China
Africa
Explore chapters and articles related to this topic
Physiology of Obesity
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Two groups of neurons in the arcuate nuclei of the hypothalamus can stimulate or inhibit feeding and energy expenditure: (i) pro-opiomelanocortin (POMC) neurons which produce α-melanocyte stimulating hormone and cocaine-amphetamine regulated transcripts (CART) and (ii) neurons that produce neuropeptide Y (NPY) and agouti-related protein (AGRP). Activation of NPY and AGRP neurons increase appetite and feeding and decrease energy expenditure (orexigenic), whereas activation of POMC neurons decrease appetite and feeding and increase energy expenditure leading to reduced energy stores (anorexigenic). NPY, AGRP, ghrelin, melanin-concentrating hormone, glutamate, γ-aminobutyric acid, cortisol, endocannabinoids, endorphins, galanin and orexins A and B are the neurotransmitters that increase appetite and feeding (orexigenic), whereas Leptin, α-melanocyte stimulating hormone, cholecystokinin (CCK), serotonin, norepinephrine, insulin, glucagon-like peptide 1, peptide YY, corticotropin-releasing hormone and CART have a role in satiety. The amygdala (in the limbic system) and prefrontal cortex play an important role in the control of appetite and their activities are coupled with those of the hypothalamus.
Anorexia in Cancer
Published in Victor R. Preedy, Handbook of Nutrition and Diet in Palliative Care, 2019
Alessio Molfino, Maria Ida Amabile, Alessandro Laviano
Under physiological conditions, the hypothalamus plays a relevant role in the control of appetite and food intake and in the regulation of energy expenditure (Molfino et al. 2010). It receives peripheral drives and transduces them into neuronal activities (Laviano et al. 2008). Within the arcuate nucleus, a relevant hypothalamic area for the regulation of energy expenditure, two different neuronal cells are involved in energy balance regulation. The first population of neurons synthesizes proopiomelanocortin (POMC), a polypeptide precursor molecule of smaller active peptides, the melanocortins, which exert anorexigenic effects (Abdel-Malek 2001; Cone 2005). The second subset of neurons expresses neuropeptide Y (NPY) and agouti-related protein (AgRP). Both AgRP and NPY highly stimulate appetite. Several hormones, such as insulin, ghrelin and leptin, reach NPY/AgRP and POMC neurons from the periphery, increasing or downregulating food intake (Laviano et al. 2008; Molfino et al. 2010). The melanocortin system plays a crucial role in the homeostasis of energy metabolism, starting with activation of POMC neurons, in specific conditions, and releasing melanocortins from POMC axon terminals leading to suppressed food intake and increased energy expenditure. Simultaneously, the activity of the arcuate AgRP/NPY system is suppressed (Laviano et al. 2008). Anorexia is related, at least in part, to dysfunction of the melanocortin system, consisting of hyperactivity of POMC neurons and decreased activity of NPY/AgRP neurons, leading to hypothalamic resistance to peripheral inputs signaling energy depletion (Laviano et al. 2008).
Noninsulin-Dependent Animal Models of Diabetes Mellitus
Published in John H. McNeill, Experimental Models of Diabetes, 2018
Christopher H. S. McIntosh, Raymond A. Pederson
Recently, a human gene, located on Chromosome 16q22, was identified and named agouti-related transcript (Agrt; Art)153 or agouti-related protein (Agrp),168 because of its similarity to Agouti. This gene encodes a 132 amino acid protein that is 25% identical to human agouti, the highest degree of identity residing within the C-terminus. The murine homologue is a 131 amino acid protein and 81% identical to the human version. The gene is expressed primarily in the adrenal (cortex and medulla), subthalamic nucleus, and hypothalamus in both human and mouse,153,168 with low-level expression in the testis, lung, and kidney. Although the function of the gene product is at present unclear, it is a selective antagonist of MC-4R, is concentrated in the ARN and median eminence, and there is a tenfold upregulation in the hypothalamus of ob and db mice. This protein is therefore probably important in feeding, and may act via MC receptors. The fact that Bardet-Biedl syndrome maps near to this locus (16q21) may also be of significance.153 Overexpression of Art protein in transgenic mice resulted in weight gain, increased circulating insulin, delayed hyperglycemia, but no change in coat color.168,169 Hypertrophic adipose tissue and pancreatic islets were also evident.
