This presentation discusses the neural mechanisms that control food and water intake in the human body. It begins with distinguishing between hunger and appetite, with hunger being the physiological drive to eat and appetite being the psychological drive. The hypothalamus plays a key role in regulating eating behavior through centers that initiate eating in the lateral hypothalamus and inhibit eating in the ventromedial hypothalamus. Peripheral signals like ghrelin, CCK, and leptin also influence these centers. Similarly, osmoreceptors detect water levels and stimulate thirst centers in the hypothalamus to maintain water balance. Damage to certain areas can impact intake, like lesions in the ventromedial hypothalamus causing overeating.
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Neural mechanism of food and water intake
1. COLLEGE OF HEALTH SCIENCES
SCHOOL OF MEDICINE
DEPARTMENT OF MEDICAL PHYSIOLOGY
12/13/2018 1
ADVANCED NUEROPHYSIOLOGY
PRESENTATION ON
NEURAL MECHANISM OF FOOD AND WATER INTAKE
By :-KIFLAY MULUGETA
2. Presentation outline
• Objective
• Introduction
• Hunger vs appetite
• Role of neural mechanisms in control of eating behavior
• Role of neural mechanisms in Control of water intake and thirsty
• Summary
• Reference
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3. Objectives
• Explain the difference between appetite and hunger
• Discuss Role of neural mechanisms in control of eating behavior
• Discuss Role of neural mechanisms in Control of water intake and
thirsty
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4. Introduction
• The maintenance of the body weight at a stable level is a major
determinant in keeping the higher animals and mammals survive.
• The body weight depends on the balance between the energy intake
and energy expenditure.
• Increased food intake over the energy expenditure of prolonged time
period results in an obesity.
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5. Con’d
• A complex of central and peripheral physiological signals is involved in
the control of the food intake.
• Centrally, the food intake is controlled by the hypothalamus, the
brainstem, and endocannabinoids and peripherally by the satiety and
adiposity signals.
• This regulatory system is formed by multiple interactions between the
gastrointestinal tract (GIT), adipose tissue, and the central nervous
system (CNS).
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6. Hunger vs Appetite
Hunger
• Physiological (internal) drive to eat
• The feeling that prompts thought
of food and motivates food
consumption
• Influenced by nutrients in the
bloodstream, eating patterns,
climate, etc
• Controlled internally
Appetite
• Psychological (external) drive to eat
• Often in the absence of hunger
• Often for particular type of food
• Combination of internal and
external signals drive us to eat
• Appetite is affected by a variety of
external forces
• Not a perfect system; desire to eat
can be overwhelming
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8. Role of neural mechanisms in eating behavior
• Homeostasis is maintained via a negative feedback loop: this
assumes that all body variables have a set point (range)
• The digestive tract and the hypothalamus play a significant role in
homeostasis in eating behaviour.
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9. Homeostasis
• Involves mechanisms that can detect and correct.
• Detect – check whether the body has enough nutrients (internal
environment)
• Correct – restore the body to its optimal state.
• Body evolved 2 separate systems in order to cope with the time lag
between restoring equilibrium and body registering their effect.
• Turning eating on and turning eating off!
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11. Neural Centers for regulation of food intake
• Most hormones are secreted from the glands that produce them
under the influence of stimulating hormones from the hypothalamus.
• The hypothalamus is a part of the brain involved in the control of
involuntary activity in the body; contains many centers of neural
control such as temperature, hunger, appetite and thirst.
• These hormones in turn are activated by releasing hormones from
the pituitary gland. 11
12. The lateral hypothalamus
• Contains the feeding centre
• This initiates eating.
• It responds to decreased blood glucose and increase in ghrelin a
hormone released from the stomach when it is empty.
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14. Ventromedial hypothalamus
• Contains the satiety centre
• This inhibits eating behaviour when we are full.
• Responds to – an increase in blood glucose,
– a decrease in ghrelin and to release of CCK, a hormone released when food is
detected in the duodenum
– leptin a long term satiety signal released by fat cells.
• Evidence= Rats whose VMH had been lesioned developed overeating and
obesity 14
15. Other Neural Center that enter into feeding
• Another area of the hypothalamus Mammillary bodies activate feeding
reflexes such as licking the lips and swallowing
• Another area higher centers than hypothalamus control feeding mainly
appetite include amygdala and cortical areas of the limbic system which is
coupled with the hypothalamus
• Amygdala is responsible for detecting the flavor intensity of particular food
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16. Con’d
• Evidence
• Destructive lesions in the amygdala increase feeding
• The cortical regions of the limbic system have areas when stimulated
can increase or decrease feeding activities
• It is believed that theses centers with amygdala and hypothalamus
responsible of the quality of food that is eaten
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17. Role of peripheral metabolic signals to the brain
• Neuropeptide Y –Rats injected with neuropeptide Y continue eating
large amounts of food even when full
– It also seems to cause a preference for carbohydrates
• CCK –released into bloodstream during meals
– Causes reduction in appetite.
