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Obesity & Hormones
MJ Rasaee TMU
2022
1
Fat
Stores
Obesity Is Caused by Long-Term Positive Energy Balance  Heredity
 Leptin :Protein produced by the body; anti-obesity hormone—the
more leptin you produce, the fuller you feel
 Set point :the weight maintained when no effort is put into gaining or
losing weight—the more you eat, the larger your set point becomes
 Metabolism : basal metabolism rate-BMR—the minimal amount of
energy an individual uses in a resting state—the more BMR
declines, the easier it becomes to gain weight
 Environmental factors : taste preferences, the availability of food,
energy-saving devices, declining physical activity. Chemical
toxicity(diethylstilbestrol (DES),bisphenol A (BPA),,phthalates, ,organotins,
polybrominated ,diphenyl ethers (PBDEs), polyfluoroalkyl chemicals
(PFCs), organochlorine (OC) pesticides, polychlorinated biphenyls (PCBs)
and some solvents caused weight gain, and it is proposed that these
chemicals were interfering with weight homeostasis by changing weight-
controlling hormones, modifying sensitivity to neurotransmitters, or altering
the sympathetic nervous system activity
 Ethnicity and gender : African American and Latino women become
obese faster than White women; Latino men become obese faster
than African American and White men
 Stress, inadequate sleep ,maternal smoking
The World Health Organization included excess weight, with a
prevalence higher than undernutrition, as one of the top 10 health risks
worldwide.It is estimated that by continuing the actual trend, the global
prevalence rate of 33.0% for overweight and obesity among adult
population (1.3 billion people) in 2005 would reach up to 57.8% (3.3
billion people) by 2030
3
(Desirable % Body Fat Men: 8-25% Women 20-30%)
The WHO regards a BMI of less than 18.5 as
underweight and may indicate malnutrition an
eating disorder, or other health problems, while a
BMI equal to or greater than 25 is considered
overweight and above 30 is considered obese.
According to the International Obesity Task
Force, obesity is defined as a body mass index
(BMI) ≥ 30 kg/m2 .Patients meeting this
criterion for obesity have a significantly
increased risk of numerous morbidities
BMI 30.0-34.9 kg/m2
Grade I
BMI 35.0-39.9 kg.m2
Grade II
BMI >40 kg/m2
Grade III (morbid
,extreme )
4
obesity is correlated with reductions in sperm
concentration and motility, increase in sperm DNA
damage and changes in reproductive hormones. Low
testosterone levels linked to excess weight.
obese men were 2.4 times more likely to have low
testosterone compared to those at a healthy weight.
Studies have also shown that as (Body Mass Index (BMI)
increases, there is proportionate reduction in testosterone
levels
1. the excessive conversion of androgens into estrogens
in redundant adipose tissue causes sexual hormone
imbalance, subsequently resulting in hypogonadism.
2. Secondly, adipokines produced by adipose tissue
induce severe inflammation and oxidative stress in
male reproductive tract, directly impairing testicular
and epididymal tissues.
3. increased scrotal adiposity leads to increase gonadal
heat, continuously hurting spermatogenesis. obesity
alters the systematic and regional environment
crucial for spermatogenesis in testis and sperm
maturation in epididymis, and finally results in poor
sperm quality including decreased sperm motility,
abnormal sperm morphology and acrosome reaction,
changed membrane lipids and increased DNA
damage
5
6
Resistin & Insulin resistance .The link between insulin
and weight gain
‫انسولین‬ ‫افزایش‬ ‫سبب‬ ‫فروکتوز‬ ‫پر‬ ‫و‬ ‫فیبر‬ ‫کم‬ ‫غذای‬
-
‫انسولین‬ ‫افزایش‬ ‫سبب‬ ‫تحرکی‬ ‫بی‬
-
‫چربی‬ ‫بافت‬ ‫به‬ ‫انرژی‬ ‫انتقال‬
‫گرسنگی‬ ‫بروز‬ ‫سبب‬ ‫و‬ ‫لپتین‬ ‫پیامهای‬ ‫در‬ ‫مداخله‬
‫را‬ ‫انسولین‬ ‫به‬ ‫ها‬ ‫ماهیچه‬ ‫وحساسیت‬ ‫است‬ ‫سوز‬ ‫کالری‬ ‫ورزشی‬ ‫تمرینات‬
‫کورتیزو‬ ‫سازی‬ ‫رها‬ ‫و‬ ‫تولید‬ ‫و‬ ‫داده‬ ‫کاهش‬ ‫را‬ ‫روحی‬ ‫فشار‬ ‫و‬ ‫میدهد‬ ‫افزایش‬
‫را‬ ‫ل‬
‫افزایش‬ ‫و‬ ‫فروکتوز‬ ‫حذف‬ ‫و‬ ‫کربس‬ ‫چرخه‬ ‫سرعت‬ ‫سبب‬ ‫و‬ ‫میدهد‬ ‫افزایش‬
‫میشود‬ ‫کبدی‬ ‫انسولین‬ ‫به‬ ‫حساسیت‬
.
