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Hunger and Obesity June 22nd, 2005

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Title: Hunger and Obesity June 22nd, 2005


1
Hunger and ObesityJune 22nd, 2005
  • Motivated Behaviors
  • Hunger
  • Why do we eat?
  • Theories of Hunger
  • Set point theory
  • Positive incentive theory
  • What, when and how much do we eat?
  • Biological basis of hunger
  • Obesity

Munch, 1893
2
Hunger and Obesity
3
Hunger and Obesity Energy Storage
  • Lipids (fats)
  • Amino acids (proteins)
  • Glucose (sugar and carbs)

When you eat a meal you provide immediate sources
of energy
4
Hunger and Obesity Sources of Energy
  • Fats (2X the energy of glycogens)
  • proteins
  • glycogen

When no immediate source of energy is available,
energy is consumed from stores
5
Hunger and Obesity Energy Metabolism
6
Hunger and Obesity Theories of Hunger
Set point Theories the body contains a negative
feedback mechanism to control food intake
  • Set point mechanism
  • How much should I eat?
  • Detector
  • How do I need to eat, how much have I eaten ?
  • Effector
  • Eating or not eating a meal.

7
Hunger and Obesity Theories of Hunger
Glucostatic and Lipostatic Set point Theories
  • Glucostatic Set Point Theory
  • We eat when blood glucose levels drop below the
    set point.
  • We are satiated when blood glucose levels return
    to the set point.

Campfield, L.A. Smith, F.J. (2003). Physiol.
Rev. 83 25-58
8
Hunger and Obesity Theories of Hunger
Glucostatic and Lipostatic Set point Theories
Short term food intake
  • Glucostatic Set Point Theory
  • We eat when blood glucose levels drop below the
    set point.
  • We are satiated when blood glucose levels return
    to the set point.
  • Lipostatic Set Point Theory
  • We eat when body fat levels drop below the set
    point.
  • We are satiated when body fat levels return to
    the set point/

Long term food intake
9
Hunger and Obesity Theories of Hunger
Glucostatic and Lipostatic Set point Theories.
However.
  • Obesity?
  • Evolutionarily eat while available, store as
    much as we can!
  • Reductions in glucose and fat needed to support
    this theory rarely occur naturally.
  • Ignores influence of social, taste, and learning
    factors.

10
Hunger and Obesity Theories of Hunger
Positive Incentive Theory we eat because it
feels good!
  • We eat because of the anticipated pleasure of
    eating, foods positive incentive value.
  • Whether you feel hungry depends on
  • Food flavor
  • Memories of the food
  • When did you last eat
  • The amount and quality of food in your gut
  • Are others eating?
  • Are your blood glucose levels in the normal
    range?

11
Hunger and Obesity what, when and how much?
Taste preferences and aversions we learn form
experience.
  • Preferences
  • Humans prefer sweet, salty and fatty tastes.
  • Rats learn to prefer tastes followed by an
    infusion of calories.
  • Rats will learn to prefer tastes they smell on
    the breath of their conspecifics social
    transmission of food preferences.
  • Aversions
  • Taste Aversion

12
Hunger and Obesity what, when and how much?
When we eat is determined by external and
internal factors
If left to snack, we would However, we tend to
eat three large and regular meals at the same
times each day. Why do we feel hungry at meal
time? We have learned to anticipate eating at
that time and our body is preparing for the
cephalic phase of metabolism.
13
Hunger and Drinkingwhat, when and how much?
How much we eat depends on volume and nutritive
density
Sham Eating
14
Hunger and Obesity what, when and how much?
How much we eat depends on volume, nutritive
density and taste
  • Sensory-specific satiety
  • palatability of foods depends on recent
    consumption
  • consumption produces overall satiety, but we will
    become satiated with one food before becoming
    overall satiated.

