Neural + Hormonal mechanisms Flashcards

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1
Q

Homeostasis

A

Mechanism that maintains a stable and constant internal environment; detects if the body has enough nutrients and if not ,corrects this

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2
Q

Turning food ON

A

One system the body has is for turning food ‘on’ where when glucose levels are low hunger increases which activates the lateral hypothalamus (LH) to create feelings of hunger to eat and rise levels again

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3
Q

Turning food OFF

A

Once glucose levels rise again this activates the ventromedial hypothalamus which creates satisfaction to inhibit further feeding

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4
Q

Lateral hypothalamus research

A
  • Began in 1950s when researches found damage to the LH in rats caused aphagia
  • Stimulation of LH elicits feeding behaviour which led to the discovery of switch on for eating
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5
Q

Neuropeptide Y

A

Neurotransmitter found in the hypothalamus which is important for turning on eating
Stanley found repeated injections of NPY into hypothalamus of rats produces obesity

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6
Q

Ventromedial hypothalamus

A
  • Opposite effects; damage to VMH caused rats to over eat leading to hyperphagia
  • Stimulation inhibited feeding suggesting it stops eating due to glucose receptors
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7
Q

Paraventricular nucleus

A
  • Damage to nerve fibres passing through VMH also damages the area of the hypothalamus called the paraventricular nucleus
  • Damage to this area alone can cause hyperphagai (Gold)
  • Also detects specific foods our body needs + responsible for our cravings
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8
Q

Hormonal mechanisms

A
  • 2 main hormones in controlling eating; Ghrelin(increases appetite) and Leptin(decreases)
  • Maintains our body weight at an optimal level by working together
  • Both peripheral signals with central effects
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9
Q

Ghrelin

A

It is released into the stomach + stimulates the hypothalamus ; when bodily resources are low/ under eating gherelin levels increase
-Play a role in determining how quickly we feel hungry after eating ; levels raise high before we eat and go down again for about 3 hours after a meal

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10
Q

Obesity

A

Ghrelin has been important in the development of obesity as stimulating appetite leads to an increase in body weight

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11
Q

Research

A

Ghrelins role in appetite control was first discovered when injected into the blood stream of rats , stimulated food intake.

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12
Q

Leptin

A

Normally produced by fat tissue + secreted into bloodstream then travel to the brain
-Circulating leptin acts as a long term signal of amount of fat stored while short term fluctuations in levels give information on changes in calorific intake

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13
Q

2 major functions

A
  1. By binding receptors in the hypothalamus it counteracts the effects of neuropeptide Y
  2. Increases sympathetic NS activity which stimulates fatty tissue to burn energy
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14
Q

Research

A

Researchers noticed when they administered a new substance to genetically altered obese mice they lost weight becoming known as the substance leptin

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15
Q

*Evaluation

Limitation of homeostasis

A

For a hunger mechanism to be adaptive it must be able to anticipate energy deficits not just react to them therefore the theory that hunger + eating is triggered only when energy levels fall below a desired level is not reality
An adaptive mechanism would promote consumption to maintain bodily resources above the optimum level for the future lack of food availability

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16
Q

Problems with LH

A

The view that it is an on switch for eating has a few problems for example damage to the LH caused deficits in other aspects of behaviour rather than just hunger + other research has shown eating behaviour is controlled by neural circuits that run through the brain not just the hypothalamus showing it is not actually the brains ‘eating centre’

17
Q

Research support for Ghrelin

A

Wren et al conducted a double blind study of 9 healthy volunteers - either received intravenous ghrelin or saline infusion + one week later the same pps took the other condition
Was measured in terms of amount of food taken and consumed at a free choice buffet ; results showed a significant increase in food consumption in ghrelin condition compared to saline infusion with a mean difference of about 28%