Control of food intake Flashcards
What are the definitions of hunger, appetite, satiety and aphagia
Hunger- discomfort caused by the lack of food and desire to heat- psychological craving for food
Appetite- psychological drive to satisfy the body’s need of food
Satiety- state of being full after eating food
Aphagia- the inability or refusal to swallow
Give examples of cues that tell you when to stop eating
Hunger, satiation and satiety are cues that tell you when to start and stop eating
What are reasons for differences in BMI
-genes (70%)
-how much we eat and its composition
-there are diurnal variation in food metabolism
-hypothalamus responds to the switch between carbohydrate and fat metabolism
What is the role of the hypothalamus
hypothalamus- control centre for appetite and food intake. Controls hunger and thirst
How does the hypothalamus control food intake
The base of the hypothalamus has several nuclei that regulates energy homeostasis
-these nuclei control the appetite; size of helping and our ingestive behaviour
Explain where the satiety centre is located and how it responds when damaged and healthy
Location: ventromedial hypothalamus
If the satiety centre is stimulated (healthy)—-> you stop eating if you have trouble swallowing aphagia via the stimulation of ventromedial nuclei
If the satiety centre is damaged you may experience increased appetite (hyperphagia)
What are other inputs control feeding behaviour?
-Orexigenic and anorexigenic neurotransmitters have been found in the hypothalamus
-Orexigenic neurotransmitters increases appetite
-anorexigenic neurotransmitters decrease appetite
-the Orexigenic and anorexigenic neurotransmitters model feeding behaviour by binding to the hypothalamic nuclei
How is feeding behaviour modulated
feeding behaviour is module by the following hypothalamic sites:
-lateral hypothalamus= hunger/thirst centre
-ventromedial nucleus= satiety centre
Explain the experimental data on the effects of hypothalamic lesions on the food consumption in cats.
Ventromedial hypothalamic lesion- when stimulated it stops the feeling of fullness so the cat overeats and becomes fat
Lateral hypothalamic lesion- when stimulated, the cat feels fullness and the cat undereats and becomes underweight
Explain the roles of dorsomedial, paraventricular and arcuate nucleus
1) Dorsomedial nucleus:
-modulates energy intake
-release of NPY into DMN (Increased eating)
2) Paraventricular nucleus:
-modulates feeding behaviour
Paraventricular nucleus and perifornical hypothalamus;
-controls feeding behaviour
-NPY, opioids —-> increased feeding
-leptin —-> decreased food intake
3) Arcuate nucleus:
-its neurons produce Orexigenic signals (NPY, the opioids, dynorphin, B-endorphin, gelanin, glutamate) —> increased feeding
Explain the roles of the suprachiasmatic nuclei’s and medial amygdaloid complex
1) Suprachiasmatic nucleus:
-location of human body clock
-perception of light-dark cycle
-appetite or the sensation of hunger
2) Medial amygdaloid nucleus:
-sub region of the amygdaloid complex;
-a role for medial amygdaloid nucleus in feeding behaviour has been proposed
-participants in the regulation of food intake
Explain the role of ligands in control of food intake
ligands (agents that mediate their effects via this site):
-5-HT via the 5HT2C and 5-HT1A
-these agents/ligands regulate appetite and food intake by binding to the medial amygdaloid nucleus
Explain what Zimelidine does
Zimelidine- inhibits the reuptake of 5-HT from the synaptic cleft, allowing 5-HT to persist in the synaptic cleft
What is the role of the prefrontal cortex in control of food intake
The prefrontal cortex:
-influences food seeking behaviour
-integrates sensory information from inside and outside the body
-receives emotional and cognitive information from the lambic system
-helps make choices by translating all homeostatic and environmental information into behavioural responses
What is the role of the limbic system in control of food intake
limbic system is a complex system of nerves and networks in the brain; involved in learning, reproductive behaviour, emotions, pleasure etc
-the act of ‘satiation of feeding behaviour’ is associated with motor planning and execution
-overall the corticosteroid-limbic mechanisms of reward are under executive control
What are factors that affect if food is sought or not and the type we ingest
-food preferences
-emotions
-environment
-life style
What signals our appetite?
-glucose blood stimulates glucose-receptors in hypothalamus
Brain has a glucostat:
-decreased glucose in blood —-> induces hunger
-increased glucose in blood —-> induces satiety
Explain the role of gut hormones in control of food intake
-hormones and factors released with a meal play a role in regulating food intake.
-fat ingestion causes CCK release and slowing of gastric emptying (state of fullness)
-CCK and samotastatin are satiety factors
-ingestion of CCK in the brain —-> suppresses appetite
-therefore CCK derivatives may have utility in obesity
Explain the tole of leptin in control of food intake
-fat cells secrete leptin- gene expressed mainly in adipocytes
-controls fat stores by operating a feedback mechanism between adipose tissue and brain
-high correlation of leptin levels with body fat in humans + animals
-administration of leptin can decrease food intake and induce weight loss
-leptin acts on hypothalamus
-increases expression of anorexigenic factors (POMC, CART and CRH)
-inhibits neuropeptide Y
Explain the role Ghrelin in the control of food intake
Ghrelin is an appetite inducing hormone wich stimulates hungry and is released by stomach, pancreas and adrenals.
-it increases central orexins (circulating levels of Ghrelin increase and pre pandial decrease after a meal
-leptin can inhibit secretion of Ghrelin
-Ghrelin suppresses ability of leptin to stimulate anorexigenic factors
Explain the role of obestatin
-produced by epithelial cells of the stomach
-encoded by Ghrelin gene, however opposes effects of Ghrelin on food intake
-suppresses food intake
-antagonises Ghrelin-induced food intake
-obestatin mediates its effects via different receptors to Ghrelin