15
Hunger and Obesity Biological Basis of Hunger
The Hypothalamus
  • Ventromedial hypothalamus satiety center
  • Lateral Hypothalamus feeding center

16
Hunger and Obesity Biological Basis of Hunger
The Hypothalamus
  • Ventromedial hypothalamus lesions produce
    hyperphagia
  • dynamic phase
  • static phase

17
Hunger and Obesity Biological Basis of Hunger
The Hypothalamus
  • lateral hypothalamus lesions produce aphagia
  • adipsia
  • rats can be kept alive and will survive

http//www.awa.com/norton/figures/fig0307a.gif
18
Hunger and Obesity Biological Basis of Hunger
The Hypothalamus revisited
  • Ventromedial hypothalamus lesions
  • Increase insulin levels in the blood which
    increases the storage of fat (lipogenesis) and
    decreases the breakdown of fat (lipolysis).
  • Lesions of the VMH damage the ventral
    noradrenergic bundle projecting from the
    paraventricular nucleus of the thalamus.

19
Hunger and Obesity Biological Basis of Hunger
The Hypothalamus revisited
  • Lateral hypothalamus lesions
  • produce severe motor deficits.
  • general lack of sensory responsiveness.

20
Hunger and Obesity Biological Basis of Hunger
The role of stomach pangs and stomach
distension..
  • Cannon and Washburn

21
Hunger and Obesity Biological Basis of Hunger
Chemicals released from the stomach..
  • Koopmans.

22
Hunger and Obesity Biological Basis of Hunger
  • CCK. Injection of CCK reduces hunger. LOX, a CCK
    antagonist blocks reduction in hunger produced by
    CCK.

Gutzweler (2000). Interaction between CCK and a
preload on reduction of food intake is mediated
by CCK-A receptors in humansAm J Physiol
Regulatory Integrative Comp Physiol, Jul 2000
279 189 - 195
23
Hunger and Obesity Biological Basis of Hunger
  • CCK. Injection of CCK and GLP (glucagen-like
    peptide) inhibits feeding and reduces blood
    glucose.

Gutzweler (2004). Interaction between GLP-1 and
CCK-33 in inhibiting food intake and appetite in
menAm J Physiol Regulatory Integrative Comp
Physiol, Sep 2004 287 562 - 567.
24
Hunger and Obesity Biological Basis of Hunger
  • CCK and serotonin. A 5HT-3 antagonist blocks the
    reduction of food intake produced by CCK in rats.

Hayes, et al. (2004). HT3 receptors participate
in CCK-induced suppression of food intake by
delaying gastric emptyingAm J Physiol Regulatory
Integrative Comp Physiol, Oct 2004 287 817 -
823
25
Hunger and Obesity Biological Basis of Hunger
  • NPY..
  • Injection of NPY into cerebral ventricles (or
    directly into the hypothalamus) of rats potently
    stimulates food intake

Hwa et al (1999). Activation of the NPY Y5
receptor regulates both feeding and energy
expenditureAm J Physiol Regulatory Integrative
Comp Physiol, Nov 1999 277 1428 - 1434
26
Hunger and Obesity Biological Basis of Hunger
NPY.. Mice lacking the gene for NPY decrease
feeding.
Segal-Lieberman (2003) NPY ablation in C57BL/6
mice leads to mild obesity and to an impaired
refeeding response to fastingAm J Physiol
Endocrinol Metab, Jun 2003 284 1131 - 1139.
27
Hunger and Obesity Biological Basis of Hunger
  • Serotonin. Serotonin inhibits NPY..

Fenfluramine Dexfenfluramine
28
Hunger and Obesity Obesity
  • Obesity is a disease that affects nearly
    one-third of the adult American population
    (approximately 60 million).
  • The number of overweight and obese Americans has
    continued to increase since 1960.
  • Today, 64.5 percent of adult Americans (about 127
    million) are categorized as being overweight or
    obese.
  • Each year, obesity causes at least 300,000 excess
    deaths in the U.S., and healthcare costs of
    American adults with obesity amount to
    approximately 100 billion.