‫آنهار‬ ‫که‬ ‫ای‬ ‫روده‬ ‫باکتریهای‬ ‫توسط‬ ‫چرب‬ ‫های‬ ‫اسید‬ ‫جذب‬ ‫از‬ ‫فیبر‬ ‫مصرف‬
‫ا‬
‫ج‬ ‫میکنند‬ ‫تبدیل‬ ‫انسولین‬ ‫کننده‬ ‫کوچکترمهار‬ ‫های‬ ‫واحد‬ ‫به‬ ‫و‬ ‫داده‬ ‫برش‬
‫گیری‬ ‫لو‬
‫میکنند‬
7
7
obesity and diabetes
Pancreatic hormones
The insulin, glucagon and pancreatic polypeptide content in
obese mice was greater than that of lean controls
Insulin resistance & FFA
Second mechanism
8
9
Reciprocal relations between obesity and stress
Chronic stress, manifested with depressive or anxiety
symptoms, can induce prolonged activation of the
hypothalamic-pituitary-adrenal (HPA) axis and
sympathetic nervous system (SNS) which together
with health risk behaviors, can progressively lead to
visceral obesity and vice .
11
monocyte chemoattractant protein–1
(
MCP-1
)
plasminogen activator inhibitor type 1 (PAI-1).
12
Esterogen and Body fat distribution
Estrogen deficiency causes central leptin
resistance and increased hypothalamic
NPY
‫لپتین‬ ‫افزایش‬ ‫بدلیل‬ ‫رس‬ ‫زود‬ ‫منس‬
‫انسولین‬ ‫مقابل‬ ‫در‬ ‫مقاومت‬ ‫و‬ ‫چاقی‬ ‫بدلیل‬ ‫تخمدانی‬ ‫کیست‬
Obesity and tumour development
13
Obesity and cancer
14
• 1)GH → Lipolysis ( adipose tissue ) →
↑ FFA → Negative feed back secretion
GH ( increase FFA in obesity )
2) Increase insulin
• 3) Adipocytes seem to secrete IGF-1
in response to GH, and in obesity,
individual fat cells may secrete less
IGF-1 than in normal subjects. The
net overall effect of the increased
number of fat cells in obese subjects
would offset this, leading to the
observed elevation in IGF-1. The
depressed GH due to elevated IGF-1
in obesity
Reduction GH secretion in obesity
Unbound IGF-1 mediates a negative feedback control
of GH secretion by acting directly onthe somatotroph
and on hypothalamic GHRH and somatostatin neurons
In animal models of genetic
obesity there is a decrease in the
number of somatotroph cells in the
pituitary gland. GH responses to a
variety of stimuli such stimuli
included GHRH, Arginine, and
GHRPs (growth hormone
releasing peptides) have also been
shown to be reduced and
Increased GH Clearance Rate In
Obesity
 Drugs that primarily decrease appetite or increase satiety
 Ciliary neurotrophic factor
 Cannabinoid (CB1) receptor antagonist (rimonabant)
 P57
 Dopamine antagonist (risperidone)
 Selective 5-HT2C receptor agonists
 Topiramate
 Dopamine and norepinephrine reuptake inhibitors
 Melanocortin-4 receptor (MC4R) agonists
 Neuropeptide Y antagonists
 Drugs that primarily increase RMR or thermogenesis
 Adipocyte complement – related protein of 30kD (Acrp30)
 β-3 adrenergic receptor stimulators (β-agonists)
 Thyroid receptor agonists
 Drugs that increase RMR and thermogenesis and decrease appetite
 ‘Second-generation’leptin
 Gastrointestinal-acting drugs
 Cholecystokinin-A promoter (CCK-A promoter)
 Glucagon-like peptide–1 (GLP-1)
 Lipase inhibitor
 Phytostanol
 Ghrelin antagonists
 Growth hormone fragment
 Insulin sensitizers (protein tyrosine phosphatase drugs, peroxisome proliferation activator gamma receptor antagonists, short-acting
bromocriptine, carboxypeptidase inhibitors, somatostatin agonists
Anti-obesity drugs in development
16
Hormones & Weight
•Thyroid hormones is a major regulator energy metabolism
(BMR) .Defects in thyroid status are frequently associated
with changes in body weight. the function of the
hypothalamic-pituitary-thyroid axis in obesity can be
essentially normal.
