HUNGER_EATING_HEALTH

 ROLE OF GLUCOSE
 Glucose- normally known as blood sugar. It is a monosaccharide so it’s the simplest form of carbohydrates. type
of sugar that you get from the food that you eat. It is moves by insulin is a hormone
~Experiment by camp field and smith there was a development regarding the role of glucose with eating.
They had rats with free access of food and water and their glucose level was monitored. 10 mins. Before the meal the
level quickly dropped by 8%. However, this incident does not suggest that the decline in glucose before meal produces
hunger and eating. Rather, the causation foes into opposite direction. Meaning to say that the intention to start eating
triggers the decline in glucose. [Blood glucose drops prior to a meal as a preparation to eat but not as a cue to eat.
~decline in blood glycose (bg) is not consistent it just really occurs suddenly before eating
~if an expected meal is not served bg returns to its previous level
HYPOTHALAMIC HUNGER
 Eating behavior is controlled by 2 different regions of hypothalamus: VENTROMEDIAL HYPOTHALAMUS
(VHM) and the LATERLA HTPOTHALAMUS (LH)
 VHM HYPOTHALAMUS
the ventromedial hypothalamus, it's part of the brain that deals with several body systems. This long
scientific name can be broken into three component parts that mostly describe its location in the brain.
'ventral' is front, 'medial' means near the middle, and 'hypothalamus' is a region of the brain just
underneath the thalamus. Ventromedial hypothalamus is the area toward the front of the hypothalamus in
the brain
hypothalamus
So the VMH is a portion of the hypothalamus gland in the brain, underneath the thalamus, near the
middle of the brain, and towards the front of the hypothalamus. Got it? Well, at least that little exercise
tells us where this brain part is, but what does it do?

The Functions of the VMH

Experiments in rats have shown the VMH to be involved in food satiety, temperature regulation, fear
response, and sexual activity. This is one busy little area of the brain. Imagine what would be happening
in our bodies without it! Let's take a look at some of these functions.

Appetite Suppression/VHM SYNDROME

When the VMH of rats were intentionally damaged in early experiments, the results were dramatic; the
damaged rat became quite overweight, leading scientists to believe the VMH was responsible for the
telling the rat when to stop eating. This led to the VMH being known as the 'satiety center'. However, it
turns out that appetite control is surprisingly complex. While the most important regulation does seem to
come from the VMH, further experiments have revealed that other areas of the brain, endocrine system,
and nervous system also affect appetite.

Now we know it's not accurate to label the VMH as the 'center' of satiety, but it is the most important
cog in the complex system that determines satiety. This new label doesn't have quite the same ring to it
as the old one, but it gets closer to the truth.

Large bilateral lesion hyperphagia (excessive eating) and extreme obesity.

2 dynamic phases; dynamic process- several week of excessive eating and rapid weight
gain. After that food consumption gradually declines. To a level just suffocoent to
mainatin the lebel of obesiity. w/c marks the 2nd phase
-static phase- the rat maintains its new weight.
NOT A STIETY CENTER
 The ecidenr proved that the primary role of the hypothalamus is actually to refulate metabalosim
and not eating. Rats overeat bc theyr were povese. The lesion increase blood insulin level which
increases in the lipogenesis (production of fat abd decrease oif lipolysis (breakdown of the fat). Calories
na iniintake ng rat ay naococnvert into fat that’s why they vecame ibses

 LH
Feeding center
Regulating matebolism and food intake
-lesion: aphagia( complete cessation of eating
2 features: adipsia- cessation of drinking
Recover thru tube feeding. 1st to eat wet palatavle foods
NOT A FEEDING CENTER

LH is more genereally involved inresponing to sensory stimuli nor specifically deidicated to feeding
since the lesion produce wide range severe motor disturbances
ROLE OF GASTROINTESTINAL TRACT IN SATIETY
-hunger is the feeling of contractions caused by an empty stomach.
-satiety us the feeling of stomach distension.
REHECTED since people whose stomach was removed still report hunger and satiety
-KOOPMANS implanted extra stomach and length of intestine into rats. It was found out that the food injected in
the stomach decreased eating in proportuion both its caloric content and volujme.. so since no nerve blood So since
nutrients are not absorbed in the stomach the gastrointestinal satiety signal niya is not accpeted as nutrient as well as the
blood signal so chemical signal siya.

HUNGER AND PEPTIDE

-it is discovered already that the stomach and other parts of the gastrointestinal tract release cgemucal signals to
the brain they started to accumulate that these chemical are actually perptides.
It is believed that the ingested interacts with a receptor that cause the release of peptides

They ingested gut peptide into the rats namely the Cholecystokinin (cck) plays a key role in facilitating digestion within
the small intestine. And the rats actually ate smaller amount of meals
So these experiments is accepted to be a supporting evidence that peptides can actually fxn as satiety signals. In fact
some gut peptides were actually found binding in the brain particularly in the hypothalamus which is involved in the
regulating of metabolism and have reportedly reduced food intake they were later in called satiety peptides.

Several hunger peptides (peptides that increase appetite) have also been discovered. These peptides tend to be
synthesized in the brain, particularly in the hypothalamus. The most
widely studied of these are neuropeptide Y, galanin, orexin-A, and ghrelin

SEROTONIN AND SATIETY

Serotonin is a neurotransmitter that is involved with our mood.
~Experiment (serotonins produced satiety)
-resist highly palatable food
-reducee food consumption during each meal and not the number of meal
-shift if food preference: away from fatty foods

>These results suggest that Serotonin can be use to combat obesity in humans
eed, serotonin agonists (e.g., fenfluramine, dexfenfluramine, fluoxetine) have been shown to reduce hunger, eating, and
body weight in obese humans under some conditions
 PRADER WILLI SYNDROME
-result of accident in chromosomal replication
-experience insatiable hunger
 -little or no satiety
-crucial to neural mechanism and hunger and eating but unfortunately it has no direct evidence yet