BMI weight / height 704.5
A BMI of 30 or more is considered obese and a BMI
between 25 to 29.9 is considered overweight.
http//www.obesity.org/subs/fastfacts/obesity_what
2.shtml
29
Hunger and Obesity Obesity
  • In many developing countries, obesity co-exists
    with under-nutrition.
  • Globally, women generally have higher rates of
    obesity than men do, although men may have higher
    rates of overweight.
  • Obesity is relatively uncommon in African and
    Asian developing countries, although when
    present, it is more prevalent in urban than in
    rural populations.
  • Many South-East Asian countries are presently
    undergoing a nutrition transition involving a
    shift in the structure of diet, decreased
    physical activity and rapid increases in the
    prevalence of obesity.
  • The prevalence of obesity has increased by about
    10 to 40 in the majority of European countries
    over 10 years.
  • Economic development leads to a shift in BMI in
    developing countries. As the proportion of
    under-nutrition decreases, the proportion of the
    overweight population increases.

http//www.obesity.org/subs/fastfacts/obesity_what
2.shtml
30
Hunger and Obesity Obesity causes
Evolution the fittest were those who preferred
a high-calorie diet ate larger meals converted
excess calories to fat for efficient later
use Cultural Influences 3 meals a day food is
the focus of social gatherings foods are served
in order of increasing palatability salt, sugar
and fat are added to foods to increase
palatability Modernization food is more readily
available decrease in exercise increase in
non-traditional foods examples Australian
Aborigines Pima Indians living in
Arizona Native Hawaiians
http//www.obesity.org/subs/fastfacts/obesity_what
2.shtml
31
Hunger and Obesity Obesity causes
ENERGY INPUT ? ENERGY OUTPUT
Eat too much.. strong preference for high
calorie foods cultures/families promoting
excessive eating larger than normal cephalic
Energy output.. too little exercise basal
metabolic rate can metabolism adjust to changes
in consumption? diet-induced thermogeneisis
body fat increases body temperature which in
turn requires more energy. nonexercise activity
thermogenesis
http//www.obesity.org/subs/fastfacts/obesity_what
2.shtml
32
Hunger and Obesity Obesity genes
Ob/Ob mouse lacking the gene that encodes
leptin Leptin is found only in fat cells Role
for leptin in reducing food intake? higher
leptin is associate with higher fat
deposits injections of leptin reduce food intake
and reduce weight leptin receptors are located
in the paraventricular nucleus leptin inhibits
NPY
33
Hunger and Obesity Obesity genes
Tubby mouse gradual increase in body weight
resembling late-onset obesity experience
hearing-loss and loss of visual function weight
gain is due to insulin resistance.
34
Hunger and Obesity Obesity treatments
Dietary Therapy reducing caloric
intake Physical Activity increase energy
usage Behavior Therapy Rewarding specific
actions Changing unrealistic goals and false
beliefs about weight loss and body image.
Developing a social support network Drug
Therapy Orlistat - works by blocking about 30
percent of dietary fat from being
absorbed. Phentermine - an appetite
suppressant. Sibutramine - is an appetite
suppressant. Surgery Obesity surgery is
recommended when BMI 40 or 35 to 39.9 with
serious medical conditions. Obesity surgery is
used to modify the stomach/intestines to reduce
the amount of food that can be eaten.
Restrictive Surgery - uses bands or staples to
create food intake restriction. The bands or
staples are surgically placed near the top of the
stomach to section off a small portion that is
often called a stomach pouch.  A small outlet,
about the size of a pencil eraser, is left at the
bottom of the stomach pouch.  Since the outlet is
small, food stays in the pouch longer and you
also feel full for a longer time. Combined
Restrictive and Malabsorptive Surgery - is a
combination of restrictive surgery (stomach
pouch) with bypass (malabsorptive surgery), in
which the stomach is connected to the jejunum or
ileum of the small intestine, bypassing the
duodenum.8
Restrictive Surgery
Combined Restrictive and Malabsorptive Surgery
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