Regulation Of Eating Behavior And | Verified Test Bank Ch.5

Chapter 5

Regulation of Eating Behavior and Body Weight

Learning Objectives

Upon successful completion of this chapter, students should be able to:

1. Apply the concept of homeostasis to regulation of body weight.
2. Distinguish between the terms hunger, appetite, satiety, and satiation.
3. Outline some of the ways that the brain and its neurotransmitters are involved in regulating weight and energy balance.
4. Outline some of the ways that the digestive system is involved in regulating weight and energy balance.
5. Describe the factors involved in development of body fat stores (fat cell size and number and location of stored fat).
6. Discuss how adipose tissue functions as an endocrine organ.
7. Describe the role of brown adipose tissue in regulation of body weight.
8. Discuss genetic factors thought to be involved in regulation of weight and how these interact with the environment.

Chapter Outline/Summary

1. Homeostasis and regulation of weight:

Weight is maintained by the balance between energy consumption and energy expenditure. Fat storage may be regulated by a set point, which attempts to maintain homeostasis (stability) by controlling physiologic processes that influence energy metabolism.

1. The brain: central regulator of weight
2. Hunger, appetite, satiety, satiation:

The brain is the primary integrator of body systems that initiate and terminate feeding. We do not always eat solely in response to hunger (biological drive to eat), nor do we automatically cease eating due to satiation or satiety.

1. The role of the brain in regulating weight:

The hypothalamus is the most important area of the brain for regulating food intake.

1. Neurotransmitters involved in regulating weight:

Neurotransmitters that promote food intake are classified as orexigenic and include Neuropeptide Y, agouti gene-related protein, melanin-concentrating hormone, galanin, dynorphin, and norepinephrine. Neurotransmitters that turn off feeding are classified as anorexigenic and include pro-opiomelanocortin, a-melanocyte-stimulating hormone, cocaine and amphetamine regulated transcript, serotonin, and several peptides that originate in the gut but find their way to the brain.

1. Other ways the brain regulates energy balance:

The prefrontal cortex, circumventricular organs, and limbic system are also thought to play a role in hunger, appetite, and satiety, but in a different way than the hypothalamic areas.

III. Digestive system: receptor and effector in regulation of weight

1. Taste and smell of food:

The gustatory system (tongue and several areas of the brain) is responsible for the sense of taste, and the olfactory system is responsible for the sense of smell. Both systems influence appetite and satiation.

1. Digestive system:

The gastrointestinal tract contains both mechanical and chemical sensors that affect hunger, appetite, satiety, and satiation. Ghrelin is the only digestive tract hormone that stimulates food intake. All other gastrointestinal signals are involved in satiety.

1. Insulin’s role in hunger and satiety:

Insulin secretion is at its lowest when eating occurred several hours ago. The presence of glucose stimulates secretion of insulin. The hyperinsulinemia seen in type 2 diabetes and in some obese individuals may stimulate food intake.

IV. Storage fat: active participant in weight regulation

1. How fat stores develop:

Storage fat tissue is comprised of fat cells (adipocytes), blood vessels, nerves, and connective tissue. Preadipocytes are fat cells that contain no lipid. Some of these will never become adipocytes; others begin to accumulate lipid deposits during the first year of life. The enlargement of fat cells is called hypertrophy and is reversible. An increase in the number of adipocytes is called hyperplasia and is permanent.

1. Determination of fat cell number and size:

When conditions are favorable, the size of fat cells can grow throughout life and the number of fat cells can increase at least into early adulthood. Lipogenesis (the accumulation of storage fat) is regulated by lipoprotein lipase and acylation-stimulation protein and facilitated by α-adrenergic receptors on the fat cells. Lipolysis (release of fatty acids from fat cells) is regulated by hormone-sensitive lipase and facilitated by β-adrenergic receptors on the fat cells.

1. Other functions of adipose tissue:

Storage fat plays a role in eating, energy expenditure, weight management, and disease. It secretes the hormone leptin, which is a messenger between the fat cells and the brain that provides information about the size of the fat stores, and can affect energy intake and expenditure in a way that preserves the size of storage fat. In addition, adipose tissue produces cytokines and adiponectin (proteins involved in inflammation), which may make some obese individuals metabolically unhealthy.

