The electrophysiology of feeding circuits

Jobst, Erin E; Enriori, Pablo J.; Cowley, Michael A.

doi:10.1016/j.tem.2004.10.007

Cited by 125 publications

(84 citation statements)

References 125 publications

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“…There are several subtypes of the melanocortin peptides, such as adrenocorticotrophin (ACTH) and alpha-melanocyte-stimulating hormone (α-MSH), which act at G-protein-coupled melanocortin receptors such as the MC 1-5 receptors [118,138,139]. In the brain, POMC is mainly expressed in the Arc [138,140], and projects to various regions of the hypothalamus [118,141]. Certain POMC gene mutations may contribute to obesity in healthy human populations [142,143], while mouse knockout for POMC also shows the obese phenotype [138,144].…”

Section: The Role Of Pomc and Cart In Sga-induced Weight Gainmentioning

confidence: 99%

Ameliorating antipsychotic-induced weight gain by betahistine: Mechanisms and clinical implications

Lian

Huang

Pai

et al. 2016

Pharmacological Research

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Second generation antipsychotic drugs (SGAs) cause substantial body weight gain/obesity and other metabolic side-effects such as dyslipidaemia. Their antagonistic affinity to the histaminergic H1 receptor (H1R) has been identified as one of the main contributors to weight gain/obesity side-effects. The effects and mechanisms of betahistine (a histaminergic H1R agonist and H3 receptor antagonist) have been investigated for ameliorating SGA-induced weight gain/obesity in both animal models and clinical trials. It has been demonstrated that co-treatment with betahistine is effective in reducing weight gain, associated with olanzapine in drug-naïve patients with schizophrenia, as well as in the animal models of both drug-naïve rats and rats with chronic, repeated exposure to olanzapine. Betahistine co-treatment can reduce food intake and increase the effect of thermogenesis in brown adipose tissue by modulating hypothalamic H1R-NPY-AMPKα (NPY: neuropeptide Y; AMPKα: AMP-activated protein kinase α) pathways, and ameliorate olanzapineinduced dyslipidaemia through modulation of AMPKα-SREBP-1-PPARα-dependent pathways (SREBP-1: Sterol regulatory element binding protein 1; PPARα: Peroxisome proliferator-activated receptor-α) in the liver. Although reduced locomotor activity was observed from antipsychotic treatment in rats, betahistine did not affect locomotor activity. Importantly, betahistine co-treatment did not influence the effects of antipsychotics on serotonergic receptors in the key brain regions for antipsychotic therapeutic efficacy. However, betahistine co-treatment reverses the upregulated dopamine D2 binding caused by chronic olanzapine administration, which may be beneficial in reducing D2 supersensitivity often observed in chronic antipsychotic treatment. Therefore, these results provide solid evidence supporting further clinical trials in treating antipsychotics-induced weight gain using betahistine in patients with schizophrenia and other mental disorders.

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Section: The Role Of Pomc and Cart In Sga-induced Weight Gainmentioning

confidence: 99%

Ameliorating antipsychotic-induced weight gain by betahistine: Mechanisms and clinical implications

Lian

Huang

Pai

et al. 2016

Pharmacological Research

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“…A large-scale study of global gene expression in normal human tissues show that CCK is expressed at highest levels in brain and placenta, but its role in the placenta has not been investigated (6). Many polymorphisms have been reported in the CCK gene (31), and the association of CCK polymorphisms with appetite and satiety remains to be determined (32). It would be interesting to determine whether there is a correlation between placental CCK expression and diet intake, satiety, and͞or weight gain during pregnancy.…”

