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The Central Effects of Thyroid Hormones on Appetite  [PDF]
Anjali Amin,Waljit S. Dhillo,Kevin G. Murphy
Journal of Thyroid Research , 2011, DOI: 10.4061/2011/306510
Abstract: Obesity is a major public health issue worldwide. Current pharmacological treatments are largely unsuccessful. Determining the complex pathways that regulate food intake may aid the development of new treatments. The hypothalamic-pituitary-thyroid (HPT) axis has well-known effects on energy expenditure, but its role in the regulation of food intake is less well characterised. Evidence suggests that the HPT axis can directly influence food intake. Thyroid dysfunction can have clinically significant consequences on appetite and body weight. Classically, these effects were thought to be mediated by the peripheral effects of thyroid hormone. However, more recently, local regulation of thyroid hormone in the central nervous system (CNS) is thought to play an important role in physiologically regulating appetite. This paper focuses on the role of the HPT and thyroid hormone in appetite and provides evidence for potential new targets for anti-obesity agents. 1. Introduction Obesity, its complications, and the associated mortality are major public health issues worldwide. The major central nervous system (CNS) areas important in the regulation of appetite are the hypothalamus and brainstem. The hypothalamus interprets and integrates afferent signals from the periphery and brainstem to modulate efferent signals that regulate food intake and energy expenditure. Neural and hormonalperipheral signals communicate information including acute nutritional states and energy stores. The hypothalamus is subdivided into a number of interconnecting nuclei, including the paraventricular nucleus (PVN), the ventromedial nucleus (VMN), and the arcuate nucleus (ARC), which are particularly important in regulating energy homeostasis. The ARC is located near the median eminence, where the blood-brain barrier is incomplete, and is thus well positioned to respond to circulating factors involved in appetite and food intake [1]. Recent evidence suggests that thyroid hormones may access the ARC and other regions of the hypothalamus to regulate appetite (Figure 1). Figure 1: Schematic diagram of central appetite regulation. T3 can access the hypothalamus and brainstem via the incomplete blood brain barrier. PVN: paraventricular nucleus; ARC: arcuate nucleus; VMN: ventromedial nucleus; BBB: blood-brain barrier; T3: triiodothyronine; POMC: Pro-opiomelanocortin; NPY: neuropeptide Y; AgRP: agouti-related protein; BDNF: brain-derived neurotrophic factor; HPT: hypothalamic-pituitary thyroid; SNS: sympathetic nervous system. It is well established that the hypothalamic-pituitary-thyroid (HPT)
Gul Tiryaki-Sonmez,Serife Ozen,Guler Bugdayci,Umid Karli
Biology of Sport , 2013,
Abstract: Over the past decade, our knowledge of how homeostatic systems regulate food intake and body weight has increased with the discovery of circulating peptides such as leptin, acyl ghrelin, des-acyl ghrelin and obestatin. These hormones regulate the appetite and food intake by sending signals to the brain regarding the body’s nutritional status. The purpose of this study was to investigate the response of appetite-regulating hormones to exercise. Nine overweight women undertook two 2 h trials in a randomized crossover design. In the exercise trial, subjects ran for 60 min at 50% of maximal oxygen uptake followed by a 60 min rest period. In the control trial, subjects rested for 2 h. Obestatin, acyl ghrelin, des-acyl ghrelin and leptin concentrations were measured at baseline and at 20, 40, 60, 90 and 120 min after baseline. A two-way ANOVA revealed a significant (P<0.05) interaction effect for leptin and acyl ghrelin. However, changes in obestatin and des-acyl ghrelin concentration were statistically insignificant (P>0.05). The data indicated that although acute treadmill exercise resulted in a significant change in acyl ghrelin and leptin levels, it had no effect on plasma obestatin and des-acyl ghrelin levels.
