Obesity

Mandy Adine
405080040

Hunger and Satiety

Hunger is afeelingexperienced when one has a need
toeatfood. Hunger is different fromappetite, the desire
(rather than need) to eat food.
Satietyis the absence of hunger. The often unpleasant
feeling of hunger originates from
thehypothalamusreleasing hormones that
targetreceptors.
The fluctuation ofleptinandghrelinhormone levels
results in themotivationof an organism to consume
food. When an organism eats,adipocytestrigger the
release of leptin into the body.
Increasing levels of leptin results in a reduction of one's
motivation to eat.After hours of non-consumption, leptin
levels drop significantly. These low levels of leptin cause
the release of secondary hormone, ghrelin, which in turn
reinitiates the feeling of hunger.

Leptin and Ghrelin

Leptin:
-Produced in the adipose tissue
-to signal fat storage in the body and
mediates long term appetite controls (to eat
more when fat storages are low, and to eat
less when fat storages are high)
Ghrelin:
-Produced in the fundus of human stomach
and epsilon cells of the pancreas.
-mediates short term appetite controls (eat
when stomach is empty and stop when
stomach is streched)

Leptin and Ghrelin (2)

The actions of both leptin and ghrelin is in the CNS, mainly in

hypothalamus.
The circuit begins in the arcuate nucleus(an area in the
hypothalamus) that has output to the lateral hypothalamus
(LH) and ventromedial hypothalamus (VMH), which are the
brains feeding and satiety centers.
The arcuate nucleus contains two distinct groups of neurons:
-Neuropeptide Y (NPY) and Agouti-related Peptide (AgRP)
stimulate inputs to the LH and inhibit inputs to the VMH.
-Pro-opiomelanocortin (POMC) and Cocaine and
Ampethamine Regulated Transcript (CART) stimulate
inputs to the VMH and inhibit inputs to the LH.
NYP/AgRP neurons stimulate feeding and inhibit satiety, while
POMC/CART neurons stimulate satiety and inhibit feeding.
Both groups are regulated by Leptin Leptin inhibits
NY/AgRP and stimulates POMC/CART, thus a Leptin deficiency
may explain the excessive weight gain in obesity.

Oxidation Competition
Carbs and fats compete for tissue oxidation.
Fat utilization produces NADH, acetyl-CoA,
and ATP. Simply, these component inhibit
carbs oxidation.
Carbs utilization produces Malonyl-CoA,
alpha glycerophospate, oxaloacetate,
citrate, and thereby, inhibit fat oxidation.
Interestingly, when carbs and fat present
together, carbs oxidation tends to win out
over fat oxidation.

Energy Balance
Is thebiological homeostasisofenergyin
living systems.
Measured by an equation :
Energy intake = internal heat produced +
external work + storage
Energy expenditure is mainly a sum of
internal heat produced and external work.
The internal heat produced is, in turn,
mainly a sum ofbasal metabolic rate(BMR)
and thethermic effect of food.
External work may be estimated by
measuringphysical activity level(PAL).

Energy Imbalance
A gaining energy imbalance is a result ofenergy
intakebeinghigherthan what is consumed in
external work and other bodily means of energy
expenditure.
The main preventable causes are:
-Overeating, resulting in increased energy intake
-Sedentary lifestyle, resulting in decreased
energy expenditure through external work
A gaining imbalance results in energy being
stored, primarily asfat, causingweight gain. In
time,overweightandobesitymay develop, with
resultant complications.

Obesity
Excess body weight, mainly fat.
WHO classification for obesity based
on body mass
index(BMI=kilograms/meters2 )

Causes
Obesity is caused by several origin
that related each other resulting in
obesity :
-Genetics
-Thyroid or leptin deficiency
-Sedentary lifetstyle
-Lack of exercise
-Excess food intake

About Obesity
Obesity are associated with several
medical condition:
-DM type 2
-Hypertension
-Hyperlipidemia
-Atherosclerosis and Stroke
-Osteoarthritis
-Cancer
-Obstructive sleep apnea
Thus the patient will show the symptoms
and signs related to those conditions
above.

Treatment
Obesity is preventable condition which can be
controlled by :
-controlling dietary intake (low carbs low fat diets)
-regular exercise
-increase fiber intake
Pharmacological therapy mainly used to increase
the total energy expenditure, and fat oxidation to
match food intake, such as:
-Thyroid hormone
-Beta 3 Adrenergic Receptor Agonist
-Sympathomimetic agents
-Leptin
Surgical treatment are suggested when obesity has
caused a morbidity disturbance (unable to move, or do
regular activity due to excess weight).

Prognosis
Early diagnosis can prevent major
complication of obesity
Obesity can be controlled
The prognosis of controlled obesity
(cholesterol, triglyceride, LDL) has
shown a promising life quality.

Metabolic Syndrome
Metabolic syndromeis a combination
ofmedicaldisorders, mainly diabetes
melitus type 2, hypertension, and
obesity

American Heart Association

*Metabolic syndrome according to AHA:
Elevated waist circumference:
Men Equal to or greater than 40inches (102cm)
Women Equal to or greater than 35inches (88cm)

Elevated triglycerides: Equal to or greater than

150mg/dL (1.7mmol/L)
Reduced HDL cholesterol:
Men Less than 40mg/dL (1.03mmol/L)
Women Less than 50mg/dL (1.29mmol/L)

Elevated blood pressure: Equal to or greater than

130/85mm Hg or use of medication for hypertension
Elevated fasting glucose: Equal to or greater than
100mg/dL (5.6mmol/L) or use of medication for
hyperglycemia

Risk Factors
Several risk factors that can lead to
metabolic syndrome :
-Stress
-Obesity and overweight
-Sedentary lifestyle
-Aging
-Diabetes melitus
-Cardiovascular disease