Exam 3 - Hunger and eating Flashcards
The three phases of energy metabolism are, in sequence:
A. think, fast, and absorb
B. absorptive, cephalic, and fasting
C. fasting, absorptive, and cephalic
D. cephalic, absorptive, and fasting
D
Glucostatic theory is to lipostatic theory as:
A. glucose is to fat
B. short-term is to long-term regulation
C. long-term is to short-term regulation
D. both A and C
D
According to the dominant hypothalamic theory of eating in the 1950’s and 1960’s, hunger is to satiety as:
A. LH is the VMH
B. LH is to the paraventricular nuclei
C. VMH is to the LH
D. pancreas is to the liver
A
Koopmans transplanted a stomach with its attached section of intestine from one rat into another and connected the circulatory system of the transplant to that of the recipient. He then injected food into the implanted stomach. This experiment indicated that:
A. The gastrointestinal tract produces a satiety signal
B. Food-related signals from the gastrointestinal tract are transmitted through the blood
C. Food-related signals from the gastrointestinal tract are transmitted through the nervous system
D. Both A and B
D
Many hunger and satiety peptides have receptors in the:
A. hypothalamus
B. Amygdala
C. hippocampus
D. prefrontal cortex
A
CCK is to neuropeptide Y as:
A. serotonin is to satiety
B. hunger is to satiety
C. rats are to humans
D. satiety is to hunger
D
The peptide produced by fat cells that appears to give the brain feedback about the body’s level of stored fat is:
A. CCK
B. insulin
C. glucagon
D. leptin
D
Is there a set point for the body’s energy reserves that determines when we eat?
no
Digestion
breaking down food and absorbing its constituents
Most energy is stored as fats, why?
it’s more economical
Cephalic energy metabolism
preparation (smelling or thinking about food)
Absorptive energy metabolism
energy absorbed
Fasting energy metabolism
withdrawing energy from reserves, ends with next cephalic phase
Lipids
fats
Amino acids
proteins
Glucose
carbohydrates
Insulin, what is it produced by, and when are levels high?
- allows body cells to use glucose, promotes formation of glycogen, fat, and protein
- produced by pancreas
- high levels during cephalic and absorptive phase
Glucagon, what is it produced by, when are levels high?
- promotes the release of free fatty acids and their conversion to ketones, making stored energy available
- produced by pancreas
- high levels during fasting phase
Set point theory, what type of feedback system is this? Does evidence support this theory?
- hunger is a response to an energy need; we eat to maintain an energy set point
- negative feedback system (eating is turned on when energy is needed, and off when set point is reached)
- no
What are the problems with the set-point theory?
- eating disorders
- reduction in blood glucose or body fat does not induce eating
- doesn’t account for the external influences on eating and hunger
Positive-incentive theory
we are drawn to eat by the pleasure of eating, we evolved to crave food
What are the typical preferences and aversions that determine what we eat?
- sweet, fatty and salty foods
- bitter
What factors influence when we eat?
- tend to get hungry at mealtime
- body enters cephalic phase, leading to a decrease in blood glucose
- pavlovian conditioning
What factors influence how much we eat?
- satiety - stops a meal, signals are induced by food in gut and glucose in blood
- a change in nutritive density
- appetizer effect
- social influences
- sensory-specific satiety
Sham eating, what were the results?
subject chews and swallows, but food then leaves the body (no energy is consumed)
- animals still eat the same portions, and at the same time
Appetizer effect
small amounts of food may increase hunger
Sensory-specific satiety
eat more with a cafeteria diet (satiety is taste specific)
Ventromedial hypothalamic center
satiety center, makes you feel full
Lateral hypothalamic center
hunger center, makes you eat
Hypothalamus
regulates energy metabolism
CCK, what is it produced by ?
- cholecystokinin - causes nausea at high doses, but suppresses food intake at doses insufficient to induce taste aversions - makes you feel full
- released by GI tract
What is Prader-Willi syndrome?
unable to feel full
Hunger peptides, where are they produced?
- increase appetite
- hypothalamus
Serotonin ______ food intake by increasing _______ satiety signals.
reduces, short-term
Diet-induced thermogenesis
changes in body fat lead to changes in energy use
Leaky barrel model
- a.k.a. the settling point model
- body weight drifts around a natural settling point - the level at which the various factors that influence body weight achieve an equilibrium
What are ob/ob mice, and what are they deficient in?
- mice that are 3x the normal weight
- leptin
Neuropeptide Y
- released in GI tract
- causes hunger
Anorexia
restricting calories, significantly underweight
Bulimia
excessive periods of eating followed by compensatory behaviors