•Thyroid hormones regulates tub gene which when mutated
in mic causes obesity, insulin resistance and sensory defects
•Overfeeding :↑T3 ( increase conversion T4 →T3) & ↓ rT3
decrease clearance ) & caloric restriction( reverse ) can
affect the concentrations of T3 and reverse T3 with return to
normal when a steady state of the caloric balance has been
reached.
Stress → ↑ Cortisol → Glucogenesis of proteins → ↑ Glucose
→ Lipogenesis
*Exogenous cortisol --> increased food intake in humans
*Glucocorticoid antagonists prevent obesity.(Cortisol may also
play a role in poor eating habits.women who secreted higher
levels of cortisol while under stress had a much greater tendency
to snack on high-fat foods than did women who did not secrete as
much cortisol in reaction to the same stressful event)
In general, adrenal dysfunction can lead to hypothyroidism,
lowered metabolic rate, and weight gain
Adrenal hormones
DHEA & Anti-obesity
DHEA exhibits an anti-obesity effect by decreasing fat
tissue, insulin, and food intake.
‫لپ‬ ‫به‬ ‫مقاومت‬ ‫سبب‬ ‫که‬ ‫زیرا‬ ‫میشوند‬ ‫وزن‬ ‫افزایش‬ ‫سبب‬ ‫ها‬ ‫استرویید‬ ‫کورتیکو‬
‫تین‬
‫میگردند‬
.
-
‫در‬ ‫کورتیزون‬ ‫موضعی‬ ‫تبدیل‬ ‫اما‬ ‫است‬ ‫طبیعی‬ ‫چاق‬ ‫افراد‬ ‫در‬ ‫کورتیزول‬ ‫غلظت‬
‫آنزیم‬ ‫غلظت‬ ‫افزایش‬ ‫خاطر‬ ‫به‬ ‫پوستی‬ ‫زیر‬ ‫چربی‬ ‫سلولهای‬
11
‫هیدروکس‬ ‫بتا‬
‫میشود‬ ‫بیشتر‬ ‫کورتیزول‬ ‫به‬ ‫هیدروژناز‬ ‫د‬ ‫استرویید‬
.
‫د‬ ‫جی‬ ‫بی‬ ‫سی‬ ‫ضمناغلظت‬
‫ر‬
‫میابد‬ ‫کاهش‬ ‫چاقی‬
Ghrelin Hunger Hormone opposite of leptin
Ghrelin is an endogenous ligand for the growth hormone secretagogue receptor
secreted by the stomach and GI tract, Opposite” of Leptin. which May account for
the observed increased appetite after dieting. Inhibition of this hormone may be a
potential target in the treatment of obesity, and specially weight regain Having
Hypothalamic receptors which Rises just before meals and falls after
Ghrelin administration in rats strongly stimulates feeding, while Anti-
Ghrelin Abs suppress feeding .High Ghrelin levels in Prader-Willi
syndrome
Variations in ghrelin and
insulin relative to meal
times
Rises just before meals and falls after
Does not decline after a meal in obese people
Increased levels in blood stimulate appetite and efficient energy storage
Anti-Ghrelin Abs suppress feeding
Increased due to short sleep duration
18
Set-point model for maintaining constant mass
Decrease hunger and food consumption -
inhibition of neuropeptide Y synthesis .
Food intake linked to its ability to regulate
the neuroendocrine system .
Regulation of food intake ,energy expenditure and body weight .
Thermogenesis .
Reproductive function .
Suppressed bone formation .
Directly act on the cells of liver and muscles .
Related to inflammatory response .
