Eating Flashcards
(54 cards)
1
Q
why do humans need glucose?
A
for the body to work effectively
2
Q
how does the body store energy?
A
cannot store glucose as glucose
85% as fat in adipose tissue
14.5% as protein in muscle
0.5% as glycogen in liver
3
Q
which energy store is closest to glucose chemically?
A
glycogen is a straight conversion from glucose
4
Q
why isn’t everything stored as glycogen?
A
- Fat and protein can hold more glucose in 1g than glycogen can in 1g
- 1g of fat stores twice as much glucose as 1g of glycogen
- Glycogen attracts, absorbs and holds water so if all energy stored as glycogen body weight would be much heavier
5
Q
define metabolism
A
the chemical reactions in the body
6
Q
define respiration
A
the breakdown of glucose making energy available to the organism
7
Q
what hormones effect blood glucose?
A
insulin and glucagon
8
Q
how is blood glucose used?
A
cells use blood glucose as energy
9
Q
what is insulin and where is it created?
A
peptide hormone created in the pancreas
10
Q
what is the function of insulin?
A
Insulin changes glucose into glycogen stored in the liver
so insulin reduces blood glucose by either moving it in cells for energy or storing it in the liver as glycogen
11
Q
what is the function of glucagon?
A
Glucagon increases blood glucose by breaking down glycogen into glucose
12
Q
what are the three different phases of metabolism (breaking down glucose)?
A
cephalic phase
absorptive phase
fasting phase
13
Q
explain the cephalic phase of metabolism
A
preparatory phase
Starts at sight, smell or expectation of food
Stops as food is absorbed into bloodstream
High levels of insulin –> insulin breaks down glucose to promote energy for respiration
excess glucose converted and stored as fat –> conversion of fat to fuel is inhibited
Body gets rid of some glucose ready for the input of glucose
Low levels of glucagon
14
Q
explain the absorptive phase of metabolism
A
meeting of the body’s immediate energy requirements
High levels of insulin –> insulin breaks down glucose to promote energy for respiration
excess glucose converted and stored as fat –> conversion of fat to fuel is inhibited
Body gets rid of some glucose ready for the input of glucose
Low levels of glucagon
15
Q
explain the fasting phase of metabolism
A
Unstored energy used and stored energy being used
Ends with the beginning of the next cephalic phase
Low levels of insulin
High levels of glucagon
Promotes conversion of fat to fatty acids (utilisable fuels)
Inhibits glucose to energy except by brain as brain needs glucose and energy all the time
Inhibits storage of fat
16
Q
explain how the homeostatic system works
A
Homeostatic system wants to work at the optimal steady level
If you start feeling hungry you eat, if you get full you stop
17
Q
what starts a meal?
A
blood glucose levels
ghrelin
external factors
18
Q
explain how blood glucose levels might start a meal
A
- Mayer (1953) proposed that the levels of blood glucose is the primary basis for hunger and satiety. He reckoned that low blood glucose levels lead to hunger and high levels lead to satiety
- Campfield and Smith (1990) monitored blood glucose levels and found that they remained steady but just before regular meal times, the levels dropped by 8%.
19
Q
explain how blood glucose levels might not start a meal
A
- Le Mangen (1981) found that blood glucose levels does not normally vary even under prolonged period of fasting
- Diabetics remain hungry with high levels of blood glucose
20
Q
explain how ghrelin might start a meal
A
- Blood levels of ghrelin increase shortly before each meal, which suggests that this peptide is involved in the initiation of a meal (Cummings, 2006)
- Schmid et al. (2005) found that a single intravenous injection of ghrelin enhanced appetite and elicited vivid images of food that the subjects liked to eat.
- Ghrelin secretion is suppressed when an animal eats or when an experimenter infuses food into the animal’s stomach
- Injections of nutrients into the blood do not suppress ghrelin secretion, so the release of the hormone is controlled by the contents of the digestive system and not by the availability of nutrients in the blood (Schaller et al., 2003)
21
Q
explain how ghrelin might not start a meal
A
- Although ghrelin is an important short-term hunger signal, it clearly cannot be the only one
- e.g. people who have undergone successful gastric bypass surgery have almost negligible levels of ghrelin in the blood. Although they eat less and lose weight, they do not stop eating.
22
Q
what is ghrelin?
A
A peptide hormone released by the stomach that increases eating
A potent stimulator of food intake and it even stimulates thoughts about food
23
Q
what external factors might start a meal?
