Discussion 6

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Physiology of Behavior

Twelfth Edition

Chapter 12 Ingestive Behavior

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Chapter Preview

Drinking

Eating: What is Metabolism?

Eating: Signals to Start a Meal

Eating: Signals to Stop a Meal

Brain Mechanisms

Obesity

Eating disorders

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Learning Objectives (1 of 5)

12.1 Explain the characteristics of a physiological regulatory mechanism.

12.2 Compare osmometric and volumetric thirst.

12.3 Identify the roles of the subfornical organ and median preoptic nucleus in regulating thirst.

12.4 Describe the function, location, and contents of the short-term reservoir.

12.5 Describe the function, location, and contents of the long-term reservoir.

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Learning Objectives (2 of 5)

12.6 Compare the pathways for the use of glucose, fat, and amino acids by the brain and body in the fasting phase.

12.7 Compare the pathways for the use of glucose, fat, and amino acids by the brain and body in the absorptive phase.

12.8 Describe ghrelin’s function as a hunger signal including its origin and relationship to obesity, fasting, and absorptive phases.

12.9 Describe how metabolic signals can play a role in starting a meal.

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Learning Objectives (3 of 5)

12.10 Describe the general function of short term satiety signals.

12.11 Identify examples of environmental factors that contribute to satiety.

12.12 Identify sensory factors that contribute to satiety.

12.13 Explain how the stomach can provide satiety signals.

12.14 Describe how the intestines can provide satiety signals.

12.15 Explain how the liver provides late-stage satiety signals.

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Learning Objectives (4 of 5)

12.16 Describe how insulin can function as a satiety signal.

12.17 Contrast the function of satiety signals from adipose tissue with short-term satiety signals.

12.18 Identify the functions of the brain stem involved in eating regulation.

12.19 Describe the role of nuclei and neurochemical systems of the hypothalamus in hunger and satiety.

12.20 Discuss the contributions of environment, physical activity, and genetics to the development of obesity.

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Learning Objectives (5 of 5)

12.21 Evaluate the roles of reinforcement, stress, surgery, pharmacology, and behavioral interventions in treating obesity.

12.22 Discuss the roles of brain changes, starvation, excessive exercise, and genetic factors in eating disorders.

12.23 List strategies used in eating disorder interventions.

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Introduction

Ingestive Behavior (in jess tiv)

Eating or drinking

Homeostasis (home ee oh stay sis)

Process by which body’s substances and characteristics (such as temperature and glucose level) are maintained at their optimal level

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The Hypothalamus

The lateral and ventromedial hypothalamus.

Unnumbered Figure, page 368

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Drinking: Physiological Regulatory Mechanisms (1 of 2)

Physiological Regulatory Mechanisms

System Variable

Set Point

Detector

Correctional Mechanism

System Variable

Variable that is controlled by regulatory mechanism; for example, temperature in a heating system

Set Point

Optimal value of the system variable in a regulatory mechanism

Detector

In a regulatory process, a mechanism that signals when system variable deviates from its set point

Correctional Mechanism

In a regulatory process, the mechanism that is capable of changing value of system variable

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Drinking: Physiological Regulatory Mechanisms (2 of 2)

Negative Feedback

Process whereby effect produced by action serves to diminish or terminate that action; characteristic of regulatory systems

Satiety Mechanism

Brain mechanism that causes cessation of hunger or thirst; produced by adequate and available supplies of nutrients or water

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Figure 12.1 Example of a Regulatory System

Figure 12.1, page 369

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Figure 12.2 Outline of the System That Controls Drinking

Figure 12.2, page 369

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Drinking: Two Types of Thirst (1 of 4)

Some Facts about Fluid Balance

Intracellular Fluid

Extracellular Fluid

Intravascular Fluid

Interstitial Fluid

Intracellular Fluid

Fluid contained within cells

Extracellular Fluid

All body fluids outside cells: interstitial fluid, blood plasma, and cerebrospinal fluid

Interstitial Fluid

Fluid that bathes cells, filling space between cells of body (the “interstices”)

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Drinking: Two Types of Thirst (2 of 4)

Some Facts about Fluid Balance

Hypovolemia (hy poh voh lee mee a)