Contribute to early hematopoiesis
 Leptin's central actions :
 Increase energy expenditure (via physical
activity, sympathetic nervous system
activity)
 Decrease food intake
 Decrease body weight
 Increase insulin sensitivity
 Help signal the onset of puberty
 Regulate other pituitary hormone axes
 Leptin’s peripheral actions
 Stimulate angiogenesis
 Hematopoietic cell proliferation
 T-cell immnunity
Obesity caused by defective leptin production
19
The JAK-STAT mechanism of leptin signal
transduction in the hypothalamus
A possible mechanism for cross-talk between receptors
for insulin and leptin
20
Inhibits intracellular lipid concentration
Activate 5 –AMP-activated protein kinase (AMPK)
Inhibits acetyl coenzyme-A carboxylase (ACC)
Increase in fatty acid oxidation and reducing the fat tissue in
muscles and liver .
Increase insulin sensitivity .
Role of leptin in lipid metabolism
Inducers Effect Species
Feeding + Rodent + man
Glucocorticoids + Rodent + man
Insulin + Rodent
C or + Man
Cytokines + Rodent
Obesity + Rodent + man
Fasting - Rodent + man
Pertussis toxin - Rodent
-receptor
antagonists
- Rodent
Thiazolidinedion
es
- Rodent
cAMP - Rodent
Inducers and suppressers of leptin expression
21
Hormones & Appetite The Appetite Center
1)Some obese people may make leptin at greater rate to compensate for faulty
signaling process
2) Resistance to leptin (more leptin may be required for action)
3)Obese individuals are in a state perceived starvation →↑food intake →↑
lipogenesis →↑ Leptin
1. Regulates energy balance by
2. Increase thermogenesis by activating SNS
3. Decrease food intake by inhibition of orexigenic pathway NPY ---Agouti
related peptide (AGRP) and by activating anorexigenic pathway POMC----
corticoliberin –MSH---MC4R
4. Inhibits puberty and facilitate fertility by activating LHRH
22
Hormones that control eating
Hormones
Orexigenic ( appetite – stimulating ) : Ghrelin
Anorectic ( appetite – suppressing) : Leptin
Long-term control of energy stores : hormones produced by adipose tissue & Insulin
Acute affect on hunger and satiety : gastrointestinal hormones
Appetite control
Gastrointestinal hormones
Orexigenic
Ghrelin : biggest stimulator of hunger
Synthesised in the stomach when it is empty
regard less of fat stores
Anoretic
CCK
GLP-1
PYY
Obestatin
Major and first satiety signal is
CCK Secreted by stomach after
intake → stop food intake
24
• α-MSH activation of MC4R
•
• Occurs in the paraventricular nucleus of the
hypothalamus
• Receptor couples to heterotrimeric Gs protein
• Activates adenylyl cyclase
• Prevents hyperphagia and obesity
AGRP
46 amino acids C-terminal cysteine-rich motif
Inhibits MCR-3, 4, & 5
Competitive antagonist
Inverse agonist
25
Mutation of the gene for leptin receptors in the brain
Post receptor abnormalities in leptin signal transduction
Impaired leptin transport across blood- brain barrier
Leptin resistance
26
PANCREATIC HORMONES REGULATING FOOD INTAKE
Peptide Stimulus Site of
Production
Site of Action effect on food
intake
Insulin carbohydrate β-cell brain decrease
Amylin carbohydrate β -cell brain decrease
Glucagon cephalic
response
α-cell liver/vagal
afferents
decrease
Amylin, or islet amyloid polypeptide (IAPP), is a 37-residue peptide hormone.It is cosecreted with insulin from the
pancreatic β-cells in the ratio of approximately 100:1 (insulin:amylin). Amylin plays a role in glycemic regulation by
slowing gastric emptying and promoting satiety, thereby preventing post-prandial spikes in blood glucose levels.