1. Determination of where body fat is deposited:

Gender plays a role in determining whether fat is preferentially deposited in the abdomen or the hips and thighs. This is primarily due to hormonal differences between the genders, although other hormones may also affect location of fat deposits. Upper-body fat tends to be made up of larger adipocytes and is associated with more health problems, while lower-body fat is comprised of a larger number of smaller adipocytes, which are more metabolically healthy but more permanent.

V. BAT: effector of energy expenditure

A. How thermogenesis occurs:

Thermogenesis takes place in the brown adipose tissue (BAT), which is rich in β-adrenergic receptors and uncoupling protein. When stimulated by cold stress or food intake, BAT produces heat, resulting in caloric expenditure.

B. BAT in obesity:

Although diet-induced thermogenesis accounts for only a small proportion of daily energy use, if this process were faulty, a slow but steady increase in fat stores might occur. Research is not yet conclusive if some obese individuals have defective BAT.

VI. Genetic factors and body composition

1. How traits are inherited:

Some human obesities are known to result from defects in specific gene locations on various chromosomes. Mutations or alleles of 20-30 genes could result in genotypes for different patterns of fat storage, energy expenditure, peptide secretion, and responses to neurochemicals, resulting in multiple obesity genotypes.

1. Obesity-promoting genes:

Body composition and BMI have heritability values of 40%-70%. There may be other genes that control various aspects of metabolism and behavior, which could be obesity-promoting. Mutations in the MC4R receptor gene may account for up to 6% of cases of severe obesity in children and adults. Mutations in the leptin-receptor gene have also been reported in a small number of humans.

1. Other genetic factors involved in weight gain:

Low energy expenditure is a factor suspected to account for some instances of weight gain. For a variety of genetic reasons, people may be more or less resistant to exercise as an obesity treatment or prevention strategy. There may also be genetic influences on the effectiveness of various diets in promoting weight loss. And people may inherit factors that influence nutrient consumption.

1. Interaction of heredity and environment:

Lack of physical activity and consumption of dietary fats are two environmental factors that might interact with genetic factors and promote weight gain. Among native populations, obesity and type 2 diabetes increase among active societies consuming traditional diets who move to less-active environments with high-fat, low-fiber diets.

Suggested Activities and Applications

Application 5.1 The Obese Family, Part 1:

This application is the first of a 3-part case study of the Rhys family. Both parents are obese with comorbidities. Their 7-year-old son is in the 97th BMI percentile. Part I describes their eating habits. Students, in groups or individually, are asked to:

• Consider the potential roles of the brain and digestive system in their eating behavior.
• Consider strategies that the Rhys family could take to reduce the impact of physiological factors on eating behavior.

Application 5.2 The Obese Family, Part 2: This part of the case study introduces the idea of genetic testing for obesity. Students are assigned to do some reading about genetic testing guidelines (both the American Academy of Pediatrics and American Medical Association have guidelines) and specifically about the MC4R gene. They are assigned to answer the following questions:

• How is this type of genetic testing done? Is it painful or invasive?
• Consider some of the issues that arise when parents decide for a child that he/she should undergo genetic testing.
• Do the benefits of learning about one's MC4R gene status outweigh the risks of having such information?
• Should Joey be informed about the results of his genetic testing? Should others in the Rhys family be informed?
• How do you think the outcome of genetic testing might affect Joey's psychological status, self-esteem, and future health risks?

Application 5.3 The Obese Family, Part 3: In this part of the case study, the parents learn that Joey has one defective MC4R gene, inherited from one of them. Mr. Rhys continues to believe that his and Joey's continued weight gain is inevitable and that changing their diet will have no effect. Mrs. Rhys thinks that the family's dietary choices and inactivity might play a larger role than heredity. Students will consider:

• What environmental factors might be contributing to this family's weight and health problems?
• Do they think that obesity is inevitable for the Rhys family?

Test Bank

True/False

1. The brain is the primary integrator of the body systems that initiate and terminate feeding. (True/ False)

2. The average non-obese adult has between 30-50 billion adipocytes. (True/ False)

3. Much of adult-onset obesity is due to hypertrophy. (True/ False)

4. Hyperplasia is not typically permanent. (True/ False)

5. Excess fat cells never go away. (True/ False)

6. Fat in the hips is generally more difficult to reduce than fat in the waist. (True/ False)

7. High levels of lipoprotein lipase promote the growth of fat cells. (True/ False)

8. Acylation-stimulating protein levels rise proportionately with BMI, however, research shows that they are not higher among obese individuals. (True/ False)

9. Acylation-stimulating protein levels are also higher among individuals with insulin resistance and cardiovascular disease, but levels can be reduced with weight loss and exercise. (True/ False)

10. Increased Leptin drives people to eat. (True/ False)

11. Gender determines to a great extent where fat is stored. (True/ False)

12. Gender patterns in fat storage evolved to sustain survival. (True/ False)

13. Researchers do not believe that BAT is involved in weight regulation in humans. (True/ False)

14. People likely inherit a preference for specific types of food (e.g. specific types of carbohydrates, such as spaghetti or potatoes). (True/ False)

Multiple Choice

15. _________________ is the stability of the body’s internal environment to ensure survival.