Reduction in volume of intravascular fluid

Vascular system of body can make some adjustments for loss of blood volume by contracting muscles in smaller veins and arteries

Presents smaller space for blood to fill

This correctional mechanism has definite limits

Thirst

Different things in different circumstances

Originally referred to sensation of dehydration

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Drinking: Two Types of Thirst (3 of 4)

Osmometric Thirst

Produced by increase in osmotic pressure of interstitial fluid relative to intracellular fluid

Cellular dehydration produced

OVLT (Organum Vasculosum of the Lamina Terminalis)

Subfornical Organ (SFO)

Satiety

Anterior cingulate cortex

Anticipatory mechanism triggered by act of drinking

Activation of this satiety mechanism reflected in activity of anterior cingulate cortex (Refer Figure 12.8)

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Drinking: Two Types of Thirst (4 of 4)

Volumetric Thirst

Occurs when intravascular volume of blood plasma decreases

Produced by hypovolemia

Role of Angiotensin

Renin (ree nin)

Hormone secreted by kidneys that causes conversion of angiotensinogen in blood into angiotensin

Angiotensin (ann gee oh ten sin)

Peptide hormone that constricts blood vessels, causes retention of sodium and water and produces thirst and salt appetite

As we saw earlier, when we lose water through evaporation, we lose it from all three fluid compartments: intracellular, interstitial, and intravascular.

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Figure 12.3 Water Loss Through Evaporation

Figure 12.2, page 369

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Figure 12.4 Osmoreceptors (1 of 2)

As solute concentration of the interstitial fluid increases, water leaves the cell and the cell decreases in volume. The reduction in cell volume triggers a change in firing rate, which signals thirst.

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Figure 12.4 Osmoreceptors (2 of 2)

As solute concentration of the interstitial fluid decreases, water enters the cell and the cell increases in volume. The increase in cell volume triggers a change in firing rate, which signals satiety.

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Figure 12.5 Osmometric Thirst in Humans

Functional MRI scans show brain activation produced by osmometric thirst. (a) Activation in the anterior cingulate cortex and hypothalamus, corresponding to a sensation of thirst. (b) Activation in the lamina terminalis, the location of the brain’s osmoreceptors.

(From Egan, G., Silk, T., Zamarripa, F., et al., Neural correlates of the emergence

of consciousness of thirst, Proceedings of the National Academy of Science,

USA, 2003, 100, 15241–15246.)

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Figure 12.6 The Circumventricular Organs

This sagittal section of the rat brain shows the location of the circumventricular organs. Inset: A hypothetical circuit connecting the subfornical organ with the median preoptic nucleus.

Figure 12.6, page 372

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Neural Mechanisms of Thirst (1 of 2)

Osmoreceptors that initiate drinking located in OVLT and SFO

Osmometric and volumetric signals in lamina terminalis are integrated to control drinking

Signal for volumetric thirst is provided by angiotensin II

Angiotensin II does not cross blood–brain barrier

Angiotensin II is a peptide

Angiotensin II does not cross blood–brain barrier and cannot directly affect neurons in brain except for those located in one of circumventricular organs

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Neural Mechanisms of Thirst (2 of 2)

Subfornical Organ

Low doses of angiotensin cause drinking

Destruction abolishes drinking

Median Preoptic Nucleus

Small nucleus situated around decussation of anterior commissure

Pays role in thirst stimulated by angiotensin

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Figure 12.7 Neural Circuitry Concerned with the Control of Drinking

Not all connections are shown, and some connections may be indirect. Although most of the osmoreceptors are located in the OVLT (organum vasculosum of the lamina terminalis), some are also located in the subfornical organ.

Figure 12.6, page 372

(Adapted from Thrasher, T. N. Acta Physiologica Scandinavica, 1989, 136, 141–150.)

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Eating: What is Metabolism?

When we eat: incorporate molecules of other living organisms, plant and animal, into our body

We ingest these molecules for two reasons:

to construct and maintain our own organs

to obtain energy for muscular movements and for keeping our bodies warm.

To stay alive, our cells must be supplied with fuel and oxygen.

Fuel comes from the digestive tract; its presence there is a result of eating.

