Transcript Set-Point Assumption - Bakersfield College

Chapter 12
Hunger, Eating, and Health
Why Do Many People Eat Too
Much?
Copyright © 2009 by Allyn & Bacon
Control of Eating
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Is there a “set point” for the body’s energy
reserves that determines when we eat?
The prevalence of eating disorders suggests
that this may not be the case
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Over half of the adult population in the U.S.
meets clinical criteria for obesity
The average American consumes 3,800 calories
per day – about twice the average requirement
Copyright © 2009 by Allyn & Bacon
Digestion, Energy Storage,
and Energy Utilization
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Purpose of eating is to provide the body with
molecular building blocks and energy
Digestion – breaking down food and
absorbing its constituents
Energy storage in the body
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Lipids (fats)
Amino acids (proteins)
Glucose (carbohydrates)
Copyright © 2009 by Allyn & Bacon
Copyright © 2009 by Allyn & Bacon
Energy Storage in the Body
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Energy delivered to the body as lipids,
amino acids, and glucose
Stored as fats, glycogen, and proteins
Fats are most efficient for energy storage
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One gram of fat stores twice as much energy
as one gram of glycogen
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Three Phases of Energy
Metabolism
Energy metabolism: Chemical changes
that make energy available for use
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Cephalic phase – preparation for eating
Absorptive phase – energy absorbed
Fasting phase
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Withdrawing energy from reserves
Ends with next cephalic phase
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Three Phases of Energy
Metabolism (continued)
Controlled by two pancreatic hormones
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Insulin – high during cephalic and
absorptive phases
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triggers glucose use as fuel by body cells
triggers conversion of bloodborne energy to fat,
glycogen, and protein
triggers energy storage in adipose cells, liver, and
muscles
Glucagon – high during fasting phase
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triggers change of stored energy to usable fuel: fat to
free fatty acids and then ketones; protein to glucose
Copyright © 2009 by Allyn & Bacon
Copyright © 2009 by Allyn & Bacon
Hunger and Eating: Set Points
vs. Positive Incentives
The Set-Point Assumption:
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Despite lack of evidence, most believe that
hunger is a response to an energy need; we
eat to maintain an energy set point
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Glucostatic and lipostatic theory
Positive Incentive Theory
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Problems with Set-Point Theories of Hunger and Eating
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Epidemic of eating disorders
Contrary to evolutionary pressures that
favored energy storage for survival
Reductions in blood glucose or body fat do
not reliably induce eating
Do not account for the influence of external
factors on eating and hunger
Copyright © 2009 by Allyn & Bacon
Physiological Research on
Hunger and Satiety
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Role of blood glucose levels
Myth of hypothalamic centers
Role of the GI tract
Hunger and satiety peptides
Serotonin and satiety
Copyright © 2009 by Allyn & Bacon
Role of Blood Glucose Levels
in Hunger and Satiety
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Blood glucose drops prior to a meal as
preparation to eat – not a cue to eat
Must decrease blood glucose by 50% to
trigger feeding
Premeal glucose infusions often do not
suppress eating
Reduced blood glucose may contribute to
hunger, but changes in blood glucose do not
prevent hunger or satiety
Copyright © 2009 by Allyn & Bacon
Myth of Hypothalamic Hunger
and Satiety Centers
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Experiments suggested two hypothalamic centers
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Ventromedial (VMH) – a satiety center
Lateral (LH) – a hunger center
Lesions of VMH produce hyperphagia
Lesions of LH produce aphagia and
adipsia
Copyright © 2009 by Allyn & Bacon
Copyright © 2009 by Allyn & Bacon
Myth of Hypothalamic Hunger
and Satiety Centers (continued)
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VMH lesion rats maintain a new higher
weight
LH lesion rats will recover if kept alive by
tube feeding
Hypothalamus – regulates energy
metabolism
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Myth of Hypothalamic Hunger
and Satiety Centers (continued)
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VMH lesions increase blood insulin
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Lipogenesis (fat production) increases
Lipolysis (fat breakdown) decreases
All calories are quickly stored so the rat
must eat more to meet immediate needs
Same results seen with lesions of
noradrenergic bundle or paraventricular
nuclei
Copyright © 2009 by Allyn & Bacon
Myth of Hypothalamic
Hunger and Satiety
Centers (continued)
Location of
hypothalamic
nuclei that
impact
feeding
behavior
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Role of the Gastrointestinal
Tract in Satiety
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Cannon and Washburn (1912)
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Studies suggested stomach contractions led to
hunger, distension to satiety
But – hunger is still experienced with no
stomach
Blood borne satiety signals?