Inducers Effect Species
Feeding + Rodent + man
Glucocorticoids + Rodent + man
Insulin + Rodent
C or + Man
Cytokines + Rodent
Obesity + Rodent + man
Fasting - Rodent + man
Pertussis toxin - Rodent
-receptor
antagonists
- Rodent
Thiazolidinediones - Rodent
cAMP - Rodent
Inducers and suppressers of leptin expression

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Obesity..ppt

  • 1. Obesity & Hormones MJ Rasaee TMU 2022 1
  • 2. Fat Stores Obesity Is Caused by Long-Term Positive Energy Balance  Heredity  Leptin :Protein produced by the body; anti-obesity hormone—the more leptin you produce, the fuller you feel  Set point :the weight maintained when no effort is put into gaining or losing weight—the more you eat, the larger your set point becomes  Metabolism : basal metabolism rate-BMR—the minimal amount of energy an individual uses in a resting state—the more BMR declines, the easier it becomes to gain weight  Environmental factors : taste preferences, the availability of food, energy-saving devices, declining physical activity. Chemical toxicity(diethylstilbestrol (DES),bisphenol A (BPA),,phthalates, ,organotins, polybrominated ,diphenyl ethers (PBDEs), polyfluoroalkyl chemicals (PFCs), organochlorine (OC) pesticides, polychlorinated biphenyls (PCBs) and some solvents caused weight gain, and it is proposed that these chemicals were interfering with weight homeostasis by changing weight- controlling hormones, modifying sensitivity to neurotransmitters, or altering the sympathetic nervous system activity  Ethnicity and gender : African American and Latino women become obese faster than White women; Latino men become obese faster than African American and White men  Stress, inadequate sleep ,maternal smoking The World Health Organization included excess weight, with a prevalence higher than undernutrition, as one of the top 10 health risks worldwide.It is estimated that by continuing the actual trend, the global prevalence rate of 33.0% for overweight and obesity among adult population (1.3 billion people) in 2005 would reach up to 57.8% (3.3 billion people) by 2030
  • 3. 3 (Desirable % Body Fat Men: 8-25% Women 20-30%) The WHO regards a BMI of less than 18.5 as underweight and may indicate malnutrition an eating disorder, or other health problems, while a BMI equal to or greater than 25 is considered overweight and above 30 is considered obese. According to the International Obesity Task Force, obesity is defined as a body mass index (BMI) ≥ 30 kg/m2 .Patients meeting this criterion for obesity have a significantly increased risk of numerous morbidities BMI 30.0-34.9 kg/m2 Grade I BMI 35.0-39.9 kg.m2 Grade II BMI >40 kg/m2 Grade III (morbid ,extreme )
  • 4. 4 obesity is correlated with reductions in sperm concentration and motility, increase in sperm DNA damage and changes in reproductive hormones. Low testosterone levels linked to excess weight. obese men were 2.4 times more likely to have low testosterone compared to those at a healthy weight. Studies have also shown that as (Body Mass Index (BMI) increases, there is proportionate reduction in testosterone levels 1. the excessive conversion of androgens into estrogens in redundant adipose tissue causes sexual hormone imbalance, subsequently resulting in hypogonadism. 2. Secondly, adipokines produced by adipose tissue induce severe inflammation and oxidative stress in male reproductive tract, directly impairing testicular and epididymal tissues. 3. increased scrotal adiposity leads to increase gonadal heat, continuously hurting spermatogenesis. obesity alters the systematic and regional environment crucial for spermatogenesis in testis and sperm maturation in epididymis, and finally results in poor sperm quality including decreased sperm motility, abnormal sperm morphology and acrosome reaction, changed membrane lipids and increased DNA damage
  • 5. 5
