Control of Food Intake Flashcards
What is hinger, appetite and saitety?
Hunger: a strong physiological craving/drive for food/sensation of emptiness in the stomach
Appetite: psychological desire to satisfy the body’s needs of food; a hunger-stimulated response
Satiety: state of being full after eating food
What is aphasia and hyperphagia?
Aphagia: the inability or refusal to swallow
Hyperphagia/polyphagia: an abnormal desire for food (unsatisfied extreme drive to eat)
How and why is satiety induced?
Satiety signals function to prolong the interval until hunger or the onset of the next meal
Mechanical distension of the stomach wall is relayed to the brain (afferent neural fibres) to induce satiety
CCK (satiety signal) sensitises the vagal nerves to mechanical stimulation
CCK also reaches the brain (inhibits feeding= a catabolic effect)
What physiological factors cause early satiety?
Reduced capacity to eat
A small meal → state of early satiety. Could be the effect of gastroparesis (reduced gastric emptying)
Cancer, reflux, peptic ulcer
Vagotomy impairs accommodation and emptying, so can be a cause for early satiety in some patients
Describe how the hypothalamus is involved in food intake control
The base of the hypothalamus has several nuclei that regulate energy homeostasis.
Feeding/hunger/thirst centre= lateral hypothalamus
Stimulation of lateral hypothalamus ↑ feeding
Lesion of lateral hypothalamus leads to aphagia
The satiety centre = hypothalamus [ventromedial nuclei]
Stimulation of ventromedial nuclei → aphagia (swallowing difficulty)
Lesions of ventromedial nuclei → hyperphagia
What are orexigenic and anorexigenic neurotransmitters?
Orexigenic and anorexigenic neurotransmitters have been found in the hypothalamus and ventromedial nuclei
Orexigenic neurotransmitters: ↑appetite
Anorexigenic neurotransmitters: ↓ appetite
The orexigenic and anorexigenic neurotransmitters module feeding behaviour by crossing the bbb and binding to hypothalamic nuclei
Arcuate nucleus: Its neurons produce orexigenic signals (eg NPY) to cause ↑ feeding
What is the DMN?
Dorsomedial nucleus (DMN) = hunger centre Release of Neural peptide Y (NPY) into DMN stimulates feeding
Describe the role of the prefrontal cortex in control of food intake
The prefrontal cortex:
Integrates sensory info from in and outside the body
Receives emotional and cognitive info from the limbic system
Helps u make food choices by translating all of the homeostatic and environmental info into (adaptive) behavioural response
What is the effect of glucose on feeding behaviour?
[glucose]blood: Stimulates gluco-receptors in hypothalamus
↓[glucose]blood in the brain →induces hunger
↑[glucose]blood → induces satiety
How can fat deposition control food intake?
Fat cells (adipocytes) secrete leptin
Leptin controls fat stores by increasing expression of anorexigenic factors.
It inhibits NPY, which stimulates feeding
The larger the adipose tissue, the greater the leptin secreted by the adipose tissue.
Leptin administration can decrease food intake, induce weight loss (and increase energy expenditure)
What can leptin resistance lead to?
Leptin resistance may lead to binge eating, despite being obese
Hyperphagia and severe obesity occurs in in humans with leptin deficiency or leptin receptor defects
What is Ghrelin?
Fast-acting and stimulates food intake. Released by stomach, pancreas, adrenals
Increases central orexins, e.g. NPY, and AgRP (= hunger signals)
Circulating levels of ghrelin ↑ fasting and ↓ after a meal (post-prandial)
Ghrelin suppresses the ability of leptin to stimulate anorexigenic factors, so inhibits leptin
What is obestatin?
Produced by epithelial cells of stomach
Encoded by ghrelin gene, but it opposes the effects of ghrelin on food intake