Copyright © 2009 by Allyn & Bacon
Copyright © 2009 by Allyn & Bacon
Hunger and Satiety
Peptides
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Gut peptides that decrease meal size:
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cholecystokinin (CCK), bombesin, glucacon,
alpha-melanocyte-stimulating hormone,
somatostatin
Must first establish that peptide does not
merely create illness
CCK causes nausea at high doses, but
suppresses food intake at doses insufficient
to induce taste aversions
Copyright © 2009 by Allyn & Bacon
Hunger Peptides
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Usually synthesized in the
hypothalamus – neuropeptide Y,
galanin, orexin-A, ghrelin
Many different signals control eating
(not just glucose and fat)
Hypothalamus plays a central role –
microinjections of some peptides have
major effects on eating
Copyright © 2009 by Allyn & Bacon
Serotonin and Satiety
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Serotonin agonists consistently reduce
rats’ food intake
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Even intake of palatable food is affected
Reduces amount eaten per meal
Preferences shift away from fatty foods
Similar effects seen in humans
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Serotonin and Satiety: PraderWilli Syndrome
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Possible key to understanding neural basis of
obesity
Symptoms
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Food-related: insatiable appetite, extremely slow
metabolism; eventual death in adulthood from obesityrelated diseases
Other symptoms: weak muscles, small hands and feet,
triangular mouth, stubbornness, feeding difficulties in
infancy, tantrums, compulsivity, skin picking
Damage or absence of a section of chromosome 15
Copyright © 2009 by Allyn & Bacon
Why Is There an Epidemic of
Obesity?
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Evolution favored preferring highcalorie food, eating to capacity,
storing fat, and using energy
efficiently
Cultural practices and beliefs promote
consumption
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The five stages of a typical weight-loss program.
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Why Do Some People Become Obese and Some Not?
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Energy input differences
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Craving for high-calorie foods
Cultural norms
Large cephalic-phase response to sight and
smell of food
Energy output differences
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Exercise
Diet-induced thermogenesis
NEAT (nonexercise activity thermogenesis)
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Leptin and the Regulation of
Body Fat
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Leptin – a negative feedback fat signal
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ob/ob mice are three times normal weight
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Hormone released by fat cells
Leptin receptors found in the brain
Homozygous for a mutant gene ob
Lack leptin
Eat more, and store fat more efficiently than
controls
Human leptin research
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However, most obese humans have high leptin
levels. Leptin injections help the few ob/ob humans
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Insulin, Leptin, and the
Arcuate Melanocortin System
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Insulin brain levels reflect visceral fat;
leptin levels reflect subcutaneous fat
Both insulin and leptin receptors found
in the arcuate nucleus of the hypothalamus
Copyright © 2009 by Allyn & Bacon
Serotonergic Drugs and the
Treatment of Obesity
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Serotonin appears to increase short-term satiety
signals associated with the consumption of a meal and
decrease…
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urge to eat high-calorie foods
consumption of fat
intensity of hunger
size of meals
number of snacks and bingeing
Early serotonin agonists produced heart disease in
some patients, was withdrawn, and not yet replaced
Copyright © 2009 by Allyn & Bacon
Anorexia Nervosa and Bulimia
Nervosa
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Anorexia
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Voluntary self-starvation
Fatal in 10% of patients
Bulimia – bingeing and purging
Similar symptoms, difficult to distinguish
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Distorted body image
Strike educated, affluent young females
Associated with obsessive-compulsive disorder
and depression
Copyright © 2009 by Allyn & Bacon