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Table 12.1 Use of Reservoirs by the Nervous System

Time	Activity	Phase	Reservoir Used by the Nervous System
0:00—Day 1	Sleeping	Fasting	Short-term
6:00	Eating breakfast	Absorptive	None
10:00	Working	Fasting	Short-term
18:00	Exercising	Fasting	Short-term
20:00	Missed dinner	Fasting	Short-term
0:00—Day 2	Sleeping	Fasting	Long-term (Long-term reservoirs are used when short-term reservoirs are depleted during prolonged fasting)
6:00	Eating breakfast	Absorptive	None

Table 12.1 page 374

Glycogen (gly ko jen)

Polysaccharide often referred to as animal starch; stored in liver and muscle; constitutes the short-term store of nutrients

Insulin

Pancreatic hormone that facilitates entry of glucose and amino acids into cell, conversion of glucose into glycogen, and transport of fats into adipose tissue

Glucagon (gloo ka gahn)

Pancreatic hormone that promotes the conversion of liver glycogen into glucose

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Figure 12.8 Effects of Insulin and Glucagon on Glucose and Glycogen

Figure 12.8, page 375

Glycogen (gly ko jen)

Polysaccharide often referred to as animal starch; stored in liver and muscle; constitutes the short-term store of nutrients

Insulin

Pancreatic hormone that facilitates entry of glucose and amino acids into cell, conversion of glucose into glycogen, and transport of fats into adipose tissue

Glucagon (gloo ka gahn)

Pancreatic hormone that promotes the conversion of liver glycogen into glucose

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The Long-Term Reservoir

Triglyceride (try gliss er ide)

Glycerol (gliss er all)

3 Fatty Acids

Triglyceride (try gliss er ide)

Form of fat storage in adipose cells; consists of molecule of glycerol joined with three fatty acids

Glycerol (gliss er all)

Substance (also called glycerine) derived from breakdown of triglycerides, along with fatty acids; can be converted by liver into glucose

Fatty Acid

Substance derived from breakdown of triglycerides, along with glycerol; can be metabolized by most cells of body except for brain

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Fasting Phase and Absorptive Phase

Fasting Phase

Phase of metabolism during which nutrients are not available from digestive system

Absorptive Phase

Phase of metabolism during which nutrients are absorbed from digestive system

Fasting Phase

Phase of metabolism during which nutrients are not available from digestive system: glucose, amino acids, and fatty acids are derived from glycogen, protein, and adipose tissue during this phase

Absorptive Phase

Phase of metabolism during which nutrients are absorbed from digestive system: glucose and amino acids constitute principal source of energy for cells during this phase, and excess nutrients are stored in adipose tissue in form of triglycerides

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Figure 12.9 Metabolic Pathways During the Fasting Phase and Absorptive Phase of Metabolism

Figure 12.9, page 376

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Eating: Signals to Start a Meal

Signals from the Digestive System

Ghrelin (grell in)

Peptide hormone released by stomach that increases eating; also produced by neurons in brain

Duodenum

First portion of small intestine; attached directly to the stomach

In humans, too, injections of ghrelin increase eating.

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Figure 12.11 Ghrelin Signals

Ghrelin relays signals from the stomach and digestive tract to the hypothalamus.

Figure 12.11 page 378

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Figure 12.12 Level of Ghrelin in Human Blood Plasma

A rise in the level of this peptide precedes each meal. (Based on data from Cummings et al., 2001.)

Figure 12.11 page 378

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Metabolic Signals

Glucoprivation

Lipoprivation

Hepatic Portal Vein

Glucoprivation

Dramatic fall in level of glucose available to cells; can be caused by fall in blood level of glucose or by drugs that inhibit glucose metabolism

Lipoprivation

Dramatic fall in level of fatty acids available to cells; usually caused by drugs that inhibit fatty acid metabolism

Hepatic Portal Vein

Vein that transports blood from digestive system to liver

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Figure 12.13 Nutrient Receptors for Glucose and Lipids in the Liver

Receptors for glucose and lipids are located in the liver, and convey signals about gluco- and lipoprivation to the brain through the vagus nerve. These receptors are located outside the blood–brain barrier. Receptors for glucose are also located in the brain, inside the blood–brain barrier.