Hypothalamic metabolic compartmentation during appetite regulation as revealed by magnetic resonance imaging and spectroscopy methods  [PDF]
Sebastián Cerdán
Frontiers in Neuroenergetics , 2013, DOI: 10.3389/fnene.2013.00006
Abstract: We review the role of neuroglial compartmentation and transcellular neurotransmitter cycling during hypothalamic appetite regulation as detected by Magnetic Resonance Imaging (MRI) and Spectroscopy (MRS) methods. We address first the neurochemical basis of neuroendocrine regulation in the hypothalamus and the orexigenic and anorexigenic feed-back loops that control appetite. Then we examine the main MRI and MRS strategies that have been used to investigate appetite regulation. Manganese-enhanced magnetic resonance imaging (MEMRI), Blood oxygenation level-dependent contrast (BOLD), and Diffusion-weighted magnetic resonance imaging (DWI) have revealed Mn2+ accumulations, augmented oxygen consumptions, and astrocytic swelling in the hypothalamus under fasting conditions, respectively. High field 1H magnetic resonance in vivo, showed increased hypothalamic myo-inositol concentrations as compared to other cerebral structures. 1H and 13C high resolution magic angle spinning (HRMAS) revealed increased neuroglial oxidative and glycolytic metabolism, as well as increased hypothalamic glutamatergic and GABAergic neurotransmissions under orexigenic stimulation. We propose here an integrative interpretation of all these findings suggesting that the neuroendocrine regulation of appetite is supported by important ionic and metabolic transcellular fluxes which begin at the tripartite orexigenic clefts and become extended spatially in the hypothalamus through astrocytic networks becoming eventually MRI and MRS detectable.
Differential Roles for Octanoylated and Decanoylated Ghrelins in Regulating Appetite and Metabolism  [PDF]
Sara E. Schwandt,Sarath C. Peddu,Larry G. Riley
International Journal of Peptides , 2010, DOI: 10.1155/2010/275804
Abstract: Since its identification in 1999, ghrelin has been identified in all vertebrate groups. The “active core” of ghrelin is highly conserved among vertebrates, suggesting its biological activity to be also conserved. In fish, both acylated forms of ghrelin have been identified; however, the ratio of the ghrelin-C8 to ghrelin-C10 is not as great as observed in mammals. In the tilapia (Oreochromis mossambicus), ghrelin-C10 is the major form of ghrelin. Since fish are known to inhabit every ecological niche on earth, studies on fish have provided valuable insight into vertebrate physiology in general; it is likely that understanding the role of both acylated forms of ghrelin, in more detail, in fish will result into novel insights in the biology of ghrelin within vertebrates. In this paper we discuss ghrelin's role in regulating appetite and metabolism in fish, in general, and provide evidence that the two tilapia ghrelins exhibit different biological roles. 1. Introduction The discovery of ghrelin in 1999 [1] broadened our understanding of energy metabolism in vertebrates, resulting in a shift in our approach to investigat the regulation of energy homeostasis in vertebrates. In mammals, two major forms of ghrelin are found in circulation: octanoylated ghrelin at Ser-3 and des-acyl ghrelin [2]. The acyl modification is essential for biological activity [1]; however, some findings provide evidence that des-acyl ghrelin exhibits some biological action [3–7]. Ghrelin has also been identified in all vertebrate classes including sharks [8]. As seen in mammals, the ghrelins identified in other vertebrates are uniquely acylated by either octanoic or decanoic acid on the third amino acid residue from the N-terminus. Indeed, the first seven amino acids of N-terminal region—“active core”—in all vertebrate ghrelins display high sequence homology [8], suggesting that the biological actions of ghrelin are highly conserved across vertebrates. Interestingly, fish ghrelins possess an amide structure on the C-terminus which is not found in tetrapod and shark ghrelins [8]. In the Mozambique tilapia (Oreochromis mossambicus), a warm water teleost (fish), we have identified two forms of ghrelin, with identical amino acid sequences, acylated by octanoic or decanoic acid, ti-ghrelin-C8 and ti-ghrelin-C10, respectively [9]. It appears that ti-ghrelin-C10 is the primary form of ghrelin in tilapia. A recent report in goldfish identified 11 different forms of ghrelins; a 17-residue octanoylated form being the predominate form [10]. This finding in goldfish is similar to other
A High-Throughput Fluorescence-Based Assay System for Appetite-Regulating Gene and Drug Screening  [PDF]
Yasuhito Shimada, Minoru Hirano, Yuhei Nishimura, Toshio Tanaka
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0052549
Abstract: The increasing number of people suffering from metabolic syndrome and obesity is becoming a serious problem not only in developed countries, but also in developing countries. However, there are few agents currently approved for the treatment of obesity. Those that are available are mainly appetite suppressants and gastrointestinal fat blockers. We have developed a simple and rapid method for the measurement of the feeding volume of Danio rerio (zebrafish). This assay can be used to screen appetite suppressants and enhancers. In this study, zebrafish were fed viable paramecia that were fluorescently-labeled, and feeding volume was measured using a 96-well microplate reader. Gene expression analysis of brain-derived neurotrophic factor (bdnf), knockdown of appetite-regulating genes (neuropeptide Y, preproinsulin, melanocortin 4 receptor, agouti related protein, and cannabinoid receptor 1), and the administration of clinical appetite suppressants (fluoxetine, sibutramine, mazindol, phentermine, and rimonabant) revealed the similarity among mechanisms regulating appetite in zebrafish and mammals. In combination with behavioral analysis, we were able to evaluate adverse effects on locomotor activities from gene knockdown and chemical treatments. In conclusion, we have developed an assay that uses zebrafish, which can be applied to high-throughput screening and target gene discovery for appetite suppressants and enhancers.
