‫بنام خداوند جان و خرد‬
‫کنترل وزن‬
‫دکتر منصور سیاوش‬
‫مفاهیم اولیه‬
‫‪ ‬مقدمه‬
‫‪ ‬اهداف بحث‬
‫‪ ‬چاقی یا الغری از نظر اجتماعی و تاریخی‬
‫چاقی یا الغری از نظر اجتماعی و تاریخی‬
‫مفاهیم اولیه‬
‫‪ ‬وزن بدن ناشی از چیست؟‬
‫در یک فرد ‪ 70‬کیلوئی‪:‬‬
‫‪42 kg‬‬
‫‪12 kg‬‬
‫‪12 kg‬‬
‫‪0.5 kg‬‬
‫‪3.5 kg‬‬
‫آب‬
‫پروتئین‬
‫چربی‬
‫گلیکوژن‬
‫وزن غیر انرژی زا‬
‫‪ ‬تغییرات وزن در طول زندگی‬
‫چگونه است؟‬
‫تغییرات ‪ BMI‬از کودکی تا بلوغ‬
‫تغییرات وزن در بالغین با افزایش سن‬
‫پاتوفیزیولوژی تغییرات وزن‬
∆ E = Q – W

If ∆ E = 0 →→
Energy intake = Energy expenditure
‫سیستم های کنترل کننده وزن بدن کدامند؟‬
‫چه عواملی بر تعیین وزن بدن تاًثیر گذارند؟‬
‫‪ ‬وزن پدیده ای مولتی فاکتولایر و حاصل تداخل عوامل زیر‬
‫است‬
‫– وراثت‬
‫– میزان مصرف مواد غذائی(کسب انرژی)‬
‫– میزان فعالیت فیزیکی(برون ده انرژی)‬
‫وراثت یا محیط ؟‬
‫وراثت‬
‫‪ ‬وراثت مهمترین عامل تعیین کننده وزن در زمان طوالنی‬
‫است‪.‬‬
‫‪ ‬هنوز ژن عامل چاقی شایع در انسان شناخته نشده است‪.‬‬
‫‪ ‬برخی ژنها مثل ژن لپتین‪ ،‬گیرنده لپتین‪ MCR4 ،‬شناخته‬
‫شده است‪.‬‬
‫تمایل ژنها به سمت ایجاد چاقی است یا الغری؟‬
‫مصرف مواد غذائی‬
‫‪ ‬عوامل محیطی‪-‬اجتماعی‬
‫‪ ‬هورمونهای دستگاه گوارش‬
‫‪ ‬هورمونهای پانکرآس‬
‫‪ ‬عوامل مرکزی‬
‫مصرف مواد غذائی‬
Environment factors suggested to promote overeating
•High Fat/Energy Dense Foods
•High Glycemic Index of Foods
•Soft Drinks
•Sugar
•Fast foods
•Portion Size
•Snack foods
•Low calcium
•Accessibility of Food
•Low Cost of Food
•Taste of Food
•Variety
High Fat/Energy Dense Foods
High Glycemic Index Food
GASTROINTESTINAL PEPTIDES
REGULATING FOOD INTAKE
Peptide
Stimulus
CCK
protein and fat
GLP-1
nutrients
gut hormones
gut neural
signals
Site of
Production
Site of
Action
Effect on
food intake
vagal afferents
decrease
ileum/colon
gastric emptying
brain
decrease
small intestine
brain
Ghrelin
fasting
stomach
brain
increase
Apo A-IV
fat absorption
intestine/liver
brain
decrease
Enterostatin
fat
Stomach
intestine
vagal afferents
decrease
GRP/
Bombesin
gastric mucosa
food ingestion
vagal
afferents ,brain
decrease
Gastrointestinal signals regulate food intake.