Voglibose-mediated alterations in neurometabolomic profiles in the hypothalamus of high-fat diet-fed mice
Published in Nutritional Neuroscience, 2019
Soo Jin Yang, Hyun Ju Do, Youngae Jung, Geum-Sook Hwang, Min-Jeong Shin
The hypothalamus is the brain region responsible for sensing the nutritional status in the gastrointestinal tract and it controls food intake via anorexigenic [proopiomelanocortin (POMC)/cocaine- and amphetamine-regulated transcript] and orexigenic [agouti-related protein (AgRP)/neuropeptide Y] neuronal regulation.9,10 Peripheral hormones, including leptin, insulin, and ghrelin, are released in response to dietary intake and the energy/nutrients status and they stimulate or inhibit specific neurons via direct inputs into specific neuronal cell types at the levels of gene transcription, membrane polarization, and synaptic plasticity.11,12 Given that the brain is the main integrating center responsible for coordinating signaling related to food intake and weight changes, it is necessary to investigate brain signaling and neurometabolome profiles to explain gut–brain communication. Hypophagic effects of VO have been reported previously, but hypothalamic regulation by VO has not been investigated. Therefore, we hypothesized that VO prevents weight gain by altering the neurometabolome profile in the hypothalamus to reduce food intake. To test this hypothesis, we assessed metabolite profiles in the hypothalamus of standard or HF diet-fed mice in the absence or presence of VO.
Sex-dependent effects of MC4R genotype on HPA axis tone: implications for stress-associated cardiometabolic disease
Published in Stress, 2019
Aki T-B. Chaffin, Yanbin Fang, Karlton R. Larson, Joram D. Mul, Karen K. Ryan
The MC4R is a G protein-coupled receptor expressed widely in the adult central nervous system (Cone, 2005; Tao, 2010). Its activity is coordinated by opposing actions of its endogenous agonist, αMSH, and its endogenous antagonist, agouti-related protein (AgRP) (Fong et al., 1997; Ollmann et al., 1997; Shutter et al., 1997). In addition, the receptor has intrinsic constitutive activity on which AgRP can act as an inverse agonist (Srinivasan et al., 2004). αMSH producing neurons in the arcuate nucleus of the hypothalamus are activated by restraint stress (Liu et al., 2007) and provide melanocortinergic input to MC4R-expressing neurons in key stress and feeding-regulatory brain regions including the paraventricular nucleus of the hypothalamus (PVN), the medial amygdala (MeA), and the nucleus accumbens (NAc) (Balthasar, 2006; Wang et al., 2015). Activation of MC4Rs by αMSH or pharmacological agonists acutely stimulates the HPA axis in male rats and mice (Liu et al., 2013) and induces weight loss by reducing caloric intake and increasing energy expenditure in both sexes (Fan et al., 1997; Hamilton & Doods, 2002). Conversely, loss of MC4R function (Ryan et al., 2014) or its pharmacological blockade (Kokare et al., 2010; Liu et al., 2007; Serova et al., 2013) blunts acute restraint stress-induced corticosterone elevation in male rats and mice. MC4R loss-of-function also induces weight gain by increasing caloric intake and decreasing energy expenditure in both sexes (Huszar et al., 1997). Our results (Figure 4) are consistent with these reports.
Food Aversion during Cancer Treatment: A Systematic Review
Published in Nutrition and Cancer, 2023
Aline de Araújo Pereira, Emylliane Santana dos Reis, Mariana Julião Guilarducci, Julia Silva e Oliveira, Júnia Maria Geraldo Gomes
The immune system and CT promote the release of cytokines, mainly interleukin 1 (IL-1), interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), and interferon γ (IFN-γ) (29, 30). The cancer inflammation dysregulates the pro-opiomelanocortin (POMC) and Agouti-related protein (AgRP) neurons, as well as stimulates the hypothalamic melanocortin 4 receptor (MC4-R), favoring appetite loss and food aversion formation (31).