  • 6. 6 Resistin & Insulin resistance .The link between insulin and weight gain ‫انسولین‬ ‫افزایش‬ ‫سبب‬ ‫فروکتوز‬ ‫پر‬ ‫و‬ ‫فیبر‬ ‫کم‬ ‫غذای‬ - ‫انسولین‬ ‫افزایش‬ ‫سبب‬ ‫تحرکی‬ ‫بی‬ - ‫چربی‬ ‫بافت‬ ‫به‬ ‫انرژی‬ ‫انتقال‬ ‫گرسنگی‬ ‫بروز‬ ‫سبب‬ ‫و‬ ‫لپتین‬ ‫پیامهای‬ ‫در‬ ‫مداخله‬ ‫را‬ ‫انسولین‬ ‫به‬ ‫ها‬ ‫ماهیچه‬ ‫وحساسیت‬ ‫است‬ ‫سوز‬ ‫کالری‬ ‫ورزشی‬ ‫تمرینات‬ ‫کورتیزو‬ ‫سازی‬ ‫رها‬ ‫و‬ ‫تولید‬ ‫و‬ ‫داده‬ ‫کاهش‬ ‫را‬ ‫روحی‬ ‫فشار‬ ‫و‬ ‫میدهد‬ ‫افزایش‬ ‫را‬ ‫ل‬ ‫افزایش‬ ‫و‬ ‫فروکتوز‬ ‫حذف‬ ‫و‬ ‫کربس‬ ‫چرخه‬ ‫سرعت‬ ‫سبب‬ ‫و‬ ‫میدهد‬ ‫افزایش‬ ‫میشود‬ ‫کبدی‬ ‫انسولین‬ ‫به‬ ‫حساسیت‬ . ‫آنهار‬ ‫که‬ ‫ای‬ ‫روده‬ ‫باکتریهای‬ ‫توسط‬ ‫چرب‬ ‫های‬ ‫اسید‬ ‫جذب‬ ‫از‬ ‫فیبر‬ ‫مصرف‬ ‫ا‬ ‫ج‬ ‫میکنند‬ ‫تبدیل‬ ‫انسولین‬ ‫کننده‬ ‫کوچکترمهار‬ ‫های‬ ‫واحد‬ ‫به‬ ‫و‬ ‫داده‬ ‫برش‬ ‫گیری‬ ‫لو‬ ‫میکنند‬
  • 7. 7 7 obesity and diabetes Pancreatic hormones The insulin, glucagon and pancreatic polypeptide content in obese mice was greater than that of lean controls
  • 8. Insulin resistance & FFA Second mechanism 8
  • 9. 9 Reciprocal relations between obesity and stress Chronic stress, manifested with depressive or anxiety symptoms, can induce prolonged activation of the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS) which together with health risk behaviors, can progressively lead to visceral obesity and vice .
  • 10.
  • 12. 12 Esterogen and Body fat distribution Estrogen deficiency causes central leptin resistance and increased hypothalamic NPY ‫لپتین‬ ‫افزایش‬ ‫بدلیل‬ ‫رس‬ ‫زود‬ ‫منس‬ ‫انسولین‬ ‫مقابل‬ ‫در‬ ‫مقاومت‬ ‫و‬ ‫چاقی‬ ‫بدلیل‬ ‫تخمدانی‬ ‫کیست‬
  • 13. Obesity and tumour development 13 Obesity and cancer
  • 14. 14 • 1)GH → Lipolysis ( adipose tissue ) → ↑ FFA → Negative feed back secretion GH ( increase FFA in obesity ) 2) Increase insulin • 3) Adipocytes seem to secrete IGF-1 in response to GH, and in obesity, individual fat cells may secrete less IGF-1 than in normal subjects. The net overall effect of the increased number of fat cells in obese subjects would offset this, leading to the observed elevation in IGF-1. The depressed GH due to elevated IGF-1 in obesity Reduction GH secretion in obesity Unbound IGF-1 mediates a negative feedback control of GH secretion by acting directly onthe somatotroph and on hypothalamic GHRH and somatostatin neurons In animal models of genetic obesity there is a decrease in the number of somatotroph cells in the pituitary gland. GH responses to a variety of stimuli such stimuli included GHRH, Arginine, and GHRPs (growth hormone releasing peptides) have also been shown to be reduced and Increased GH Clearance Rate In Obesity
  • 15.  Drugs that primarily decrease appetite or increase satiety  Ciliary neurotrophic factor  Cannabinoid (CB1) receptor antagonist (rimonabant)  P57  Dopamine antagonist (risperidone)  Selective 5-HT2C receptor agonists  Topiramate  Dopamine and norepinephrine reuptake inhibitors  Melanocortin-4 receptor (MC4R) agonists  Neuropeptide Y antagonists  Drugs that primarily increase RMR or thermogenesis  Adipocyte complement – related protein of 30kD (Acrp30)  β-3 adrenergic receptor stimulators (β-agonists)  Thyroid receptor agonists  Drugs that increase RMR and thermogenesis and decrease appetite  ‘Second-generation’leptin  Gastrointestinal-acting drugs  Cholecystokinin-A promoter (CCK-A promoter)  Glucagon-like peptide–1 (GLP-1)  Lipase inhibitor  Phytostanol  Ghrelin antagonists  Growth hormone fragment  Insulin sensitizers (protein tyrosine phosphatase drugs, peroxisome proliferation activator gamma receptor antagonists, short-acting bromocriptine, carboxypeptidase inhibitors, somatostatin agonists Anti-obesity drugs in development
