Control Of Food Intake

OBESITY
Body Mass Index (BMI)

Weight (kg) Weight (lb)

BMI =
Height (m2) Height (in2)
X 705

Classification BMI (kg/m2) Risk co-morbidity

Normal values 18.524.9 Average
Overweight 25
Pre-obesity 2529.9 Increased
Obesity class I 30.034.9 Moderate
Obesity class II 35.039.9 High
Obesity class III 40.0  Very High
World Health Organization,
1998
 OBJECTIVES
1. Recognizes the centers controlling food
intake and factors affecting them.
2. Define Body Mass Index (BMI)
3. Define obesity and its types.
4. Realize the hazards and complications of
obesity.
5. Know the management of obesity.
 FOOD INTAKE
CONTROL OF FOOD INTAKE
Control of food intake is important to maintain
normal energy balance. Food intake is controlled by a
specific center in the hypothalamus (the appestat) and
the limbic lobe (particularly the amygdaloid nuclei).The
hypothalamic appestat center is formed of 2 centers: -
a) Feeding Center :
• It is present in the lateral hypothalamic nuclei.
• Its stimulation increased appetite and food intake.
• Its destruction  severe anorexia.
b) Satiety Center:
• It is present in the ventromedial hypothalamic
nuclei.
• Its stimulation decreased appetite and leads to
cessation food intake.
• Its destruction  increased appetite and leads to
severe hyperphagia (marked increased food intake)
 severe obesity (hypothalamic obesity).
N.B.
• Normallly, the feeding center is continuously active
and is inactivated only when the satiety center is
stimulated (e.g. following food ingestion). The
satiety center produces its effects through
inactivation of the feeding center.
• There is a definitive set point for the normal body
weight. The food intake controlling mechanisms
adjust feeding so that the energy input is equal to
the energy output at the set point for every
individual with the net result of keeping the body
weight constant.
The hypothalmic appestat is affected by
input stimuli from:
1) The buccal and oesophageal receptors:
• These receptors send impulses to the hypothalmic
appestat stimulation of the satiety center  
appetite and food intake.

2) Other parts of the GIT:

• Distention of the stomach and intestine 
stimulation of the satiety center and cessation of
food intake.
• Hunger contractions of the stomach  stimulation
of the feeding ceter increase appetite and food
intake.
3) Thermoreceptors:
Exposure to cold  stimulation of the feeding center and  food intake.
Exposure to hot   food intake.

4) Chemical stimuli:
Glucose:
During fasting, the blood glucose level is    glucose utilization by the cells of
the satiety center (which are called the glucostat)   activity of the satiety
centerstimulation of the feeding center   appetite and food intake. The
reverse occure if the blood glucose level is high.
Hormones:
Cholecystokinin-pancreozymin(CCK-PZ),insulin and calcitonin  appetite and
food intake.
Glucagon  stimulation of food intake.
Drugs : Amphetmine stimlate the satiety centerinhibition of appetite and food
intake.
N.B.
• Psychological factors affect the
hypothalmic appestat.Obesity commonly
occurs in psychologically unstable persons.
Over eating seems to be a release
mechanism in these persons.
• Environmental & cultural factors, in
relation to food intake also affect the
appestat center and can  or  food
intake.
 OBESITY
• It is the accumulation of excess fat in the body.
• It is produced as a result of disturbance of
energy balance so that the energy intake is more
than the energy utilized by the body (i.e. there is
a +ve energy balance).
• The excess energy is stored as fat in adipose
tissues.
• For each 9.3 C excess taken, one gram of fat is
deposited.
• So, the direct cause of obesity is hyperphagia
associated with decreased muscular activity.
• Once obesity occurs, the person remains obese
even if the energy input is equal to the energy
output. This may be due to re-setting of the
appestat center to a higher point for the body
weight than normal.
• Normally, 12-18% of the body weight of males
is due to fat (18--24% in females). Obesity is
present if more than 20% of the body weight is
due to fat in men (and if more than 25% in
women).
 Obesity predisposes to
many diseases e.g.
• Hypertension.
• Coronary Heart Diseases.
• Gall Bladder Diseases.
• Diabetes Mellitus.
Hyperphagia, which is the direct cause of obesity may be
due to :-
(1) Psychological factors:
In theses cases, hyperphagia seems to be a release
mechanism from tension psychogenic obesity.

(3) Hypothalamic abnormalities:

Disturbance of the appestat center and /or the limbic lobe
may lead to a severe type of obesity (hypothalamic
obesity).

(4) Genetic factors:

Obesity runs in families. This can be attributed to a genetic
abnormality of the appestat center and/or environmental,
cultural and food factors.
 TYPES OF OBESITY:
There are tow types of obesity:
(1) Hypertrophic obesity:
This type is characterized by an increase in the amount of fat
per fat cell but there is no increase in the number of fat
cells. It occurs usually in adults and it is not severe. So, it is
easier in treatment.

(2) Hypertrophic hyperplastic obesity:

In this type, there is an increase in both the number of fat
cells (hyperplasia) and the amount of fat deposited per fat
cell (hypertrophy). It starts early in childhood due to
overfeeding early in life. This type is difficult to treat.
Body Mass Index (BMI)

Weight (kg) Weight (lb)

BMI =
Height (m2) Height (in2)
X 705

Classification BMI (kg/m2) Risk co-morbidity

Normal values 18.524.9 Average
Overweight 25
Pre-obesity 2529.9 Increased
Obesity class I 30.034.9 Moderate
Obesity class II 35.039.9 High
Obesity class III 40.0  Very High
World Health Organization,
1998
 Energy Balance
• Sources of fuel for energy
– Input from diet: carbs, fat, prot, alcohol
– Stored energy: glycogen, fat, muscle
• Energy outgo from:
– Basal metabolism
– Physical activity
– “Dietary thermogenesis”
 TREATMENT OF OBESITY
1. The energy input is decreased by decreasing the
food intake below the energy output of the
individual. This can be done by partial starvation
using various reducing diets. These diets contain a
large amount of vegetables, salads and fruits with
suitable amounts of proteins, but with a very low
content of carbohydrates and fats.
2. The energy output is increased by increasing
muscular activity.
3. Drugs as amphetamine to reduce appetite (by
stimulation of the satiety center) but its
sympathomimetic effects and tolerance limit its use.