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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.
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.
The homeostatic feeding response to fasting is under chronostatic control
Published in Chronobiology International, 2018
David Rivera-Estrada, Raúl Aguilar-Roblero, Claudia Alva-Sánchez, Iván Villanueva
To further differentiate among these two mechanisms of control of food intake, and to evaluate the relative importance of the time drive in determining feeding behavior, we studied the effect of (a) the onset at different times of the light-dark cycle of fixed 24-h food deprivation, and (b) increasing food deprivation intervals initiated at the same time of day (thus increasing homeostatic demand) on the compensatory feeding response. If the amount of food intake is dependent only on homeostatic regulation, a 24-h fasting would result in similar intake independently of the time it starts and ends. Furthermore, increasing the time of fasting would produce a proportional increase in the ensuing food intake. We hypothesize that a chronostatic control, as depicted above, would cause the compensatory feeding response to decrease at certain time points matching the circadian feeding pattern, in spite of a strong homeostatic motivation to increase.
Interaction between central GABAA receptor and dopaminergic system on food intake in neonatal chicks: role of D1 and GABAA receptors
Published in International Journal of Neuroscience, 2018
Mona Hashemzadeh, Morteza Zendehdel, Vahab Babapour, Negar Panahi
Feeding behaviour is a complex physiologic phenomenon which interacts via diverse signals from the central and peripheral tissues [1,2]. In the central nervous system (CNS), several neurotransmitters interact by a wide distributed neurological network on food intake regulation [3]. The homeostasis of the food intake regulates by complex neurochemical mechanisms in several parts of the brain such as striatum, amygdala and hypothalamus [3]. γ-Aminobutyric acid (GABA) is an important neurotransmitter which has many physiologic actions such as anti-convulsion, pain alleviation, sleep, memory, regulation of respiration and appetite [4]. The GABAergic system acts via distinct receptors, including the GABAA, GABAB and GABAC receptors [5]. The GABAA and GABAC receptors are part of a macromolecular complex coupled to a Cl− ionophore while GABAB is a metabotropic receptor belonging to G-protein-coupled receptors (GPCRs) [6]. Intracerebroventricular (ICV) injection of GABAA and GABAB agonists increases feeding in layer [2,7] but GABAB agonist has no effect on broiler [8]. Also, the stimulatory role of GABA in the regulation of food intake was reported in the turkey [9].