Biopsychology Exam 3: Hunger and Eating

What has new research found about the lateral hypothalamus? What does the lateral hypothalamus release (2)? What do these hormones do? What does food deprivation result in?

***hunger** Releases 2 hormones related to hunger and eating: Melanin-concentrating hormone - related to increased eating behavior. Increased MCH release when highly palatable foods are around. Palatable foods = release of MCH=increased eating behavior. (explains why you eat more bad food) Orexin - higher orexin gives a preference for foods higher in sugar, salt, and fats. Both hormones trigger perception of hunger, choice, and eating behaviors. Both decrease metabolic rate, meaning that in total there is a decrease in how quickly we will expend energy. With more MCH and orexin, the body is trying to reserve the energy that's coming in. Food deprivation results in increased MCH and orexin.

Why is the "settling point theory" a better explanation for food/weight regulation?

- body weight tends to remain relatively constant in many adult animals over time - settling point theory helps to account for higher gains in weight during the adult years - weight that is less likely to come back off later because of the newly established state of homeostasis

Why is fat the body's preferred way of storing energy?

1. A gram of fat can store almost twice as much energy as a gram of glycogen. 2. Glycogen, unlike fat, attracts and holds substantial quantities of water. (Extra weight)

What are the steps in digestion? (8)

1. Chewing breaks up food and mixes it with saliva. 2. Saliva lubricates food and begins its digestion. Parotid glands - break down starches and carbohydrates 3. Swallowing moves food and drink down the esophagus to the stomach 4. The stomach acts a reservoir for storage of food before it passes through the intestines. The hydrochloric acid in the stomach breaks down food into small particles and pepsin begins the process of breaking down protein molecules to amino acid. 5. The stomach gradually empties into contents through the pyloric sphincter into the duodenum, the upper portion of the intestine, where most of the absorption takes place. Food makes it through pyloric sphincter, which opens and closes based on various chemical signals. Smaller opening = slower. Determines how quickly you will feel hungry again. 6. Duodenum is where nutrient absorption takes place. Digestive enzymes in the duodenum break down protein molecules to amino acids, and starch & complex sugar molecules to simple sugars. Simple sugars and amino acids readily pass through the duodenum wall into the bloodstream and are carried to the liver. 7. Fats are broken down by bile. Bile is manufactured in the liver and stored in the gall bladder until it is released into the duodenum. Emulsified fat cannot pass through the duodenum wall and is carried by small ducts in the duodenum wall into the lymphatic system 8. Most of the remaining water and electrolytes are absorbed from the waste in the large intestine, and the rest is waste.

Summarize the steps in digestion (8)

1. Chewing food to break up and mix with saliva 2. Saliva lubricates food and begins its digestion 3. Swallowing moves food down esophagus to stomach 4. Stomach as storage reservoir. Hydrochloric acid breaks down food. Pepsin begins breaking protein molecules to amino acids. 5. Stomach gradually empties contents through pyloric sphincter into duodenum. 6. Digestive enzymes in duodenum break down protein molecules into amino acids, starch & complex sugars into simple sugars. Sugars and amino acids pass through duodenum into liver. 7. Fats are emulsified by bile. Carried by small ducts in the duodenum wall into lymphatic system. 8. Remaining water and electrolytes absorbed. Waste is ejected.

How does the leaky barrel model serve as an analogy for the settling point model?

1. The amount of water entering the hose is analogous to to the amount of available food. 2. The water pressure at the nozzle is analogous to the incentive value of the available food. 3. The amount of water entering the barrel is analogous to the amount of consumed energy. 4. The water level in the barrel is analogous to the level of body fat. 5. The amount of water leaking from the barrel is analogous to the amount of energy being expended. 6. The weight of the barrel on the hose is analogous to the strength of the satiety signal.

What is lipostatic set point theory?

According to lipostatic set point theory, every person has a set point for body fat and deviations from this set point produce compensatory adjustments in the level of eating that return levels of body fat to their set point. When in the fasting phase, we are tapping into energy reserves and triglycerides are being converted into glucose. The reduction in energy from our fat needs to be replaced. Dropping below set point = hunger = eating to replenish what we lost. The longer you're in the fasting phase = falling of lipids below set point = hungrier. Once you eat, fats being absorbed and being put back into adipose tissue and that energy reserve is built back up.