A
smell
adverts
places you associate with food
time of day
learning
24
Q
explain how learning might start a meal
A
- Pavlov conditioned dogs to salivate when they heard a bell
- Weingarten (1983) paired buzzer with food and bell with inter-meal times, they would start pressing lever for food when they heard buzzer but not bell
- Birch (1989) showed similar results with children - the stimuli associated with food initiated the hunger
25
what stops a meal?
body fat levels
feeling of fullness
nutrient content
signals sent by the stomach and duodenum
external factors
26
explain how body fat levels might stop a meal
- Wilson et al. (1990) showed force fed rats increased weight and decreased voluntary intake of food
- Campfield et al. (1995) showed obese mice do not produce leptin
- Kahler et al. (1998) injected leptin in normal mice and found that reduced meal size suggesting it plays a role in stopping a meal
27
what is leptin?
hormone that helps maintain body weight by regulating hunger and energy balance
28
explain how feeling full might stop a meal
- Cannon and Washburn (1912) - Washburn swallowed a balloon and then inflated it, contractions coincided with hunger pains
- David & Campbell (1973) removed food from stomach of rats so they continued to eat until they had replaced the volume removed (vagus nerve records information about stretch of stomach)
- Greenberg et al. (1990) found entry of food straight into intestine inhibits feeding
29
explain how feeling full might not stop a meal
people without stomachs still have hunger pains
30
explain how nutrient content might stop a meal
- Deutsch Gonzalez (1980) removed nutrient content and replaced with water, rats kept eating until nutrient level was restored, (splanchnic nerves info on nutrient content of stomach)
- Glucose infused to duodenum caused satiation, but blood did not (Lavin et al)
- Entry of food into duodenum causes duodenum to release cholecystokinin hormone, decreases size of meal by closing pyloric sphincter causing stomach to fill faster also acts as neurotransmitter in brain to decrease eating (Greenberg et al., 1990)
31
explain how signals sent by stomach and duodenum might stop a meal
- Entry of food into duodenum stimulates release of cholecytoskinin
- CCK closes pyloric sphincter in stomach
- CCK injections suppress feeding (Gibbs et al., 1973)
- Peptide YY released by stomach after meal in proportion to calories consumed (Pederson-Bjerdgaard, 1996)
- Injections of PYY inhibits size of meals (Batterham, 2007)
32
what external factors might stop a meal?
learning from previous experience
social factors
33
explain how learning from previous experience might stop a meal
- Animals regularly given free access to food will eat set amount then stop when they have gained enough nutrients and if they eat this food over and over they learn to stop at the same time
- Weingarten showed in Sham feeding experiments, animals will stop eating at the same point even if they are getting no nutrients, due to the food not being absorbed from the stomach, however over sessions, eating will increase as the animals learn the food is not providing enough nutrients - shows that amount eaten is based on previous experience (Weingarten and Kulikovsky, 1989)
- Cafeteria diets in people - if you don't have experience in food then you are likely to overeat initially
- Rolls et al. (1981) showed participants were more likely to eat more food if there was new food on offer at the time
34
explain how social factors might stop a meal
- Redd and DeCastro (1992) asked people to keep diaries of food eaten, 60% eat more when more people present
- rats do same when eating in a group
- Polivy et al. (1979) Four female participants and one accomplice, a model, all had a meal together. Half the subjects she told she was on a diet and the half she told ate less than those she didn’t tell
- Berry et al. (1985) Males eat more lasagne when they eat in groups
- Rogers & Blundell (1980) found similar results in rats
35
what is the arcuate nucleus?
part of the hypothalamus
secretes Neuropeptide Y (NPY) as a response to ghrelin (Van den Top et al., 2004)
36
what happens when NPY is infused into hypothalamus?
leads to ravenous hunger
37
what is THC?
tetrahydrocannabinol - the chemical responsible for most of marijuana's psychological effects
38
how did they explain hunger in the 1950s?
There was thought to be two feeding centres: one for hunger, one for satiation
Recent evidence suggests that this was an oversimplication
39
how does the lateral hypothalamus explain hunger?
lesions and growths on lateral hypothalamus caused lack of eating
stimulation of hypothalamus caused high levels of hunger
40
explain how hunger works
ghrelin released by empty stomach
arcuate nucleus detects ghrelin and secretes NPY
NPY stimulates lateral hypothalamus to release melanin-concentrating hormone (MCH) and orexin
these increase eating and decrease metabolic rate thus increasing and preserving energy stores in body
which stimulates hunger
41
explain how satiation works
adipose tissue releases leptin
leptin binds to receptor on arcuate nucleus
full stomach releases PYY
PYY binds to receptors on arcuate nucleus
PYY and leptin inhibits release of NPY
PYY stimulates arcuate nucleus to release anorexigens
leptin activates anorexigens which inhibit release of orexin and MCH by lateral hypothalamus
preventing stimulatory effect on appetite so feelings of fullness occur
42
what are anorexigens?
appetite suppressing chemicals
e.g. CART and a-MSH
43
stats on obesity
- In USA, 67% of men and 62% of women are overweight
- In USA, 34 million people are overweight; 12.5 million of them severely so; economic cost of obesity related disease is 39 billion dollars per year
- In past 20 years, incidence of obesity in adolescents has tripled
- Over 10-year period, incidence in young urban children in Chine has increased by 8 times (Zorrella et al., 2006)
44
health hazards associated with obesity
cardiovascular disease, diabetes, stroke, arthritis, some forms of cancer
45
why are obesity rates increasing?
