypothalamic nuclei, and between the latter and the decreases in appetite in the rats. The loss of appetite induced by OE is not necessarily mediated by CRH, because the obese rats show an intense decrease in voluntary food intake but their hypothalamic nuclei CRH levels do not change at all. Hypothalamic nuclei CRH does not, necessarily, mediate the rise in glucocorticoids induced by OE treatment, because this is observed in lean and obese rats, lean rats increases being mismatched with those of hypothalamic CRH. The OE induced changes in hypothalamic CRH require a fully functional leptinergic pathway, because it is not observed in Zucker fa/fa rats lacking a working leptin receptor. This–indirectly–shows that leptin is needed for its synthesis or modulation.     

The influence of infantile handling, age and strain on alcohol selection in mice

Male mice from three inbred strains (C57B1/10J, BALB/cJ and C3H/2lbg) were assigned to infantile handling or control conditions. In a cross-sectional developmental design, handled and control mice were tested for two-choice selection of 10% (v/v) ethanol vs. tap water at 60, 90 or 120 days of age. The volume of fluid consumed from both tubes was recorded for fifteen days. In 60 day old mice, handling produced a trend toward increased total fluid consumption in the C57 mice and a trend toward increased ethanol selection in the BALBs. In 90 day old mice, there were trends noted toward handling-related decreased fluid consumption in BALBs. Also noted was a trend toward handling related increased ethanol selection in C57 mice. In 120 day old mice, a handling-related increase in alcohol selection was noted in the C3H strain.     

Effect of Fenfluramine on the single neuron activities of the hypothalamic feeding centers

Electrical activity of single neurons of the hypothalamic satiety and feeding centers and other adjacent areas was recorded by means of stereotaxically guided steel microelectrodes, before and after Fenfluramine infusion in doses of 1.5 mg/kg body wt. In addition arterial and venous blood glucose estimations were carried out to assess the levels of glucose utilization. The spike frequency of satiety center units increased while that of feeding center units decreased, in response to Fenfluramine while other hypothalamic units did not show any changes. The A-V glucose differences also increased showing increased level of glucose utilization. The significance of these findings in explaining the effects of Fenfluramine in depressing appetite have been discussed.