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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 Adapted from R. Unger

50 years

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

Genetic background

Hypotalamic satiety centre (neuropeptides, leptin, insulin)

Food intake

Energy expenditure

Life styl

Sympathetic nervous system - Energy expenditure, lipolysis

Gastrointestinal tract ghrelin, peptide YY

Adipose tissue leptin, adiponectin, resistin, TNF-a

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 hypothalamus (serotoninergic neurons)

Source: Morton et al. 2005

Ventromedial nuclei satiety centre (lesion 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

Hypothalamus

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 Stomach and duodenum distension (n.vagus) heat catecholamines serotonin ACTH Insulin (food in stomach) Leptin CCK (lipids in duodenum) MSH glucagon Peptide YY HUNGER FACTORS Hungry contractions cold orexins endorphins Galanin Glutamic acid cortisol Neuropeptide Y GABA ghrelin AMPK

glucose, amino acids, lipids in blood glucose, amino acids, lipids in blood

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)


BMI = Weight (kg) Height (m2)

Clasification Normal weight Overweight Obesity I Obesity II Obesity III

BMI (kg/m2) 18.524.9 2529.9 30.034.9 35.039.9 40.0

Metabolic c. average increased middle high Very high

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
>102 cm = highly increased risk1 >94 cm = increased risk1

>88 cm = highly increased risk1 >80 cm = increased risk1

1Lean

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 biological factors cultural-social, psychological,

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