  • 16. 16 Hormones & Weight •Thyroid hormones is a major regulator energy metabolism (BMR) .Defects in thyroid status are frequently associated with changes in body weight. the function of the hypothalamic-pituitary-thyroid axis in obesity can be essentially normal. •Thyroid hormones regulates tub gene which when mutated in mic causes obesity, insulin resistance and sensory defects •Overfeeding :↑T3 ( increase conversion T4 →T3) & ↓ rT3 decrease clearance ) & caloric restriction( reverse ) can affect the concentrations of T3 and reverse T3 with return to normal when a steady state of the caloric balance has been reached. Stress → ↑ Cortisol → Glucogenesis of proteins → ↑ Glucose → Lipogenesis *Exogenous cortisol --> increased food intake in humans *Glucocorticoid antagonists prevent obesity.(Cortisol may also play a role in poor eating habits.women who secreted higher levels of cortisol while under stress had a much greater tendency to snack on high-fat foods than did women who did not secrete as much cortisol in reaction to the same stressful event) In general, adrenal dysfunction can lead to hypothyroidism, lowered metabolic rate, and weight gain Adrenal hormones DHEA & Anti-obesity DHEA exhibits an anti-obesity effect by decreasing fat tissue, insulin, and food intake. ‫لپ‬ ‫به‬ ‫مقاومت‬ ‫سبب‬ ‫که‬ ‫زیرا‬ ‫میشوند‬ ‫وزن‬ ‫افزایش‬ ‫سبب‬ ‫ها‬ ‫استرویید‬ ‫کورتیکو‬ ‫تین‬ ‫میگردند‬ . - ‫در‬ ‫کورتیزون‬ ‫موضعی‬ ‫تبدیل‬ ‫اما‬ ‫است‬ ‫طبیعی‬ ‫چاق‬ ‫افراد‬ ‫در‬ ‫کورتیزول‬ ‫غلظت‬ ‫آنزیم‬ ‫غلظت‬ ‫افزایش‬ ‫خاطر‬ ‫به‬ ‫پوستی‬ ‫زیر‬ ‫چربی‬ ‫سلولهای‬ 11 ‫هیدروکس‬ ‫بتا‬ ‫میشود‬ ‫بیشتر‬ ‫کورتیزول‬ ‫به‬ ‫هیدروژناز‬ ‫د‬ ‫استرویید‬ . ‫د‬ ‫جی‬ ‫بی‬ ‫سی‬ ‫ضمناغلظت‬ ‫ر‬ ‫میابد‬ ‫کاهش‬ ‫چاقی‬
  • 17. Ghrelin Hunger Hormone opposite of leptin Ghrelin is an endogenous ligand for the growth hormone secretagogue receptor secreted by the stomach and GI tract, Opposite” of Leptin. which May account for the observed increased appetite after dieting. Inhibition of this hormone may be a potential target in the treatment of obesity, and specially weight regain Having Hypothalamic receptors which Rises just before meals and falls after Ghrelin administration in rats strongly stimulates feeding, while Anti- Ghrelin Abs suppress feeding .High Ghrelin levels in Prader-Willi syndrome Variations in ghrelin and insulin relative to meal times Rises just before meals and falls after Does not decline after a meal in obese people Increased levels in blood stimulate appetite and efficient energy storage Anti-Ghrelin Abs suppress feeding Increased due to short sleep duration
  • 18. 18 Set-point model for maintaining constant mass Decrease hunger and food consumption - inhibition of neuropeptide Y synthesis . Food intake linked to its ability to regulate the neuroendocrine system . Regulation of food intake ,energy expenditure and body weight . Thermogenesis . Reproductive function . Suppressed bone formation . Directly act on the cells of liver and muscles . Related to inflammatory response . Contribute to early hematopoiesis  Leptin's central actions :  Increase energy expenditure (via physical activity, sympathetic nervous system activity)  Decrease food intake  Decrease body weight  Increase insulin sensitivity  Help signal the onset of puberty  Regulate other pituitary hormone axes  Leptin’s peripheral actions  Stimulate angiogenesis  Hematopoietic cell proliferation  T-cell immnunity Obesity caused by defective leptin production
  • 19. 19 The JAK-STAT mechanism of leptin signal transduction in the hypothalamus A possible mechanism for cross-talk between receptors for insulin and leptin
  • 20. 20 Inhibits intracellular lipid concentration Activate 5 –AMP-activated protein kinase (AMPK) Inhibits acetyl coenzyme-A carboxylase (ACC) Increase in fatty acid oxidation and reducing the fat tissue in muscles and liver . Increase insulin sensitivity . Role of leptin in lipid metabolism Inducers Effect Species Feeding + Rodent + man Glucocorticoids + Rodent + man Insulin + Rodent C or + Man Cytokines + Rodent Obesity + Rodent + man Fasting - Rodent + man Pertussis toxin - Rodent -receptor antagonists - Rodent Thiazolidinedion es - Rodent cAMP - Rodent Inducers and suppressers of leptin expression
