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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
The hypothalamic nuclei participate in the control of food intake; the lateral nuclei serve as feeding centres and the ventromedial nuclei, the satiety centres. The arcuate nuclei of the hypothalamus are the sites in the hypothalamus where several hormones from fat tissue and the gut converge to regulate food intake as well as energy expenditure. The hypothalamus receives signals about gastric filling and blood levels of glucose, amino acids and fatty acids that indicate satiety and signals from gut hormones, hormones from adipose tissue and the cerebral cortex (e.g. smell, sight, taste) that affect feeding behaviour.
Endocrine Functions of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Early studies identified the hypothalamus as a critical feeding center, based on the induction of a significant increase in feeding behavior by lesions in the ventromedial hypothalamus (VMH) of the rat, whereas lesions in the ventrolateral hypothalamus led to reduced feeding behavior and malnutrition. Figure 4.8 illustrates the central role of the hypothalamus as an integrator of information on the nutritional status of the body and as a coordinator of endocrine, autonomic, and behavioral responses that regulate feeding behavior and appetite.
Eating – You, the World, and Food
Published in Emily Crews Splane, Neil E. Rowland, Anaya Mitra, Psychology of Eating, 2019
Emily Crews Splane, Neil E. Rowland, Anaya Mitra
All animals eat, and the study of feeding behavior of animals can give us important insights into human behavior. Further, for animals that have similar feeding habits to our own (i.e., mammalian omnivores, like rats), there is every reason to believe that some of the physiological and brain mechanisms underlying feeding are similar to our own. Although many aspects of feeding and the brain can be directly studied in humans, and many examples will be given in this book, there are some scientific procedures and measures that we cannot perform in humans but instead turn to suitable animal models to address the questions. Most such research uses rats or mice, and we will occasionally refer to such studies. All animal research is highly regulated and reviewed by both institutional and national professional entities with regard to rigorously humane treatment and scientific necessity. Likewise, all research with humans is regulated by institutional review boards, and includes not only aspects of safety but also confidentiality of records.
Five years of Avoidant/Restrictive Food Intake Disorder: no consensus of understanding among health professionals in New Zealand
Published in Speech, Language and Hearing, 2022
Bianca N. Jackson, Léa A. T. Turner, Georgina L. Kevany, Suzanne C. Purdy
Within a continuum of feeding behaviours, picky eating can be considered both a typical and atypical feeding behaviour, occurring developmentally in toddlers (Aldridge et al., 2018; Taylor, Wernimont, Northstone, & Emmett, 2015). The developmental picky eater may be differentiated from a child with a feeding disorder by factors such as the length of time the challenging eating behaviour persists (Marshall, Hill, Ware, Ziviani, & Dodrill, 2015), and the degree to which it impacts participation in mealtimes (Aldridge et al., 2018). The lack of a specific definition prevents clinicians from accurately identifying problematic picky eating in children (Marshall et al., 2015). The lack of consensus across the board not only hinders the collaborative approach to caring for individuals with feeding disorders, but inhibits health professionals and researchers to adequately determine conditions, prevalence, and therefore treatment and support for individuals and families affected by feeding disorders. This makes it difficult to differentiate picky eating behaviours that are developmentally sound compared to those presenting with more severity, which consequently influences the rate of prevalence in practice (Marshall et al., 2015). With the introduction of a new diagnostic category, many had hoped this would clarify understanding, guidelines and in turn clinical practice (Bryant-Waugh, 2013; Nakai et al., 2017; Norris & Katzman, 2015; Ornstein et al., 2013); the more extreme picky eater now being classified as having new diagnosis of Avoidant/Restrictive Food Intake Disorder (ARFID).
Central microinjection of phytohormone abscisic acid changes feeding behavior, decreases body weight, and reduces brain oxidative stress in rats
Published in Nutritional Neuroscience, 2019
Monavereh Soti, Mehdi Abbasnejad, Razieh Kooshki, Saeed Esmaeili-Mahani
Oxidative stress, an imbalance between the oxidants and antioxidants, is a major risk factor for the induction of metabolic diseases. In a normal situation, antioxidant enzymes, such as catalases and peroxidase serve a defending role in brain via inactivation of detrimental oxidants which are produced in metabolic procedures.23 It has been indicated that nutritional treatments raise antioxidant capacity and could be helpful in suppressing clinical features of disrupted metabolism.24,25 It has been demonstrated that the critical regulatory sites for the integration of metabolic signals are brain stem regions including solitary tract, dorsal vagal complex, and diencephalon centers mainly hypothalamus nuclei.26,27 Therefore, biochemical analysis of such regions might be helpful to identify the mechanism of drugs or agents on feeding behavior.
High-fat simple carbohydrate (HFSC) diet impairs hypothalamic and corpus striatal serotonergic metabolic pathway in metabolic syndrome (MetS) induced C57BL/6J mice
Published in Nutritional Neuroscience, 2019
DSouza Serena Stephen, Asha Abraham
A better understanding of the disruption of the serotonergic pathway would be possible if the mice were fed for a longer duration of time. Also, tryptophan content in the feed might have influenced the study. Unfortunately, we have not measured typtophan content in the feed. A limitation of our study is that we have not studied the enzyme aromatic amino acid decarboxylase (AADC) which catalyzes the conversion of 5-hydroxytryptophan to serotonin. It is also known to catalyze the conversion of l-DOPA to dopamine and is therefore an enzyme which controls the production of two important monoamines – serotonin and dopamine. We observed a lower dopaminergic tone in the HFSC-fed C57BL/6J mice as compared to the control-fed C57BL/6J mice.44 The path taken by the AADC depends on the concentration of the substrate. The dominating substrate that is the substrate present at a higher concentration will determine the pathway taken thereby inhibiting the other pathway (competitive inhibition).45 Thus our study clearly shows derailment of serotonergic pathway in the hypothalamus precedes peripheral pathways in HFSC-fed MetS-induced mice. These findings may have implications in the feeding behavior as well as cognitive decline and dementia associated with metabolic syndrome patients.