Figure 12.13, page 379

Detectors

Liver detectors

Brain detectors: dorsomedial and ventromedial medulla

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Eating: Signals to Stop a Meal

Regulation of Body Weight

Balance between food intake and energy expenditure

Mechanisms to maintain body weight

Increase motivation to eat if long-term reservoir depleted

Restrain food intake if we consume more than we need

Satiety signals

Short-term

Long-term

If we ingest more calories than we burn, we will gain weight; carbohydrates and proteins contain about 4 kcal/gm, and fats contain about 9 kcal/gm. (The “Calorie” you might see printed on a food label is actually a kilocalorie—1000 calories—or enough energy to raise the temperature of a liter of water by 1° C.)

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Short-Term Satiety (1 of 2)

Memory

Signals from environmental factors

de Castro and colleagues (2004)

Harrar and Spence (2013)

Signals from sensory factors

Appearance

Odor

Taste

Texture

Temperature

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Short-Term Satiety (2 of 2)

Intestinal Factors

Cholecystokinin (CCK) (coal i sis toe ky nin)

Hormone secreted by duodenum in response to presence of fats

Promotes satiety

Peptide YY (PYY)

Hormone secreted by small intestine in response to nutrients Proomotes Satiety

Duodenum

Controls rate of stomach emptying by secreting peptide hormone called cholecystokinin (CCK)

Cholecystokinin (CCK) (coal i sis toe ky nin)

Hormone secreted by duodenum that regulates gastric motility and causes gallbladder (cholecyst) to contract; appears to provide satiety signal transmitted to brain through vagus nerve

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Figure 12.14 Satiety Signals

Short-term signals are presented in blue; long-term signals in red.

Figure 12.14 page 381

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Figure 12.15 Effects of PYY on Hunger

The graph shows the amount of food (in kilocalories) eaten at a buffet meal 30 minutes after people received a 90-minute intravenous infusion of saline or PYY. Data points from each person are connected

by straight lines.

Figure 12.15 page 383

(Data from Batterham, R. L., ffytche, D. H., Rosenthal, J. M., et al., PYY

modulation of cortical and hypothalamic brain areas predicts feeding behaviour

in humans, Nature, 2007, 450, 106–109.)

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What Stops a Meal? (1 of 2)

Liver Factors

Last stage of satiety occurs in liver

First organ to learn that food is finally being received from intestines

Insulin

Permits organs other than brain to metabolize glucose

Promotes entry of nutrients into fat cells, where they are converted into triglycerides

Not until nutrients are absorbed from intestines can they be used to nourish cells of body and replenish body’s nutrient reservoirs

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What Stops a Meal? (2 of 2)

What purpose do these insulin receptors serve?

Receptors appear to detect insulin present in blood

This tells brain that body is probably in absorptive phase of metabolism

Thus, insulin may serve as a satiety signal (Woods et al, 2006)

Peptide that would not normally be admitted to brain

However, transport mechanism delivers it through blood–brain barrier,

It reaches neurons in hypothalamus that are involved in regulation of hunger and satiety

Infusion of insulin into third ventricle inhibits eating and causes loss of body weight (Woods et al., 1979).

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Long-Term Satiety: Signals from Adipose Tissue

OB Mouse

Strain of mice whose obesity and low metabolic rate caused by a mutation that prevents production of leptin

Leptin

Hormone secreted by adipose tissue; decreases food intake and increases metabolic rate, primarily by inhibiting NPY-secreting neurons in arcuate nucleus

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Figure 12.16 Effects of Force Feeding

After rats were fed an excess of their normal food intake, their subsequent food intake fell and recovered only when their body weight returned to normal.

(Based on data from Wilson et al., 1990.)

Figure 12.16, page 384

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Figure 12.17 Effects of Leptin on Obesity in Mice of the Ob Strain

The ob mouse on the left is untreated; the one on the right received

daily injections of leptin.

Amgen, Inc.)

Figure 12.17, page 384

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Brain Mechanisms

Brain Stem

Decerebration

Surgical procedure that severs brain stem, disconnecting hindbrain from forebrain (Refer Figure 12.18)

Only behaviors that decerebrate animals can display are those that are directly controlled by neural circuits located within the brain stem

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Figure 12.18 Decerebration

The operation disconnects the forebrain from the hindbrain so that the muscles involved in ingestive behavior are controlled solely by hindbrain mechanisms.

