Dietary Balances; Regulation of
Feeding; Obesity and Starvation;
• Energy Available in Foods:
• The Average Daily Requirement for Protein Is 30
to 50 Grams.
• Carbohydrates and Fats Act as “Protein Sparers.”
• Methods for Determining Metabolic Utilization
of Carbohydrates, Fats, and Proteins: by means
of “Respiratory Quotient,” : is the ratio of carbon
dioxide production to oxygen utilization.
REGULATION OF FOOD INTAKE
AND ENERGY STORAGE:
• Stability of the body’s
total mass and
long periods requires
that energy intake
NEURAL CENTERS REGULATE
• The sensation of hunger is associated with a
craving for food and several other physiological
effects, such as rhythmical contractions of the
stomach and restlessness, which cause the
person to seek food.
• A person’s appetite is a desire for food, often of a
particular type, and is useful in helping to choose
the quality of the food to be eaten.
• If the quest for food is successful, the feeling of
The Hypothalamus Contains
Hunger and Satiety Centers:
A) The lateral nuclei of the hypothalamus serve as a
1. Stimulation of this area causes an animal to eat
2. Destruction of the lateral hypothalamus causes
lack of desire for food and progressive inanition, a
condition characterized by marked weight loss,
muscle weakness, and decreased metabolism.
• The lateral hypothalamic feeding center operates by
exciting the motor drives to search for food.
B) The ventromedial nuclei of the hypothalamus serve
as a major satiety center.
• This center is believed to give a sense of nutritional
satisfaction that inhibits the feeding center.
1. Electrical stimulation of this region can cause
complete satiety, and even in the presence of highly
appetizing food, the animal refuses to eat
2. destruction of the ventromedial nuclei causes
voracious and continued eating until the animal
becomes extremely obese, sometimes weighing as
much as four times normal.
C) The paraventricular, dorsomedial, and arcuate
nuclei of the hypothalamus also play a major role in
regulating food intake.
• lesions of the paraventricular nuclei often cause
• lesions of the dorsomedial nuclei usually depress
• the arcuate nuclei are the sites in the hypothalamus
where multiple hormones released from the
gastrointestinal tract and adipose tissue converge to
regulate food intake, as well as energy expenditure
The hypothalamus receives:
(1) Neural signals from the gastrointestinal tract that
provide sensory information about stomach filling.
(2) Chemical signals from nutrients in the blood
(glucose, amino acids, and fatty acids) that signify
(3) Signals from gastrointestinal hormones.
(4) Signals from hormones released by adipose tissue.
(5) Signals from the cerebral cortex (sight, smell, and
taste) that influence feeding behavior.
The hypothalamic feeding and
satiety centers have a high
density of receptors for
neurotransmitters and hormones
that influence feeding behavior,
and are generally categorized as
(1) orexigenic substances that
(2) anorexigenic substances that
Neurons and Neurotransmitters in the
Hypothalamus That Stimulate or Inhibit Feeding:
Neural Centers That Influence the
Mechanical Process of Feeding:
• If the brain is sectioned below the
hypothalamus but above the mesencephalon,
the animal can still perform the basic
mechanical features of the feeding process.
• It can salivate, lick its lips, chew food, and
• Therefore, the actual mechanics of feeding are
controlled by centers in the brain stem.
• Neural centers higher than the hypothalamus also
play important roles in the control of feeding,
particularly in the control of appetite.
• These centers include the
2. prefrontal cortex, which are closely coupled with the
Destructive lesions in the amygdala have demonstrated that some
of its areas increase feeding, whereas others inhibit feeding.
In addition, stimulation of some areas of the amygdala elicits the
mechanical act of feeding.
“psychic blindness”: destruction of the amygdala on both sides of
the results in loses or at least partially loses the appetite control
that determines the type and quality of food it eats.