  • 21. 21 Hormones & Appetite The Appetite Center 1)Some obese people may make leptin at greater rate to compensate for faulty signaling process 2) Resistance to leptin (more leptin may be required for action) 3)Obese individuals are in a state perceived starvation →↑food intake →↑ lipogenesis →↑ Leptin 1. Regulates energy balance by 2. Increase thermogenesis by activating SNS 3. Decrease food intake by inhibition of orexigenic pathway NPY ---Agouti related peptide (AGRP) and by activating anorexigenic pathway POMC---- corticoliberin –MSH---MC4R 4. Inhibits puberty and facilitate fertility by activating LHRH
  • 22. 22
  • 23. Hormones that control eating Hormones Orexigenic ( appetite – stimulating ) : Ghrelin Anorectic ( appetite – suppressing) : Leptin Long-term control of energy stores : hormones produced by adipose tissue & Insulin Acute affect on hunger and satiety : gastrointestinal hormones Appetite control Gastrointestinal hormones Orexigenic Ghrelin : biggest stimulator of hunger Synthesised in the stomach when it is empty regard less of fat stores Anoretic CCK GLP-1 PYY Obestatin Major and first satiety signal is CCK Secreted by stomach after intake → stop food intake
  • 24. 24 • α-MSH activation of MC4R • • Occurs in the paraventricular nucleus of the hypothalamus • Receptor couples to heterotrimeric Gs protein • Activates adenylyl cyclase • Prevents hyperphagia and obesity AGRP 46 amino acids C-terminal cysteine-rich motif Inhibits MCR-3, 4, & 5 Competitive antagonist Inverse agonist
  • 25. 25 Mutation of the gene for leptin receptors in the brain Post receptor abnormalities in leptin signal transduction Impaired leptin transport across blood- brain barrier Leptin resistance
  • 26. 26 PANCREATIC HORMONES REGULATING FOOD INTAKE Peptide Stimulus Site of Production Site of Action effect on food intake Insulin carbohydrate β-cell brain decrease Amylin carbohydrate β -cell brain decrease Glucagon cephalic response α-cell liver/vagal afferents decrease Amylin, or islet amyloid polypeptide (IAPP), is a 37-residue peptide hormone.It is cosecreted with insulin from the pancreatic β-cells in the ratio of approximately 100:1 (insulin:amylin). Amylin plays a role in glycemic regulation by slowing gastric emptying and promoting satiety, thereby preventing post-prandial spikes in blood glucose levels. Inducers Effect Species Feeding + Rodent + man Glucocorticoids + Rodent + man Insulin + Rodent C or + Man Cytokines + Rodent Obesity + Rodent + man Fasting - Rodent + man Pertussis toxin - Rodent -receptor antagonists - Rodent Thiazolidinediones - Rodent cAMP - Rodent Inducers and suppressers of leptin expression

Editor's Notes

  1. Obesity is caused by long-term positive energy balance Obesity is caused by ingesting more energy than is expended over a long period of time. The excess calories that are consumed lead to an accumulation of body fat either by being stored as fat or preventing the mobilization and oxidation of endogenous fat. In general, ingesting 3500 kcal more (or less) than expended will lead to a gain (or loss) of approximately 1 lb of fat. Genetic factors may influence the amount of weight gained with overfeeding. In one study, weight gain varied greatly among 12 monozygotic twin pairs who were chronically overfed 1000 kcal/d [1]. However, weight gains were very similar within each member of a twin pair. In another study, body fat gain after 8 weeks of overfeeding also varied among study subjects but was inversely related to changes in non-volitional energy expenditure, such as fidgeting, which may be determined genetically [2]. Bouchard C, Tremblay A, Despres JP, et al. The response to long-term overfeeding in identical twins. N Engl J Med 1990;322:1477-1482. Levine JA, Eberhardt NL, Jensen MD. Role of nonexercise activity thermogenesis in resistance to fat gain in humans. Science 1999;282:212-214.