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Unit 7 Physiology Lec.7

The document discusses the regulation of appetite and hunger through various mechanisms in the body and hypothalamus. It defines concepts like hunger, appetite, and satiety and explains how centers in the hypothalamus control food intake. It also outlines factors like hormones and peptides that influence appetite and mechanisms like glucostatic, lipostatic, peptide and hormonal that regulate food intake and energy balance.

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Akeil Akeil
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15 views

Unit 7 Physiology Lec.7

The document discusses the regulation of appetite and hunger through various mechanisms in the body and hypothalamus. It defines concepts like hunger, appetite, and satiety and explains how centers in the hypothalamus control food intake. It also outlines factors like hormones and peptides that influence appetite and mechanisms like glucostatic, lipostatic, peptide and hormonal that regulate food intake and energy balance.

Uploaded by

Akeil Akeil
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Obesity and appetite control

• Differentiate between hunger sensation, appetite and satiety.


• Central control of appetite: hypothalamic hunger and satiety centres.
• Adipostat factor: leptin.
• Gut hormones: cholecystokinin; pancreatic polypeptide and peptide
YY; ghrelin.
 Hunger = physiological sensation of desiring food.

Increased by: empty stomach, hypoglycemia, ghrelin and glucagon.

• Appetite is the psychological desire to eat. Associated with sensory

experiences or aspects of food.

• Satiety: is the feeling of fullness and satisfaction that occurs after a meal

and inhibits eating until the next meal.


Regulation of hunger and food intake
Hunger center (Feeding center)

• Situated in the lateral hypothalamic nucleus.


• It is always active.
• Stimulation → (hyperphagia) → obesity.
• Destruction → (anorexia).
Satiety center

• Situated in the ventromedial nucleus of the hypothalamus.


• Causes temporary inhibition of feeding center after eating.
• Stimulation → (anorexia).
• Destruction → (hyperphagia) → obesity (hypothalamic obesity).
hunger and satiety centers
feeding satiety
center center
INHIBITION
LATERAL VENTROMEDIAL
HYPOTHALAMUS HYOTHALAMUS

food intake
Mechanism of regulation of food intake

1. Glucostatic mechanism.
2. Lipostatic mechanism.
3. Peptide mechanism.
4. Hormonal mechanism.
5. Thermostatic mechanism.
Glucostatic mechanism

Cells of satiety center function as (Glucostats), which are stimulated by


increased blood glucose level within the body`s physiological limits.
- Eating → ↑ glucose level → Glucostats stimulated → satiety center
activated → hunger center inhibited → stopping of eating.
once blood glucose level increases and the cycle repeats itself.
- After hours from stopping eating → ↓ glucose level → Glucostats
inhibited → satiety center inhibited → hunger center activated →
eating.
What happens in hyperglycemia of diabetes?
Feeding Eating
center
stimulated starts

Blood
Glucostats sugar
inhibited
rises

Blood
Glucostats
glucose
stimulated
drops

Satiety
Eating
center
stops
stimulated
Inhibition
of feeding
center
Lipostatic mechanism

• The lipostat or (adipostat) is likened to a thermostat.


• ↑ fat stores → adipostat switches on fat burning metabolic processes.
• ↓ fat stores → adipostat switches off fat burning metabolic processes.
• Thus fat stores are regulated by the lipostat increasing or decreasing fat
metabolism.
• Leptin is a peptide secreted by adipocytes that plays an important role
in lipostat mechanism.
• Leptin acts through specific neuropeptides in hypothalamus
called Neuropeptide Y which is secreted in small intestine,
medulla and hypothalamus.
• Normally, this peptide stimulates the food intake. But, leptin
inhibits neuropeptide Y, leading to stoppage of food intake.
• Adipose tissues increases → adipocytes secrete leptin → crosses the
BBB → hypothalamus → inhibits Neuropeptide Y (stimulator of hunger
center) → loss of appetite → stopping food intake and stimulates
utilization of fat stores for energy production.
• Neuropeptide Y secreted from small intestine, medulla and
hypothalamus.
Defective leptin receptors (or leptin pathways)
can lead to obesity
Leptin receptor deficiency