A. Set Point

B. Homeostasis

C. Satiety

D. All of the above

16. The _______________ is the area of the brain that serves as a link between the endocrine and autonomic nervous systems; it promotes homeostasis by regulating temperature, water balance, food intake, hormonal balance, and emotional responses.

A. hypothalamus

B. cortex

C. cerebellum

D. All of the above

17. _________________ is a branch of the nervous system that regulates involuntary physiological functions, such as sweating, circulation, and digestion.

A. Limbic System

B. Autonomic Nervous System

C. Endocrine System

D. Sympathetic Nervous System

18. _____________ is a system of glands and the hormones they secrete to deliver chemical messages to target cells throughout the body.

A. Limbic System

B. Autonomic Nervous System

C. Endocrine System

D. Sympathetic Nervous System

19. ______________ is a critical hub that contains neurons that produce appetite stimulating neurotransmitters and neurons that produce appetite-dampening neurotransmitters. This area also contains many insulin and leptin receptors.

A. Dorsomedial hypothalamic nucleus (DMN)

B. Arcuate Nucleus (ARC)

C. Limbic System

D. All of the above

20. _____________ is the most abundant neuropeptide in humans. It stimulates intake of food and reduces energy expenditure by inhibiting sympathetic nervous system activity in the brown adipose tissue.

A. Neuropeptide Y

B. Catecholamines

C. Anorexigenic peptides

D. All of the above

21. ______________ stimulate food intake, but they may have a more important role in regulating sleep.

A. Neuropeptide Y

B. Peptide YY

C. Orexins

D. All of the above

22. The opioid peptide, __________________, promotes eating and has pain-reducing properties. This morphine-like substance acts on the feeding centers of the hypothalamus to stimulate the consumption of highly palatable foods, such as fats. It may also play some role in stress-induced eating.

A. Neuropeptide Y

B. Peptide YY

C. Dynorphin

D. Galanin

23. _____________ stimulates eating particularly by increasing the size of a meal and increasing the intake of carbohydrates.

A. Peptide YY

B. Dynorphin

C. Galanin

D. Norepinephrine

24. __________________ turns off eating, and in some cases increases energy expenditures.

A. Catecholamines

B. Dynorphin

C. Norepinephrine

D. All of the above

25. A group of brain structures collectively known as ____________ integrate sensory information and transmit this information to other parts of the brain, including the hypothalamus. It exists outside the blood-brain barrier.

A. Circumventricular organs

B. the Limbic System

C. the Gustatory System

D. the Olfactory System

26. The ________________ is responsible for the sense of taste and includes the tongue and several areas of the brain, most notably the cortex and hypothalamus.

A. Olfactory system

B. Gustatory System

C. Limbic System

D. All of the above

27. __________________ are the structures and pathways involved in the sense of smell.

A. Olfactory System

B. Gustatory System

C. Limbic System

D. All of the above

Answer A

28. This hormone in the gastrointestinal tract stimulates food intake. It is secreted mainly in the stomach and reaches peak levels just before eating.

A. Leptin

B. Ghrelin

C. Insulin

D. Acylation-stimulating protein

29. _______________ means the enlargement of fat cells.

A. Adiposity

B. Adiposity Rebound

C. Hypertrophy

D. All of the above

30. ____________ is the increase in the number of fat cells.

A. Hypertrophy

B. Hyperplasia

C. Lipogenesis

D. All of the above

31. _______________ is the accumulation or production of fat, which occurs by the uptake of fatty acids into adipocytes.

A. Hypertrophy

B. Hyperplasia

C. Lipogenesis

D. Lipolysis

32. ____________ is the breakdown of fat and involves the release of fatty acids into the bloodstream after they have undergone hydrolysis.

A. Hypertrophy

B. Hyperplasia

C. Lipogenesis

D. Lipolysis

33. _________________ are receptors on fat cells that are sensitive to sympathetic activation; they respond to norepinephrine or epinephrine to regulate fat cell size and function.