The majority of signals from the GI tract
regulate the size of individual meals.
Mechanoreceptors quantitating stretch of
the stomach, and chemoreceptors
activated by nutrients in the GI tract,
transmit information via vagal and
sympathetic afferents to the hindbrain
nuclei. This information is then
transmitted to the hypothalamus and
other forebrain structures for integration
with additional signals regulating food
intake. Vagal afferents from the liver
signal the presence of specific nutrients.
Glucose and ketones act as signals to the
CNS directly on responsive neurons in
the hypothalamus. Gastrointestinal
hormones such as CCK bind receptors in
the liver to activate vagal afferents, or
access the CNS via the circulation. Other
hormones such as GLP-1 inhibit feeding
by slowing gastric emptying.
PANCREATIC HORMONES REGULATING FOOD
INTAKE
Peptide
Stimulus
Site of
Production
Site of
Action
Effect on
food intake
Insulin
carbohydrate
b-cell
brain
decrease
Amylin
carbohydrate
b-cell
brain
decrease
Glucagon
cephalic
response
a-cell
liver/vagal
afferents
decrease
‫میزان فعالیت فیزیکی‬
Environmental factors suggested to reduce physical
activity?
•Reduced need for physical labor in most jobs
•Elevators ,Remote controls, Telephone
•No required physical activity in schools
•Reductions in physical activity required for daily
living
•Competition from attractive sedentary activities:
•television, video/DVD, video/computer
games, internet
‫سیستم های کنترل کننده وزن بدن کدامند؟‬
‫کنترل وزن چگونه انجام میشود؟‬
‫‪.1‬‬
‫‪.2‬‬
‫‪.3‬‬
‫‪.4‬‬
‫‪.5‬‬
‫سیستم گیرنده وضعیت فعلی نسج چربی را می سنجد‪.‬‬
‫وضعیت فعلی به اطالع مرکز کنترل وزن میرسد‪.‬‬
‫مرکز کنترل وزن اطالعات دریافتی را با ‪Set point‬‬
‫مقایسه میکند‪.‬‬
‫مرکز کنترل وزن دستورات اصالحی را در جهت رسیدن‬
‫وزن به ‪ Set point‬صادر میکند‪.‬‬
‫مراکز عمل کننده با تغییر در ‪Intake‬‬
‫و‪ Expenditure‬اصالحات الزم را انجام میدهند‪.‬‬
Leptin
Leptin




Was discovered in 1994 by Friedman et al .
Is a 16 kd protein produced predominantly in white
adipose tissue and, to a lesser extent, in the placenta,
skeletal muscle, and stomach fundus in rats.
Has a myriad of functions in carbohydrate, bone, and
reproductive metabolism that are still being unraveled .
The major role of leptin in body weight regulation is to
signal satiety to the hypothalamus, thus :
– Reduces dietary intake and fat storage while
modulating energy expenditure and carbohydrate metabolism to
prevent further weight gain.
Pathway of leptin appetite regulation
PC-1 processing enzyme
Leptin
Leptin
receptor
POMC
expression
Alfa MSH
Melanocortin 4
Receptor
signal
AgRP
Decreased
Appetite
Leptin Rx
Other biological actions of leptin
POMC
Proopiomelanocortin (POMC) and alpha–
melanocyte-stimulating hormone (alpha-MSH)
both act centrally on the melanocortin receptor
4 (MC4R) to reduce dietary intake .
 Genetic defects in POMC production and
mutations in the MC4R gene both
 have been described as monogenic causes of
obesity in humans .
 As many as 5% of children who are obese have
MC4R or POMC mutations.

Prohormone convertase1
Involved in the conversion of POMC to
alpha-MSH.
 Patients identified to have mutations of
this,although rare, have significant
obesity,hypogonadotrophic hypogonadism,
and central adrenal insufficiency.
 It is one of the few obesity models not
associated with insulin resistance.

PPAR-gamma
Is a transcription factor that is involved in
adipocyte differentiation.
 All humans with mutations of the receptor
described so far have severe obesity.

AgRP
This protein inhibits the binding of melanocytestimulating hormone(MSH) to its receptors
(melanocortin-1 receptor), thereby reducing
melanin pigmentation.
 The agouti protein also competes with MSH for a
receptor in the hypothalamus (melanocortin-4
receptor) that modulates food intake .
 Serum concentrations of the agouti protein are
higher in obese than non-obese men .

Proposed Mechanism of Action of
Resistin in Mice.
Whether triglycerides are stored in adipocytes or
broken down and released from adipocytes
depends on whether there is a positive or negative
energy balance, respectively.The adipocyte
actively modulates energy balance through the
secretion of hormones and other signaling
molecules. For example, leptin is secreted by
triglyceride-laden adipocytes, travels through the
circulation, crosses the blood–brain barrier, and
reaches the hypothalamus, where it modulates a
host of neuroendocrine and autonomic nervous
system activities, resulting in decreased food
intake and increased energy expenditure. Resistin,
as well as tumor necrosis factor , adiponectin, free
fatty acids, and possibly other factors released by
adipocytes, act in peripheral tissues to influence
sensitivity to insulin and other cellular and
metabolic processes involved in the use and
partitioning of substrates.
Central control of weight
Categories of total body energy
expenditur