Figure 12.17, page 384

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Brain Mechanisms: Hypothalamus

Basic Findings

After lateral hypothalamus was destroyed, animals stopped eating or drinking (Anand and Brobeck, 1951; Teitelbaum and Stellar, 1954)

Electrical stimulation of same region would produce eating, drinking, or both behaviors

Lesions of ventromedial hypothalamus produced overeating that led to gross obesity, whereas electrical stimulation suppressed eating (Hetherington and Ranson, 1942)

Melanin-Concentrating Hormone (MCH)

Orexin

Lateral Hypothalamus (LH)

See Figure 12.21

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Figure 12.19 Role of the Hypothalamus

The lateral hypothalamus regulates hunger, while the ventromedial hypothalamus regulates satiety.

Figure 12.19 page 387

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Figure 12.20 Feeding Circuits in the Brain

This schematic diagram shows connections of the MCH neurons and orexin neurons of the lateral hypothalamus.

Figure 12.20 page 388

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Brain Mechanisms: Role in Hunger

Hypothalamus

Neuropeptide Y (NPY)

Dopamine

Paraventricular Nucleus (PVN)

Agouti-Related Protein (AGRP)

Endocannibinoids

Neuropeptide Y (NPY)

Potent stimulator of food intake, even in presence of aversive stimulus

Found in arcuate nuceus

Dopamine

DA neurons in VTA have ghrelin receptors

Infusion elicits eating in rodents

Paraventricular Nucleus (PVN)

Nucleus of hypothalamus located adjacent to dorsal third ventricle; contains neurons involved in control of autonomic nervous system and posterior pituitary gland

Agouti-Related Protein (AGRP)

Neuropeptide that acts as antagonist at MC-4 receptors and increases eating

Endocannibinoids

Class of orexigenic compounds – stimulate eating by increasing release of MCH and orexin

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Figure 12.21 Action of Hunger Signals on Feeding Circuits in the Brain

The diagram shows connections of the NPY neurons of the arcuate nucleus.

Figure 12.21 page 390

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Brain Mechanisms: Role in Satiety

Hypothalamus

Leptin

Inhibits neurons secreting NPY / AGRP

Activates neurons for CART / Alpha-MSH

CART

Arcuate nucleus

Alpha-MSH

Also released by CART neurons

Leptin: long term satiety signal

CART

Cocaine- and amphetamine-regulated transcript; peptide neurotransmitter found in system of neurons of arcuate nucleus that inhibit feeding

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Figure 12.22 Action of Satiety Signals on Hypothalamic

Neurons Involved in Control of Hunger and Satiety

Figure 12.22 page 391

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Obesity

Obesity is a widespread problem that can have serious medical consequences.

Increase incidence in both developed and developing countries

Increase in incidence over 20 years

Known health risks

Possible Causes

Environmental Factors

Physical Activity Factors

Genetic Factors

only account for extreme cases of obesity

Obesity is a widespread problem that can have serious medical consequences.

Increasing incidence in both developed and developing countries

In United States, approximately 67 percent of men and 62 percent of women are overweight, which is defined as body mass index (BMI) of over 25.

In the past twenty years, the incidence of obesity, defined as a BMI of over 30, has doubled in the population as a whole and has tripled for adolescents.

Known health risks: cardiovascular disease, type 2 diabetes, stroke, arthritis, and some forms of cancer

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Table 12.2 BMI Categories

(indicative of poor liver function) and insulin resistance (a predictor of developing type II diabetes) returned to within normal ranges.

Category	BMI Scores (kg/m2)
Underweight	< 18.5
Normal range	18.5–25
Overweight	>25
Obese	> 30

Table 12.2 page 393

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Obesity: Possible Causes

If we consume more calories than we expend as heat and work, we gain weight.

If we expend more than we consume, we lose weight.

Another modern trend that contributes to the obesity epidemic involves changes in people’s expenditure of energy.

The proportion of people employed in jobs that require a high level of physical activity has decreased considerably, which means that on the average we need less food than our forbears did.