A. Cholinergic receptors

B. Adrenergic receptors

C. Both A & B

34. ________________ are receptors on cells that are sensitive to parasympathetic activation; they respond to acetylcholine; fat cells do not contain cholinergic receptors.

A. Cholinergic receptors

B. Adrenergic receptors

C. A& B

35.________________ is an enzyme produced in many tissues to help remove fatty acids from the bloodstream. This has been referred to as the gatekeeper of the fat cells because of its role in fat storage.

A. Lipogenesis

B. Lipoprotein lipase

C. Hypertrophy

D. Acylation-stimulating protein

36. ___________________ is a protein produced by the fat cells that provide a satiety signal to the brain. It is derived from a Greek work that means “thin” because people who secrete normal amounts of it are frequently lean.

A. Ghrelin

B. Leptin

C. Acylation-stimulating protein

D. Both A & B

37. _____________________ is a specialized form of fat tissue that contributes to energy expenditure through its capacity for thermogenesis, or production of heat.

A. Brown adipose tissue (BAT)

B. Leptin

C. Lipoprotein lipase

D. Lipolysis

38. Which of the following defines the body’s “set point.”

A. minimum healthy weight of a person that can be maintained for 10 years after age 21

B. maximum healthy weight of a person

C. point at which a dieter plateaus and then drops weight quickly

D. point above which the body tends to lose weight and below which it tends to gain weight

39. What is the role of the hypothalamus in hunger and satiety?

A. it produces leptin at abnormally high levels in some people, stimulating hunger

B. it contains hunger and satiety centers that are responsive to neuropeptides

C. it signals the duodenum to secrete cholecystokinin after eating

D. all are roles of the hypothalamus

40. ß-adrenergic receptors in fat cells stimulate

A. homeostasis

B. lipogenesis

C. lipolysis

D. hyperplasia

41. When leptin secretion occurs

A. an individual is driven to eat

B. triglyceride uptake by the fat cells increases

C. BMR rises

D. food consumption slows and then stops

42. Which of the following is NOT a characteristic of normal brown adipose tissue?

A. hyperplasia after it is stimulated

B. rich in UCP-1

C. sensitive to cold exposure and food intake

D. important fat storage tissue in gluteofemoral region

43. The enzyme called the “gatekeeper of the fat cells,” because it stimulates fat uptake is:

A. lipoprotein lipase

B. insulin

C. neuropeptide Y

D. bombesin

Answer B

44. The psychological desire to eat that accompanies the sight, smell, or thought of food is known as:

A. appetite

B. satiety

C. hunger

D. palatability

45. Which of the following describes the process of thermogenesis?

A. burning of fat

B. synthesis of fat

C. generation of heat

46. Obesity resulting from an increase in the size of fat cells is termed:

A. hyperplastic obesity

B. hypertrophic obesity

C. hypometabolic obesity

D. leptin-dependent obesity

47. Research with moderately obese people seems to show that there is no increase in the risk for strokes and hypertension provided excess body fat is distributed around the

A. abdomen

B. arms and chest

C. neck and shoulders

D. hips and thighs

Short Answer/ Fill in the Blank

48. ________________ is a level of body weight or fatness maintained by a complex combination of body systems.

49. _________________ is the termination of eating after hunger has been satisfied.

50. _________________ represents a psychological desire to eat and includes selecting particular nutrients, having a taste for specific foods, and craving specific foods in response to the sight, smell or thought of them.

51. Describe the non-homeostatic mechanisms of the brain that influence energy balance.

52. _____________ is a hormone secreted by the pancreas in response to an increase in the blood glucose level; it permits glucose to be taken up by the cells and is responsible for fat storage.

53. Describe one of the ways that the brain works to regulate body weight.

54. Describe one of the ways that the digestive system works to regulate body weight.

55.__________________ is now understood to be a messenger between fat cells and the brain that provides vital information about the size of the body’s energy stores.

56. How are fat storage patterns different for many women and men?

57. Describe one way that genetics influences body weight, fat storage/ patterning, and food preference.

58. How does the environment interact with heredity among overweight individuals?

59. How do family factors influence obesity?

60. In terms of weight management issues, what do Pima Indians and Pacific Islanders have in common?

61. Discuss the major differences between upper and lower body fat depots.

62. Briefly discuss the contribution of adipocyte size and number to the development of obesity.