– Suppresses weight gain
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18. Con’d
• Ghrelin: also called hunger hormone
Is produced in the stomach and brain
induces food intake
• Orexin: Also called Hypocretins – neurotransmitter hormones that
increase food intake,
• Synthesized in neurons located in the lateral Hypothalamus
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19. Neural mechanism of water intake
• By two mechanisms:
1. Osmoreceptors in the supraoptic N. are sensitive to osmolarity of
plasma and ECF.
Excess water loss and dehydration, causes an ↑ in osmolarity of ECF,
→stimulate osmoreceptors → release ADH
↑ water reabsorption → normal osmolarity of ECF.
Excess water intake leads to → ↓ osmoreceptors → ↓ ADH.
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20. Con’d
2. By thirst mechanism
• A thirst centre is in the Lateral Hypothalamus → stimulated by
intracellular dehydration → causes water drinking
• Increase in plasma osmolarity, decrease in ECF volume, haemorrage,
Angiotensin II and dryness of mouth promote water drinking and
thirst mechanism thus maintains water balance
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21. Clinical importance
Prader-willi syndrome
• In Prader-Willi syndrome over production of ghrelin → hyperphagia →
obesity
Diabetes Mellitus
• In Diabetes Mellitus the Ventromedial Nucleus (VMN) is deprived of
glucose due to the deficiency of Insulin →↑ activity of Feeding centre →
Hyperphagia
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23. Reference
• Endocrine regulations, Vol. 51, No. 1, 52–70, 2017
• Walter F Boron, Emile L Boulpaep. (2017)(Third). Medical Physiology.
• Broberger, C. Brain Regulation of Food Intake and Appetite Molecules
and Networks. Journal of Internal Medicine 2005
• The Regulation of Food Intake in Humans Mark Hopkins, John
Blundell, Jason Halford, Neil King, and Graham Finlayson 2016
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Glosary
appetite: the integrated response to the sight, smell, thought, or taste of food that initiates or delays eating.
• hunger: the painful sensation caused by a lack of food that initiates food-seeking behavior
• hypothalamus: a brain center that controls activities such as maintenance of water balance, regulation of body temperature, and control of appetite.
satiation: the feeling of satisfaction; and fullness that occurs during a meal and stop eating. Satiation determines how much food is consumed during a meal.
• satiety: the feeling of fullness and satisfaction that occurs after a meal and inhibits eating until the next meal. Satiety determines how much time passes between meals.
The results show that when we eat for pleasure, the body releases chemicals that trigger a feeling of reward, and this may lead to overeating, the researchers said. "Understanding the physiological mechanisms underlying this eating behavior may shed some light on the obesity epidemic,“
The researchers periodically measured levels of two chemicals involved in the body's reward system: 2-arachidonoylglycerlo (2-AG) and ghrelin.
The found that the blood levels of these chemicals increased when participants ate their favorite foods, but not when they ate the less palatable foods.
This increase suggests that the body's reward system overrides the body's signal that enough has been eaten to restore energy,
Set Point Theory We have seen that the Dual-Centre hypothesis - which visualized the LH as a feeding centre and the VMH as a satiety centre - could not explain the long term effects of lesions to these areas. One solution to this problem was to suggest that these nuclei controlled body weight through a set-point mechanism .
According to this view:
LH lesions reduced the set point for body weight. Lesioned rats maintain body weight at a new lower level
VMH lesions increased the set point for body weight . Lesioned rats maintain body weight at a new higher level
2 areas of the hypothalamus involved in eating behavior
– Ventro Medial Hypothalamus (VMH) as a "satiety centre" = full up!
– Lateral Hypothalamus (LH) as a "Hunger centre".
• NOTE: VMH and LH are also called VMN and LN sometimes
Centre is a cluster of nerve cells governing a specific bodily process
a place where some particular activity is concentrated
CCK= Neurotransmitters and modulators that decrease food intake
Neuropeptide Y=Neurotransmitters that increase food intake A neuropeptide that stimulates the
contraction of the gallbladder with release
of bile and the secretion of pancreatic
enzymes into the small intestine. CCK is
secreted by cells lining the upper intestine
and by the hypothalamus. Hypothalamic
cholecystokinin is a neurotransmitter.
Arcuate nucleus of hypothalamus
– Contains two clusters of appetite regulating neurons
• Neurons that secrete neuropeptide Y (NPY) – Increases appetite and food intake
• Neurons that secrete melanocortins – Suppress appetite and food intake
Oleoylethanolamide (OEA) produced in the duodenum and acts via the vagus nerve decrease body weight through activation of the nTS to decrease appetite