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Obesity: Environmental Factors

The food of modern industrialized societies

Inexpensive

Convenient

Palatable

High-calorie

Snack foods

Sugars

We expend energy in two basic ways

Through physical activity

Through production of heat

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Physical Activity Factors

Physical activity at work

Less expenditure than hunter-gatherer ancestors

Nonexercise activity thermogenesis (NEAT)

Modern decrease in energy expenditure

NEAT: Levine et al., 2005

Involuntary activity: muscle tone, postural changes, and fidgeting (genetic basis)

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Genetic Factors

Contributions to metabolism, activity level, or appetite

Gene for MC4 receptor and FTO (fat mass and obesity related) gene

Other rare genes account for few cases

Thrifty Phenotype

Leptin

Leptin resistance

Thrifty phenotype;

Those with an efficient metabolism have calories left over to deposit in the long-term nutrient reservoir, and these calories accumulate in the form of increased adipose tissue

Perhaps people whose ancestors lived in regions where food was scarce or subject to periods of famine are more likely to have inherited efficient metabolisms

E.g. Pima native americans

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Obesity: Treatment (1 of 4)

Obesity extremely difficult to treat

Wide range of treatment approaches

Lose weight is quickly regained

Similar physiological mechanisms explain difficulty in weight loss versus stopping drug use.

e.g. Reinforcement and stress

What do you think?

Is overeating a form of addiction?

Enormous financial success of diet books, health spas, and weight reduction programs attests to the trouble people have in losing weight

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Obesity: Treatment (2 of 4)

Similarities with drug addiction

Initial success then relapse (weight regained)

Stress and anxiety contribute to relapse

Role of dopamine

Note: food required for survival, drugs are not

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Obesity: Treatment (3 of 4)

Treatment: Roux-en-Y gastric bypass, or RYGB

Most effective form of bariatric surgery

Small pouch in upper end of stomach produced

Jejunum (second part of the small intestine, immediately “downstream” from duodenum) cut

Upper end attached to stomach pouch

The most effective form of bariatric surgery is a special form of gastric bypass called the Roux-en-Y gastric bypass, or RYGB

This procedure produces a small pouch in the upper end of the stomach

The jejunum (the second part of the small intestine, immediately “downstream” from the duodenum) is cut, and the upper end is attached to the stomach pouch

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Obesity: Treatment (4 of 4)

Pharmacological Intervention

Many potential targets

To suppress appetite: difficulty with side effects

Prevent digestion

Behavioral Interventions

E.g. to increase physical activity

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Figure 12.26 Roux-en-Y Gastric Bypass (RYGB)

This procedure almost totally suppresses the secretion of ghrelin. (a) The stomach and small intestine before surgery. (b) The small pouch made from the stomach and the connection to the roux limb of the small intestine (the second part of the small intestine, downstream of the duodenum). This procedure reduces the size of the stomach and bypasses the duodenum.

Figure 12.26, page 397

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Table 12.3 Neuropeptides and Peripheral Peptides Involved in Control of Food Intake and Metabolism (1 of 3)

Neuropeptides Name	Location of Cell Bodies	Location of Terminals	Interaction with Other Peptides	Physiological or Behavioral Effects
Melanin-concentrating hormone (MCH)	Lateral hypothalamus	Neocortex, periaqueductal gray matter, reticular formation, thalamus, locus coeruleus, neurons in spinal cord that control the sympathetic nervous system	Activated by NPY/AGRP; inhibited by leptin and CART/α-MSH	Eating, decreased metabolic Rate
Orexin	Lateral hypothalamus	Similar to those of MCH Neurons	Activated by NPY/AGRP; inhibited by leptin and CART/α-MSH	Eating, decreased metabolic Rate
Neuropeptide Y (NPY)	Arcuate nucleus of Hypothalamus	Paraventricular nucleus, MCH and orexin neurons of the lateral hypothalamus	Activated by ghrelin; inhibited by leptin	Eating, decreased metabolic Rate
Agouti-related protein (AGRP)	Arcuate nucleus of hypothalamus (colocalized with NPY)	Same regions as NPY neurons	Inhibited by leptin	Eating, decreased metabolic rate; acts as antagonist at MC4 receptors

