PUSAT LAPAR &

KENYANG
PENGATURAN
PEMASUKAN
MAKANAN
PEMASUKAN MAKANAN?
Berapa kali sehari kita makan?
Apa yang mendorong kita
makan?
Apa saja yang kita makan?
Tujuan apa yang dicapai dengan
pemasukan makanan?
Adakah bahaya makanan bagi
tubuh?
 BERAPA KALI SEHARI KITA
MAKAN?
Pengaruh selera?
Pengaruh keuangan?
Pengaruh aktivitas?
Pengaruh emosi?
 APA YANG MENDORONG
KITA MAKAN?
Rasa lapar/kenyang?
Di mana pusatnya?
Apa yang merangsang?
Bagaimana prosesnya?
Apa efektornya?
Bagaimana relasinya dng sistem
di tubuh?
 The progression of mankind development

2.5 milion of years 50 years

Adapted from R. Unger

Historical view of the regulation of
food intake
Lipostatic hypothesis (Kennedy 1953)
adipose tissue produces specific lipostatic
factor

Glucostatic hypothesis (Mayer and Thomas

1967) fluctuations in glycaemia lead to
stimulation/inhibition of food intake
(regulating organs brain and the liver)

Combination of above mentioned

The physiological regulation of food intake is a complex
homeostatic process that is regulated by many endocrine
and metabolic factors in a combination with visual,
olfactory, taste sensation, emotions, memory and the
life conditions
 The balance between energy intake and
expenditure is tightly regulated and body weight
is stable despite day-to-day food intake
fluctuations......

..but when the border is overestimated the

balance is broken.
Interactions between
emotions and
metabolic/endocrine
regulations

Berthoud et al. 2006

 Hypotalamic satiety centre
Genetic background (neuropeptides, leptin, insulin)

Energy
Food intake expenditure
Sympathetic nervous system
Life styl - Energy expenditure, lipolysis

Gastrointestinal tract
ghrelin, peptide YY

Adipose tissue
leptin, adiponectin, resistin,
TNF-
 Hypothalamus and brain stem are crucial in central
regulation of feeding
Integration of brain neurotransmiters, peripheral neurohumoral afferents,
adipocyte-derived signals, GIT peptides

Modulated by
neocortex
N. arcuatus (ARC) receptors
for hormones and neuropetides that
regulate feeding

N. paraventricularis (PVN)
integration of signals from ARC with
thyroid and HPA axes

N. vagus satiety signals to the

brain stem after ingestion of a meal

N. tractus solitarius + PVN

connection of brainstem with Source: Morton et al. 2005
hypothalamus (serotoninergic
neurons)
 Ventromedial nuclei
satiety centre (lesion
Hypothalamus
leads to hyperfagia)

Lateral nuclei hunger

centre (lesion leads to
anorexia)

N.arcuatus pivotal
role in the integration
of signals regulating
appetite

N. suprachiasmaticus
timing (lesions in
humans lead to night
hyperfagia and obesity
Energy homeostasis is controlled by peripheral signals from
adipose tissue, pancreas, and the GIT.
Gut-derived peptides and adiposity signals influence central
circuits in the hypothalamus and brain stem to produce a
negative () or positive (+) effect on energy balance. Thus
the drive to eat and energy expenditure are adjusted so that
over time, body weight remains stable.
 Adipose tissue plays an
important role in the regulation
of energy homeostasis
 Factors regulating food intake
SATIETY FACTORS HUNGER FACTORS
Stomach and duodenum Hungry contractions
distension (n.vagus)
heat cold
glucose, amino acids, lipids glucose, amino acids, lipids
in blood in blood
catecholamines orexins
serotonin endorphins
ACTH Galanin
Insulin (food in stomach) Glutamic acid
Leptin cortisol
CCK (lipids in duodenum) Neuropeptide Y
MSH GABA
glucagon ghrelin
Peptide YY AMPK
 APA SAJA YANG KITA
MAKAN?
Macam makanan?
Sumber tenaga?
Sumber bahan bangunan?
Sumber bahan pengatur?
Sumber bahan pelarut/media
reaksi kimia?
TUJUAN APA YANG DICAPAI
DENGAN PEMASUKAN
MAKANAN?
Kenyang?
Puas?
Pemenuhan kebutuhan tubuh?
ADAKAH BAHAYA MAKANAN
BAGI TUBUH?
Tidak ada bahayanya?
Ada bahayanya?
Apa saja bahayanya?
Bagaimana
mencegah/menanggulangi
bahaya makanan?
OBESITY
Obesity is classified by
Body Mass Index (BMI)

Weight (kg)
BMI =
Height (m2)

Clasification BMI (kg/m2) Metabolic c.

Normal weight 18.524.9 average

Overweight 2529.9 increased

Obesity I 30.034.9 middle
Obesity II 35.039.9 high
Obesity III 40.0

WHO, 1998
 Waist circumference is a helping indicator
of visceral fat this fat is the most
metabolically active and thus the most
harmful

Women cm Men
>88 cm = highly increased risk1 >102 cm = highly increased risk1
>80 cm = increased risk1 >94 cm = increased risk1

1
Lean MEJ, et al. Lancet;1998:351:8536
 Complications of obesity

Mechanical joint illness, dyspnoe,

sleeping apnoe, heart hypetrophy,..

Metabolic - diabetes, hypertension,

hyperlipoproteinemia, ischemic heart
disease, ictus, tumours, sterility,
depression,.. = Reaven metabolic
syndrome
More slim and more fit means
more success and beauty..

.. but sometimes this motto of modern

societies leads to death
 Anorexia Nervosa
(AN)
Severe psychiatric disorder of unclear etiology
associated with significant morbidity and
mortality (Hsu 1996)

Prevalence 0.3% of young girls, mortalty of

6%/decade (Dardeness 2007)

Irrational fear of becoming fat even if patient

is of normal or usually underweight

Phobic response to food, abnormal eating

behavior, hyperactivity, weakness, muscle
aches, sleep disturbances, GIT complications,
mood disturances, alterations of wide variety
of hormonal and metabolic systems

Combination of cultural-social, psychological,

biological factors
 Complications of AN
Hematological and electrolyte: leukopenia with
leukocytosis, alkalosis, hypokalemia, hypochloremia,
elevated serum bicarbonate (vomiting), acidosis
(laxatives), dehydration, lethargy, weakness

Chemistry: elevated liver enzymes, elevated serum

cholesterol, carotinemia, elevation of amylase
(vomiting)

GI: delay in gastric emptying sense (pp discomfort-

early satiety-restricting behavior cycle), gastritis,
esophageal erosions (vomiting) or rupture (binge
eating)

Long-term complications:
Osteoporosis
Amenorrhea - persisting after weight recovery in 50%
of AN (warren and Vande Wielle 1973)
Skeletal-muscular injuries (sprains, fractures)
 Cancer anorexia
Cancer anorexia-cachexia syndrome
(Tisdale 1997)
Observed in 80% of advaced-stage cancer
One of the most frequent causes of death
(Mantovani 2001)
The role of proinflammatory cytokines
(serotonin) released by cancer cells or
immune systm in inducing satiety and
anorexia, activation of anorexigenic
pathway
Regulation of the feeding in cancer patients

Anorexia
satiety

inhibition