Step-by-step conversion of fuel into ATP and then ATP
into biological work within the cell. Free fatty acids
(FFAs) and glucose are oxidized generating NADH and
FADH2 which donate electrons to the electron transport
chain. Ubiquinone (Q) shuttles electrons from both
complexes I and II to complex III while cytochrome C
(C) shuttles electrons from complex III to complex IV.
Molecular oxygen (O2) is the terminal electron acceptor.
Protons are pumped out by complexes I, III and IV of
the electron transport chain creating a proton
electrochemical potential gradient (?uH+). Protons may
reenter the mitochondrial matrix via the F0F1 ATPase,
with energy being used to generate ATP from ADP and
Pi. Protons may also reenter via an uncoupling protein
(UCP), with energy being released in the form of heat.
Proton rentry via ATP synthase depends upon the
availability of ADP which is generated in the cytosol from
reactions utilizing ATP.
Abbreviations: ANC, adenine nucleotide carrier; CC, carnitine carrier; complex I,
NADH-ubiquinone oxidoreductase; complex II, succinate:ubiquinone oxidoreductase;
complex III, ubiquinone-cytochrome-c oxidoreductase; complex IV, cytochrome-c
oxidase; PiC, phosphate carrier; PyC, pyruvate carrier.

Coupling of reactions in energy metabolism and the operation of
"futile cycles". Metabolism of fuel generates a stoichiometric amount
of NADH and FADH2. Oxidation of NADH and FADH2 results in 10
and 6 protons, respectively, being pumped out of the mitochondrial
matrix. Three protons enter via ATP synthase in order to synthesize
one molecule of ATP from ADP and Pi. One additional proton enters
the matrix as it is co-transported with Pi via the phosphate carrier.
ATP is then utilized to perform a fixed amount of work. The major
consumers of ATP are shown above. Muscle relaxation, ion leaks,
protein degradation and dephosphorylation create the possibility for
"futile cycles".
Energy Expenditure is Regulated by
the Brain

Central and efferent pathways regulating energy
expenditure. Diet and cold is sensed by the brain. In the
case of diet-induced thermogenesis, a strong case can
be made for the role of aMSH neurons in the arcuate
nucleus of the hypothalamus which project to neurons in
the paraventricular nucleus of the hypothalamus
controlling sympathetic outflow, as well as to
sympathetic preganglionic neurons located in the
intermedial lateral column of the spinal cord. As
discussed in the text, MC4Rs are likely to play an
important role. These pathways lead to increased activity
of sympathetic nerves which release norepinephrine,
activating bARs. This has acute and chronic effects on
brown adipocytes which promote increased
thermogenesis. This figure was adapted from reference
‫وزن متناسب چیست؟‬
Classification of Obesity
WHO
Classification
Popular
Description
BMI (kg/m2)
Risk of comorbidities
Underweight
Thin
<18.5
Low (but risk of
Normal range
Normal
18.5 - 24.9
Average
other clinical
problems increased)
> 25.0
Overweight
Pre-obese
Overweight
25 - 29.9
Increased
Obese Class I
Obese
30.0 - 34.9
Moderate
Obese Class II
Obese
35.0 - 39.9
Severe
Morbidly Obese
> 40.0
Very severe
Obese Class III
‫برای ارزیابی وزن چه شیوه هائی وجود دارد؟‬
Weight
 Weight chart
 BMI
 Anthropometric assessment
 MRI/CT
 Hydrodensitometry

BMI
‫ادازه گیری های آنتروپومتریک‬






1) vertical triceps skinfold thickness halfway between the
acromion and olecranon processes,
2) vertical biceps skinfold thickness at the same level as
the triceps skinfold thickness above the antecubital
fossa,
3) subscapular skinfold thickness just below the inferior
tip of the scapula,
4) suprailiac skinfold thickness as an oblique fold on the
iliac crest in the midaxillary line,
5) midaxillary skinfold thickness in the midaxillary line at
the level of the zyphoid process in a vertical plane, and
6) vertical abdominal skinfold thickness adjacent to the
umbilicus.
Anthropometric measures
Anthropometric measures
‫روش های تحقیقی ارزیابی وزن‬
Hydrodensitometry
 CT
 MRI
 Radionuclide