• is a condition that causes severe obesity beginning in the first


few months of life. Affected individuals are of normal weight
at birth, but they are constantly hungry and quickly gain
weight.
• Most obese people appear to have defective leptin receptors
(or leptin pathways) in the appetite centers of the CNS. Their
circulating leptin levels are already several times higher than
those in individuals of normal body weight.
Peptide Mechanism
• Peptides, which increase the food intake (orexigenics):
1. Ghrelin.
2. Neuropeptide Y.
• Peptides, which decrease the food intake (anorexigenics):
1. Leptin.
2. Peptide YY.
Ghrelin "hunger hormone“.

• Secreted from gastric mucosa during fasting.

• Stimulates feeding center  increases appetite.

• Ghrelin + leptin  balance between hunger and satiety.


Neuropeptide Y (NPY)

• Extremely potent stimulator of feeding center.


• Stimulated by hypoglycemia.
• Increases the desire for sweet and starchy foods.
• Leptin inhibits NPY synthesis and release in the hypothalamus → ↓ appetite.

Q: Why does most people prefer to have rice at lunch or may be unsatisfied if
no bread was there?
Neuropeptide Y (NPY)

Skipping breakfast → ↑ NPY → by afternoon, a person usually overeats


a carbohydrate rich lunch.
Peptides, which decrease the food intake (anorexigenics):
Peptide YY:

• Released from L-cells in the small intestine.


• Activates satiety center  decreased appetite.
• Stimulated by:
 Proteins and fat. (This may explain the efficacy of the protein-rich,
carbohydrate-poor diet in losing weight)
 Bile.
 CCK.
• High peptide YY cause a decrease in appetite and
food intake.
• High peptide YY concentrations are associated with
diseases where there is dramatic weight loss, such as
anorexia nervosa, coeliac disease and some cancers.
• Low peptide YY concentrations are associated with
an increase in appetite and food intake.
• Low peptide YY levels are seen in obesity and before
the onset of type 2 diabetes and may contribute to
weight gain in these conditions.
• The amount secreted increases with the number of
calories ingested and especially when these are derived
from proteins rather than carbohydrates or fats. (This
m ay ex p l a i n t h e eff i ca c y o f t h e p ro te i n - r i c h ,
carbohydrate-poor diet in weight reduction.)
Hormonal Mechanism (gut hormones)

Cholecystokinin:
It is involved in appetite suppression by increasing the sensation of
fullness during a meal rather than between meals.
Stimulants: partially digested fats and proteins.
Pancreatic Polypeptide (PP):
• Produced by Islets of Langerhans.
• Acts as a satiety factor by activating satiety center.
• Released by vagal signals in response to food ingestion.
• Food in the stomach → gastric distension → activation of stretch
receptors → induce a vagal stimulation of PP cells → PP is released.
• moderate doses given in the form of chewing gum, can reduce the
amount of food eaten by healthy volunteers by 15–20 percent by
suppressing appetite.
Thermostatic Mechanism

• Food intake is inversely proportional to body temperature.


• In fever, the food intake is decreased.
• Hunger center is inhibited directly by.
 The preoptic thermoreceptors.
 The cytokines.
Obesity

• Obesity is a medical condition in which excess body fat has


accumulated to the extent that it may have a negative effect on health.

• People are generally considered obese when their body mass


index (BMI), a measurement obtained by dividing a person's weight
by the square of the person's height, is over 30 kg/m2, with the
range 25–30 kg/m2 defined as overweight.
or
• Obesity: was traditionally defined as an increase in body
weight that was greater than 20 percent of an individual's ideal
body weight (the weight associated with the lowest risk of
death, as determined by certain factors, such as age, height,
and gender).

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