- Jordan & Speigel (1977) - good to like sweet things
- Wurtman & Wurtman (1979) - born to like sugar - as children we want to eat sweet things to help us grow - leads to a preference for sweet things
- James & Trayhurn (1981) - good to store food reserves
46
is obesity adaptive?
- Fast changing society coupled with slow changing evolution means it is no longer adaptive to store large amounts of food
- Gossler et al. (1995) - natural experiment - no pressure on sparrows due to lack of predators which led to increased sparrows becoming obese - no set point at which the animals stopped eating - did not need to store food
- Gibbs (1996) - population becomes obese with increase in wealth
47
why is obesity getting worse?
- Ravussin et al. (1994) Populations of similar genetic backgrounds but located in US and Mexico with different jobs and diets show different incidence of obesity
- Levine, Eberhardt and Jensen (1999) found that the overweight people remained seated 2.5 hours more per day than the lean people. The difference in energy expenditure amounted to 350 kcal per day
- Snack food containing high fructose corn syrup. Fructose unlike glucose does not stimulate insulin or leptin production (Bray, Neilsen and Popkin, 2004)
- 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.
48
what are some possible causes obesity?
genetic predisposition
inability to produce leptin
insensitivity to leptin
receptors in hypothalamus
different metabolism
49
explain the genetic predisposition that might cause obesity
- Sims and Horton (1968) Non-obese prisoners increased calorie intake, eating 8,000 a day, despite similar sedentary lifestyle and same food only some prisoners had weight gain
- Bouchard et al. (1990) 12 pairs of twins overfed by 1,000 calories a day, low correlation over the group as a whole but high correlation in weight gain of two twins in a pair. Also they gained weight in the same place
- Price and Gottesman (1991) 85% of variability due to heredity
- Stunkard et al. (1986) body weight of adopted children is correlated to biological parents and not adoptive parents, same with biological and not adoptive siblings
50
explain how not producing leptin may cause obesity
- Leptin deficiency (Licino et al., 2004) - some populations of people do not produce leptin - genetic
51
explain how insensitivity to leptin might cause obesity
- Schwartz et al (1996) Plasma levels of leptin is correlated with total body fat in both lean (control) and obese people.
- Leptin is a peptide and peptides can't cross blood brain barrier, an active transport process is necessary, maybe this is not present in obese people
- Caro et la. (1996) showed that there was an 320% increase in blood plasma levels in obese people but only a 30% increase in the cerebrospinal fluid
52
explain how receptors in the hypothalamus might cause obesity
- Mutations in genes controlling activation of receptors in hypothalamus have been found in overweight Labradors (Wallace et al, 2025)
- Mutation in the gene, found in a quarter of pet Labrador retrievers, is associated with increased weight, adiposity and hunger
- If the receptors in the hypothalamus are not activated then signals of satiation (leptin) will not be effective
- Comparative genomics identified that these canine obesity genes were also associated with human obesity
53
explain how different metabolisms might cause obesity
- Rose & Williams (1961) matched people for weight, height, age and activity. Some of these individuals ate twice as many calories as their matched partner. Efficient metabolism will have excess glucose after satisfying the body energy needs which is converted to fat - have more glucose left over
- Calles-Escandon and Horton (1992) 70-85% of energy expenditure is during resting metabolism, heat production and energy needed to digest food
- Levine, Eberhardt and Jensen (1999) fed people a diet for 8 weeks that contained 1000 calories more than usual: 39% increased conversion into fat tissue; 26% increased resting metabolic rate; 33% increase in involuntary activity - fidgeting 'nonexercise activity thermogenesis' or NEAT; the amount of fat tissue that a person gained was inversely related to their level of NEAT
54
what causes people to store more or increase metabolic rate?
- Uncoupling protein (UCP) found in muscles plays important role in metabolisms efficiency (Scarpace et al. 2000)
- Increasing levels of UCP associated with increasing metabolic rate (spendthrift) and so less glucose left over to store as fat (Schrauwen et al. 1999)
- Dittman et al. (2024) showed that Labradors that have a genetic mutation will loose fewer calories when working for the food e.g. have a more efficient metabolism