‫اهمیت توزیع چربی‬
‫‪ ‬چاقی مردانه‪ /‬شکمی‬
‫– زمینه ساز مشکالت کاردیووسکوالر‬
‫– زمینه ساز هیپرلیپیدمی‬
‫‪ ‬چاقی زنانه‪ /‬گلوتئال‬
‫‪ ‬چاقی سیب یا گالبی‬
‫انواع چاقی‬
‫راههای ارزیابی نوع چاقی‬
‫‪ ‬اندازه گیری دور شکم‬
‫– در مردان بیشتر از ‪102 cm‬‬
‫– در زنان بیشتر از‪88 cm‬‬
‫‪ ‬نسبت کمر به شکم‬
‫– در مردان بیشتر از ‪1‬‬
‫– در زنان بیشتر از ‪0.85‬‬
‫سندرم متابولیک چیست؟‬
‫‪ ‬اختالل شایعی است که در آن عالوه بر چاقی‪،‬هیپرلیپیدمی‬
‫و اختالل تحمل گلوکز نیز دیده میشود‪.‬‬
‫‪ ‬اهمیت سندرم متابولیک زمینه سازی برای عوارض متعدد‬
‫قلبی عروقی‪ ،‬دیابت‪ ،‬فشار خون‪ ،‬عدم تخمک گذاری‪ ،‬و‬
‫سنگ صفرا می باشد‪.‬‬
‫معیارهای تشخیص سندرم متابولیک چیست؟‬
‫ معیار از پنج معیار زیر‬3 ‫ سندرم متابولیک در حضور‬
:‫تشخیص داده میشود‬
1. Abdominal obesity: waist circumference,
>102 cm
2. Hypertriglyceridemia: > 150 mg/dl
3. Low HDL cholesterol:<40 mg/dl in men,
<50 mg/dl in women
4. High blood pressure: >130/85 mm
5. High fasting glucose: >110 mg/dl
‫سندرم متابولیک‬
‫چاقی چه عوارضی دارد؟‬
COMPLICATIONS OF OBESITY
1. Metabolic-hormonal complications
Metabolic syndrome
oType II diabetes
oInsulin resistance, hyperinsulinemia
oDyslipidemia
oHypertension
oGout
oSleep disorders
Abnormalities of hormones and other circulating factors:
oCytokines
oGhrelin
oGrowth hormone (GH)
oHypothalamic-pituitary-adrenal (HPA) axis
oLeptin
oRenin-angiotensin system
2. Diseases of organ systems
Cardiac and vascular diseases
oCerebrovascular disease
oCongestive heart failure
oCoronary heart disease
oHypertension
oThromboembolic disease
Respiratory system abnormalities
oObesity-hypoventilation syndrome
oSleep apnea
Digestive system abnormalities
oGall bladder disease
oHepatic disease
Reproductive system abnormalities
oHormonal complications: Females
oHormonal complications: Males:
oObstetric complications
Nervous system
oAdiposis dolorosa
oPseudotumor cerebri
Immune system dysfunction
Skin diseases
Eye disease
3. Cancer
Breast
Colon
Female reproductive: cervix, endometrium, ovary
Gallbladder
Kidney
Prostate
4. Mechanical complications of obesity
Arthritis
Increased intra-abdominal pressure
5. Surgical complications
Perioperative risks: anesthesia, wound complications,
infections
Incisional hernias
6. Psycho-social complications
Psychological complications
Social complications
Economic impact
‫راه های کاهش وزن‬
‫‪ ‬رژیم غذائی‬
‫‪ ‬افزایش فعالیت ورزشی‬
‫‪ ‬اصالح رفتار (رفتار درمانی)‬
‫‪ ‬دارو‬
‫‪ ‬جراحی‬
‫رژیم غذائی‬
‫‪ ‬مقدار مواد غذائی‬
‫‪ ‬نوع مواد غذائی‬
‫فعالیت ورزشی‬
‫‪ ‬ورزش های مناسب‬
‫‪ ‬میزان مناسب ورزش‬
‫‪ ‬شدت فعالیت های ورزشی‬
‫داروها‬
Xenical
 Sibutramin
 Metformin
 Others

‫جراحی‬
‫رفتار درمانی‬
‫‪ ‬افزایش فعالیت های روزمره‪،‬کاهش استفاده از آسانسور و‬
‫دستگاه های کنترل از راه دور‬
‫‪ ‬کاهش استفاده از غذاهای آماده و پرانرژی‬
‫‪ ‬مراقبت مداوم از تغییرات وزن‬
‫اقدامات ممنوعه‬
‫‪ ‬استفاده از دیورتیک ها‬
‫‪ ‬استفاده از قرص های تیروئید‬
‫‪ ‬ایجاد سوء تغذیه‬
‫‪ ‬رژیم های غذائی غیرعلمی‬
‫وظایف پزشک تیم های ورزشی‬
‫‪ ‬آموزش کافی به ورزشکاران‬
‫‪ ‬پیشگیری از اقدامات ممنوعه‬
‫‪ ‬کمک به اصالح وزن ورزشکاران‬
‫‪ ‬تاًمین کالری کافی در برنامه غذائی ورزشکاران‬
‫خالصه‬