Control of food intake Flashcards
How does an impaired ability of the stomach to accommodate and a delay in the rate of gastric emptying give rise to early satiety
If vagotomy is undergone (removal of vagus nerve), accommodation and emptying is impaired. This leads to early satiety and the feeling of fullness in 5% of vagotomy cases.
Other tissues and organs release other factors which can mediate satiety (hunger or urge to eat), from the deposits from the GI tract, the CNS, and etc.
What are the differences between hunger, appetite and satiety (and aphagia and hyper/polyphagia)
Hunger- Discomfort caused by lack of food and the desire to eat - Physiological craving/drive for food/sensation of emptiness in the stomach
Appetite - Psychological desire/drive to satisfy the body’s needs of food, hunger-stimulated response
Appetite can be influenced by factors such as presentation, smells, ethnic origins, emotional factors etc
Satiety - State of being full after eating food. Tells you to stop eating and satisfaction between meals.
Aphagia: Inability or refusal to swallow
Hyperphagia/polyphagia: Abnormal desire for food
What is the role of afferent nerves from the stomach and small intestine in the regulation of food intake and the genesis of the sensation of fullness
What is the hypothalamic nuclei
Nuclei found at the base of the hypothalamus that regulate enery homeostasis - Appetite, size of helping and ingestive behaviour
Discuss the roles of the important nuclei and their neurotransmitters
Neurotransmitters/factors are released by cells that stimulate each nuclei, causing a response.
Satiety centre - Hypothalamus (ventromedial nuclei) - Stimulation leads to aphagia.
Lesions of ventromedial nuclei lead to hyperphagia.
Feeding/hunger/thirst centre - At the lateral hypothalamus - Lateral hypothalamic nuclei
Stimulation - Increased feeding
Lesion - Aphagia
Orexigenic and anorexigenic neurotransmitters in the hypothalamus can bind to the nuclei and cause increase/decrease in appetite
It is possible to experimentally modulate feeding behaviour in animals. Hypothalamic lesions in the VM nuclei, a cat would gain weight as it eats more. A LH nuclei lesion, there is a loss of appetite and the cat loses weight.
Dorsomedial nucleus (DMN) - Modulates energy intake (hunger centre)
Release of NPY (neural peptide Y) into DMN - increases feeding
Paraventricular nucleus (PVN) - Modulates feeding behaviour - Paraventricular nucleus and perifornical hypothalamus
Secretes NPY, opioids -> Increase feeding
Leptin -> Decreases food intake (although this may be bypassed by other factors)
Arcuate nucleus
Neurons produce orexigenic signals (NPY, opioids, etc) to increase feeding.
Suprachiasmatic nucleus - Human body clock
Perception of circadian rhythms, appetite -> mood/drive to eat
Medial amygdaloid nucleus
Participates in regulation of food intake
Ligands - 5-HT regulate appetite and food intake by binding to medial amygdaloid nucleus. Zimelidine inhibits 5-HT reuptake, so 5-HT persists in the synaptic cleft. Binds to brain nuclei and stimulates, reducing food intake.
What is the role of endocrine in the short and long term regulation of food intake
Prefrontal cortex - influences food-seeking behaviour
Integrates sensory information frm in and out of body, receives emotional and cognitive information frm the limbic system, helps the indivdual made a behavioural response
Limbic system - Complex system of nerves and networks in the brain, areas concerned with instinct, learning, reproductive behaviour, emotions/mood, pleasure
Satiation - associated with motor planning and execution.
How do blood glucose levels signal our appetite
Stimulates gluco-receptors in hypothalamus
Brain has glucostat
Decrease blood glucose -> Hunger
Increase blood glucose -> Satiety
Diabetic patients feel hungry as blood glucose is not taken up.
Cold -> Increase in appetite
Hot -> Decrease in appetite