Interleukin 6 Deficiency Modulates the Hypothalamic Expression of Energy Balance Regulating Peptides during Pregnancy in Mice  [PDF]
Patricia Pazos, Luis Lima, Felipe F. Casanueva, Carlos Diéguez, María C. García
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072339
Abstract: Pregnancy is associated with hyperphagia, increased adiposity and multiple neuroendocrine adaptations. Maternal adipose tissue secretes rising amounts of interleukin 6 (IL6), which acts peripherally modulating metabolic function and centrally increasing energy expenditure and reducing body fat. To explore the role of IL6 in the central mechanisms governing dam's energy homeostasis, early, mid and late pregnant (gestational days 7, 13 and 18) wild-type (WT) and Il6 knockout mice (Il6-KO) were compared with virgin controls at diestrus. Food intake, body weight and composition as well as indirect calorimetry measurements were performed in vivo. Anabolic and orexigenic peptides: neuropeptide Y (Npy) and agouti-related peptide (Agrp); and catabolic and anorectic neuropeptides: proopiomelanocortin (Pomc), corticotrophin and thyrotropin-releasing hormone (Crh and Trh) mRNA levels were determined by in situ hybridization. Real time-PCR and western-blot were used for additional tissue gene expression and protein studies. Non-pregnant Il6-KO mice were leaner than WT mice due to a decrease in fat but not in lean body mass. Pregnant Il6-KO mice had higher fat accretion despite similar body weight gain than WT controls. A decreased fat utilization in absence of Il6 might explain this effect, as shown by increased respiratory exchange ratio (RER) in virgin Il6-KO mice. Il6 mRNA levels were markedly enhanced in adipose tissue but reduced in hypothalamus of mid and late pregnant WT mice. Trh expression was also stimulated at gestational day 13 and lack of Il6 blunted this effect. Conversely, in late pregnant mice lessened hypothalamic Il6 receptor alpha (Il6ra), Pomc and Crh mRNA were observed. Il6 deficiency during this stage up-regulated Npy and Agrp expression, while restoring Pomc mRNA levels to virgin values. Together these results demonstrate that IL6/IL6Ra system modulates Npy/Agrp, Pomc and Trh expression during mouse pregnancy, supporting a role of IL6 in the central regulation of body fat in this physiological state.
Appetite Regulating Hormone  [cached]
Nirmala G.C.,Suchitra B.R. and Pavankumar K.N.
Veterinary World , 2009,
Abstract: [Vet World 2009; 2(6.000): 242-246]
The Peripheral Hypotheses of Hypothalamic Aging
Zi-Jian Cai
Open Access Library Journal (OALib Journal) , 2018, DOI: 10.4236/oalib.1104445
It is well known that the hypothalamic changes in control of hormones determine the chronological sequence of aging in mammals. For decades, it has been demonstrated in humans that the hypothalamic nuclei manifest heterogeneity in degeneration during aging, with the neuron number decreasing in both the suprachiasmatic nucleus (SCN) and the preoptic sexually dimorphic nucleus (SDN-POA) in the process of senescence, while the neuron number remains unchanged in the paraventricular nucleus (PVN). Recently, it was newly hypothesized some peripheral mechanisms responsible for the senescent changes of the hypothalamic nuclei. It was proposed by Cai that the decrease in slow-wave sleep (SWS) caused the degeneration of the suprachiasmatic nucleus (SCN). Besides, when reviewing the proposal by the European people in television about the senescent pathway for male reproduction on the degeneration of hypothalamic preoptic area by the common knowledge of reduction of sperm production from adipose accumulation in the middle/old age, it was as well demonstrated that the reduced testosterone level from the increased body fat caused the degeneration of the male preoptic sexually dimorphic nucleus (SDN-POA). It seems both the activity-dependent and hormonal regulation of the neuronal numbers are involved in the mechanisms causing the senescence of the hypothalamic nuclei. It is further pointed out that the paraventricular nucleus (PVN) maintaining its neuronal number unchanged in aging may cause many cellular and molecular changes of aging from chronic stress. It is expected that these preliminary considerations could elicit more investigations on the other peripheral causes for the hypothalamic aging, such as the cholesterol, hypertension, and so on.