FACTORS THAT REGULATE
QUANTITY OF FOOD INTAKE:
1. Short-term regulation, which is concerned
primarily with preventing overeating at each
2. Long-term regulation, which is concerned
primarily with maintenance of normal
quantities of energy stores in the body.
1- Short-Term Regulation of
1. Gastrointestinal Filling Inhibits Feeding.
2. Gastrointestinal Hormonal Factors Suppress Feeding:
(CCK, Peptide YY, Glucose Like Peptide).
3. Ghrelin, a Gastrointestinal Hormone, Increases Feeding.
4. Oral Receptors Meter Food Intake:
• When an animal with an esophageal fistula is fed large
quantities of food several “oral factors” related to feeding,
such as chewing, salivation, swallowing, and tasting,
“meter” the food as it passes through the mouth, and
after a certain amount has passed, the hypothalamic
feeding center becomes inhibited (20 to 40 min).
2- Intermediate- and Long-Term
Regulation of Food Intake
1. Effect of Blood Concentrations of Glucose, Amino
Acids, and Lipids on Hunger and Feeding: (Glucostatic,
Aminostatic, Lipostatic theory of hunger and feeding
(A) A rise in blood glucose level increases the rate of firing
of glucoreceptor neurons in the satiety center in the
ventromedial and paraventricular nuclei of the
(B) The same increase in blood glucose level
simultaneously decreases the firing of glucosensitive
neurons in the hunger center of the lateral
2. Temperature Regulation and Food Intake:
• When an animal is exposed to cold, it tends to increase
feeding; when it is exposed to heat, it tends to decrease its
3. Feedback Signals From Adipose Tissue Regulate Food Intake:
• Stimulation of leptin receptors in these hypothalamic nuclei
initiates multiple actions that decrease fat storage, including:
(A) decreased production in the hypothalamus of appetite
stimulators, such as NPY and AGRP.
(B) Activation of POMC neurons.
(C) increased production in the hypothalamus of substances, such
as corticotropin-releasing hormone, that decrease food intake;
(D) increased sympathetic nerve activity.
(E) decreased insulin secretion by the pancreatic beta cells.
FOOD INTAKE AND
• As an excess of body fat.
• BMI greater than 30 kg/m2.
• The impact of obesity on the risk for various
disorders such as cirrhosis, hypertension, heart
attack, stroke, and kidney disease.
• Obesity Results From Greater Intake Than
Expenditure of Energy.
• Hyperplastic obesity (in children).
• Hypertrophic obesity (in adults).
• Decreased Physical Activity and Abnormal
Feeding Regulation as Causes of Obesity.
1. Sedentary Lifestyle Is a Major Cause of Obesity.
2. Abnormal Feeding Behavior Is an Important Cause of Obesity.
3. Childhood Overnutrition as a Possible Cause of Obesity.
4. Neurogenic Abnormalities as a Cause of Obesity.
5. Genetic Factors as a Cause of Obesity.
Cause of Obesity.
Inanition, Anorexia, and
• Inanition: is a extreme weight loss.
• It can be caused by inadequate
availability of food or by
pathophysiological conditions that
greatly decrease the desire for food,
including psychogenic disturbances,
hypothalamic abnormalities, and factors
released from peripheral tissues.
• Anorexia: a reduction in food intake
caused primarily by diminished
• pain and nausea, may also cause a
person to consume less food.
• Cachexia: is a metabolic disorder of
increased energy expenditure leading
to weight loss greater than that caused
by reduced food intake alone.
• Depletion of Food Stores in the Body
Tissues During Starvation.
• the tissues prefer to use carbohydrate
rather than either fat or protein for
energy, the quantity of carbohydrate
normally stored in the entire body is
only a few hundred grams.
• the rate of fat depletion continues
unabated, until most of the fat stores
in the body are gone.
• Protein undergoes three phases of
depletion: rapid depletion at first,
followed by greatly slowed depletion,
and finally rapid depletion again
shortly before death.