Figure 12.26, page 397

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Table 12.3 Neuropeptides and Peripheral Peptides Involved in Control of Food Intake and Metabolism (2 of 3)

Neuropeptides Name	Location of Cell Bodies	Location of Terminals	Interaction with Other Peptides	Physiological or Behavioral Effects
Cocaine- and amphetamine regulated transcript (CART)	Arcuate nucleus of hypothalamus	Paraventricular nucleus, lateral hypothalamus, periaqueductal gray matter, neurons in spinal cord that control the sympathetic nervous system	Activated by leptin	Suppression of eating, increased metabolic rate
α-melanocyte stimulating hormone (α-MSH)	Arcuate nucleus of hypothalamus (colocalized with CART)	Same regions as CART neurons	Activated by leptin	Suppression of eating, increased metabolic rate; acts as agonist at MC4 receptors

Figure 12.26, page 397

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Table 12.3 Neuropeptides and Peripheral Peptides Involved in Control of Food Intake and Metabolism (3 of 3)

Peripheral Peptides Name	Where Produced	Site of Actions	Physiological or Behavioral Effects
Leptin	Fat tissue	Inhibits NPY/AGRP neurons; excites CART/α-MSH neurons	Suppression of eating, increased metabolic rate
Insulin	Pancreas	Similar to leptin	Similar to leptin
Ghrelin	Gastrointestinal system	Activates NPY/AGRP neurons	Eating
Cholecystokinin (CCK)	Duodenum	Neurons in pylorus	Suppression of eating
Peptide YY3–36 (PYY)	Gastrointestinal system	Inhibits NPY/AGRP neurons	Suppression of eating

Figure 12.26, page 397

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Eating Disorders (1 of 2)

Anorexia Nervosa

Bulimia Nervosa

Binge eating disorder

Possible Causes of Eating Disorders

Brain changes

Starvation: symptoms as cause or consequence

Excessive exercise

Genetic factors

Anorexia Nervosa

Disorder that most frequently afflicts young women; exaggerated concern with being overweight that leads to excessive dieting and often compulsive exercising; can lead to starvation

Bulimia Nervosa

Bouts of excessive hunger and eating, often followed by forced vomiting or purging with laxatives; sometimes seen in people with anorexia nervosa

Binge eating disorder: eating large qualities of food in a relatively short time period (without compensatory behavior)

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Eating Disorders (2 of 2)

Very difficult to treat successfully

Cognitive behavior therapy considered most effective approach

Pharmacology

Alterative therapies

Cognitive behavior therapy, considered by many clinicians to be the most effective approach, has a success rate of less than 50 percent and a relapse rate of 22 percent during a 1-year treatment period (Pike et al., 2003

A meta-analysis by Steinhausen (2002) indicates that the success rate in treating anorexia has not improved in the last fifty years

A therapeutic protocol based on findings such as these has shown promise in helping anorexic patients overcome the disorder.

Researchers have tried to treat anorexia with drugs that increase appetite, but none has been found to be helpful.

However, fluoxetine, a serotonin agonist used to treat depression, may help to suppress episodes of bulimia.

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Table 12.4 Criteria for Eating Disorders

Anorexia Nervosa	Bulimia Nervosa	Binge-Eating Disorder
Restricted eating that leads to low body weight	Episodes of binge-eating	Episodes of binge-eating
Fear of gaining weight	Compensatory behaviors to prevent gaining weight that follow binge eating	Distress related to binge-eating
Persistent behavior to prevent weight gain	Critical evaluation of body weight or shape	No use of compensatory behaviors
Disturbance in self-perception or failure to perceive seriousness of low body weight

Figure 12.26, page 397

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Figure 12.27 Brain Comparison of Individuals with Anorexia

(a) Patient with anorexia nervosa, showing enlarged sulci (yellow circle), third ventricle (red circle), and lateral ventricle (green circle). (b) Healthy control patient shows typical anatomy in same regions.

(Based on Golden, N. H., Ashtari, M., Kohn, M. R., Patel, M., Jacobson, M. S., Fletcher, A., and Shenker, I. R., Reversibility

of cerebral ventricular enlargement in anorexia nervosa, demonstrated by quantitative magnetic resonance imaging,

Discussion 6

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