Effects of Insulin Detemir and NPH Insulin on Body Weight and Appetite-Regulating Brain Regions in Human Type 1 Diabetes: A Randomized Controlled Trial  [PDF]
Larissa W. van Golen, Dick J. Veltman, Richard G. IJzerman, Jan Berend Deijen, Annemieke C. Heijboer, Frederik Barkhof, Madeleine L. Drent, Michaela Diamant
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0094483
Abstract: Studies in rodents have demonstrated that insulin in the central nervous system induces satiety. In humans, these effects are less well established. Insulin detemir is a basal insulin analog that causes less weight gain than other basal insulin formulations, including the current standard intermediate-long acting Neutral Protamine Hagedorn (NPH) insulin. Due to its structural modifications, which render the molecule more lipophilic, it was proposed that insulin detemir enters the brain more readily than other insulins. The aim of this study was to investigate whether insulin detemir treatment differentially modifies brain activation in response to food stimuli as compared to NPH insulin. In addition, cerebral spinal fluid (CSF) insulin levels were measured after both treatments. Brain responses to viewing food and non-food pictures were measured using functional Magnetic Resonance Imaging in 32 type 1 diabetic patients, after each of two 12-week treatment periods with insulin detemir and NPH insulin, respectively, both combined with prandial insulin aspart. CSF insulin levels were determined in a subgroup. Insulin detemir decreased body weight by 0.8 kg and NPH insulin increased weight by 0.5 kg (p = 0.02 for difference), while both treatments resulted in similar glycemic control. After treatment with insulin detemir, as compared to NPH insulin, brain activation was significantly lower in bilateral insula in response to visual food stimuli, compared to NPH (p = 0.02 for right and p = 0.05 for left insula). Also, CSF insulin levels were higher compared to those with NPH insulin treatment (p = 0.003). Our findings support the hypothesis that in type 1 diabetic patients, the weight sparing effect of insulin detemir may be mediated by its enhanced action on the central nervous system, resulting in blunted activation in bilateral insula, an appetite-regulating brain region, in response to food stimuli. Trial Registration ClinicalTrials.gov NCT00626080.
Nonsocial Functions of Hypothalamic Oxytocin  [PDF]
Hai-Peng Yang,Liwei Wang,Liqun Han,Stephani C. Wang
ISRN Neuroscience , 2013, DOI: 10.1155/2013/179272
Abstract: Oxytocin (OXT) is a hypothalamic neuropeptide composed of nine amino acids. The functions of OXT cover a variety of social and nonsocial activity/behaviors. Therapeutic effects of OXT on aberrant social behaviors are attracting more attention, such as social memory, attachment, sexual behavior, maternal behavior, aggression, pair bonding, and trust. The nonsocial behaviors/functions of brain OXT have also received renewed attention, which covers brain development, reproduction, sex, endocrine, immune regulation, learning and memory, pain perception, energy balance, and almost all the functions of peripheral organ systems. Coordinating with brain OXT, locally produced OXT also involves the central and peripheral actions of OXT. Disorders in OXT secretion and functions can cause a series of aberrant social behaviors, such as depression, autism, and schizophrenia as well as disturbance of nonsocial behaviors/functions, such as anorexia, obesity, lactation failure, osteoporosis, diabetes, and carcinogenesis. As more and more OXT functions are identified, it is essential to provide a general view of OXT functions in order to explore the therapeutic potentials of OXT. In this review, we will focus on roles of hypothalamic OXT on central and peripheral nonsocial functions. 1. Introduction Recent progress in studying therapeutic potential of hypothalamic nonaneuropeptide oxytocin has resumed our enthusiasm of its classical physiological functions. In the hypothalamus, OXT is predominantly expressed in two types of neurons, that is, magnocellular neurons in the paraventricular (PVN) and supraoptic (SON) nuclei, and parvocellular neurons in the parvocellular division of the PVN. In magnocellular OXT neurons, OXT and its carrier, neurophysin I, are packaged in membrane-bound large dense-core vesicles and transported down the long axons to the nerve endings in the posterior pituitary or neurohypophysis [1]. In response to increased activity of OXT neurons, OXT is released from the neurohypophysis into the blood [2] to act on variety of peripheral tissues. The magnocellular neurons and the neurohypophysis that contain OXT and its partner peptide, vasopressin (VP, antidiuretic hormone) together form the hypothalamoneurohypophysial system. Lately, OXT is found to be released into other regions of brain [3–5], likely from the terminals of the OXT neurons of the parvocellular division of the PVN and axon collaterals and distal dendrites of magnocellular neurons [6]. In addition to the hypothalamic origin, OXT is also produced in extrahypothalamic regions and peripheral
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