Section: Genes That Define Interindividual Variation In Villus Sectiomentioning

confidence: 99%

Gene expression patterns in human placenta

Sood¹,

Zehnder²,

Druzin

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

399

289

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The placenta is the principal metabolic, respiratory, excretory, and endocrine organ for the first 9 months of fetal life. Its role in fetal and maternal physiology is remarkably diverse. Because of the central role that the placenta has in fetal and maternal physiology and development, the possibility that variation in placental gene expression patterns might be linked to important abnormalities in maternal or fetal health, or even variations in later life, warrants investigation. As an initial step, we used DNA microarrays to analyze gene expression patterns in 72 samples of amnion, chorion, umbilical cord, and sections of villus parenchyma from 19 human placentas from successful full-term pregnancies. The umbilical cord, chorion, amnion, and villus parenchyma samples were readily distinguished by differences in their global gene-expression patterns, many of which seemed to be related to physiology and histology. Differentially expressed genes have roles that include placental trophoblast secretion, signal transduction, metabolism, immune regulation, cell adhesion, and structure. We found interindividual differences in expression patterns in villus parenchyma and systematic differences between the maternal, fetal, and intermediate layers. A group of genes that was expressed in both the maternal and fetal villus parenchyma sections of placenta included genes that may be associated with preeclampsia. We identified sets of genes whose expression in placenta was significantly correlated with the sex of the fetus. This study provides a rich and diverse picture of the molecular variation in the placenta from healthy pregnancies.microarray ͉ pregnancy ͉ transcriptome ͉ preeclampsia T he placenta is a temporary organ that performs the functions of several adult organs for the growing fetus. The placenta is designed uniquely for exchange of oxygen, nutrients, antibodies, hormones, and waste products between the mother and fetus and may carry valuable information about the pregnancy. Although a placenta after delivery is among the most easily accessible human tissues, it is usually discarded after a cursory evaluation (1). Several pregnancy disorders including preeclampsia (PE) and preterm labor are associated with placental pathology. Also, epidemiologic studies suggest that there are ''fetal origins'' that predispose adults to cardiovascular, metabolic, and endocrine diseases (2). Also, low-birth-weight fetuses associated with large placentas are associated with increased neonatal morbidity indicating abnormal placental activity in such scenarios (3, 4). The investigation of placenta may provide valuable insights into placental functions and help identify molecular mechanisms that have both immediate and long lasting effects on health of the fetus.A schematic representation of the placenta is given in Fig. 1, with both the placental disk proper and the reflected membranes. The placenta is a composite organ of trophectoderm-derived cells and cells that are derived from the inner cell mass (ICM)͞epiblast, and a minor co...

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“…These neurons project to melanocortin-4-receptor (MC4R) expressing neurons in other hypothalamic regions like the paraventricular nucleus (PVN). In states of high caloric excess, elevated leptin levels stimulate anorexigenic Pomc neurons and inhibit orexigenic Agrp neurons [12,31]. In second order neurons MC4R-signaling promotes negative energy balance by increasing energy expenditure and reducing food intake [10,29,49].…”

Section: Obesitymentioning

confidence: 99%

Mouse models for the central melanocortin system

Bolze

Klingenspor

2009

Genes Nutr

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Obesity is characterized by an excess storage of body fat and promotes the risk for complex disease traits such as diabetes mellitus and cardiovascular diseases. The obesity prevalence in Europe is rising and meanwhile ranges from 10 to 20% in men and 15-25% in women. Body fat accumulation occurs in states of positive energy balance and is favored by interactions among environmental, psychosocial and genetic factors. Energy balance is regulated by a complex neuronal network of anorexigenic and orexigenic neurons which integrates peripheral and central hormonal and neuronal signals relaying information on the metabolic status of organs and tissues in the body. A key component of this network is the central melanocortin pathway in the hypothalamus that elicits metabolic and behavioral adaptations for the maintenance of energy homeostasis. Genetic defects in this system cause obesity in mice and humans. In this review we emphasize mouse models with spontaneous natural mutations as well as targeted mutations that contributed to our understanding of the central melanocortin system function in the control of energy balance.Keywords Energy balance Á Melanocortin Á Mouse models Á Obesity ObesityObesity is characterized by an excess of body fat and promotes the risk for the development of complex disease traits like diabetes mellitus, cardiovascular dysfunctions, certain forms of cancer and sleep-breathing disorders. World Health Organization defines obesity by a body mass index (BMI) larger than 30 kg/m 2 , whereas overweight is defined by a BMI between 25 and 29.9 kg/m 2 . The obesity prevalence in Europe ranges from 10 to 20% in men and 15-25% in woman. Body fat mass is influenced by interactions among environmental, psychosocial and genetic factors. Promotion of positive energy balance causes obesity in humans as well as in mice (for review see [4,20,33]).The mouse has proven itself as an excellent model for investigations on human diseases as development and genetics are similar in mouse and man. Furthermore, genetic engineering techniques in the mouse became wellestablished and reliable tools in the last two decades. In this mini review we highlight different mouse models which have been instrumental to study body weight regulation and the development of obesity.The melanocortin system and its role in the regulation of energy homeostasisThe lipostatic hypothesis for the control of food intake postulates that adipose tissue produces a hormone in proportion to the amount of fat and acts on the central nervous system to reduce feeding and increase energy expenditure for maintaining energy balance [32].

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The electrophysiology of feeding circuits

Cited by 125 publications

References 125 publications

Ameliorating antipsychotic-induced weight gain by betahistine: Mechanisms and clinical implications

Ameliorating antipsychotic-induced weight gain by betahistine: Mechanisms and clinical implications

Gene expression patterns in human placenta

Mouse models for the central melanocortin system

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