What is the positive incentive theory? What is a problem with the theory?

Animals and humans are drawn to eating by the anticipated pleasure of the eating experience (positive incentive value of eating). Degree of hunger felt at any given period in time is dependent on all the factors affect the incentive value of eating Flavor of food (palatable, tasty, fatty, salty) Conditioning of food in past experiences Time since last meal Presence of other people Blood glucose out of normal range (too high or too low) Implies that if eating is all about pleasure, we should only eat these tasty and fatty foods. This model predicts everyone shifting to that preference, but not everyone is.

What happens to positive-incentive value as you eat one food?

As you eat one food, the positive-incentive value of all foods declines slightly, but the positive-incentive value of that particular food plummets.

What is modeling of food preferences?

Babies prefer flavors found in mother's milk and on breath of others. Indicator of food available, so natural preference grows for survival. May learn to prefer foods eaten by others.

Why is eating stressful on the body?

Before a meal, the body's energy reserves are in reasonable homeostatic balance. As a meal is consumed, there is a major homeostasis-disturbing influx of fuels into the bloodstream. The body does what it can to defend its homeostasis.

What is a set point theory? What are the 2 set point theories?

Belief that we eat to bring our energy resources back up to an optimal level...to an energy set point Whether we are hungry or sated depends on whether we cross the set point. Functions like a thermostat. Bodies have a set point (point at which we want to maintain energy reserves) Glucostatic and lipostatic

What are the 3 satiety peptides and 1 satiety neurotransmitter?

Cholecystokinin (CCK) Peptide YY Leptin Serotonin

What is Cholecystokinin (CCK)? Where is it secreted from and in response to what?

Cholecystokinin is a satiety peptide secreted by the duodenum in response to fats in the intestines. Consuming lipids and fats = increased release of CCK. CCK slows rate of stomach emptying and closing of sphincter. When closed, it reduces how quickly food is passing through and slows the rate of stomach emptying. Results in a decrease in hunger because there is decreased ghrelin.

What is conditioning of hunger?

Cues related to eating will trigger cephalic phase. If you don't eat any food, the feeling of hunger will pass. If you continuously are exposed to these foods, insulin will spike and the feeling of hunger will continue. (ex. restaurants)

(PVN) What do elevated levels of NPY/AGRP lead to? What does activation of the PVN by AGRP lead to? What effect does thyrotropin releasing hormone have on AGRP?

Elevated levels of NPy/AgRp leads to increasing eating (via thyrotropin-releasing hormone and corticotropin-releasing hormone) Activation of the PVN by AGRP leads to decreased activity in thyrotropin releasing hormone. However, thyrotropin releasing hormone has an excitatory affect on AgRP. So, while one is trying to suppress thyrotropin-releasing hormone, one is increasing it. Overall PVN activity is related to decreased eating and increased energy expenditure.

What is energy metabolism and what are the 3 phases of energy metabolism?

Energy metabolism are the chemical changes by which energy is made available for an organism's use. Cephalic, absorptive, fasting phase

What are the 3 factors the influence what we eat?

Evolution of tastes, modeling of food preferences, vitamins and minerals

What are the 3 forms of energy storage?

Fats (majority) Glycogen Proteins

What are some satiety signals?

Food in the gut = Decrease in food consumption because you're less hungry as food is being absorbed. Once you start eating = increase in satiety Glucose in the blood = more insulin. Energy is put away into storage if not used immediately. Volume of food= Stomach contractions occur when you're hungry Nutritive density of food= low-calorie foods lead to more consumption. Appetizer effect - triggers cephalic phase with small amount of food = sudden drop in glucose levels= feeling more hungry = eating more. So when the meal comes, you're more likely to eat more of your dinner as a result of ordering the appetizer.

NYP and AGRP neurons have receptors for what? (4) Where does each come from and what does increase of each result in?

Ghrelin (from stomach). Increased ghrelin = increase NPY. Leptin (from adipose tissue), Increased leptin = decreased NPY and AgRP and decreased orexin because leptin is a satiety peptide. Increased leptin = decrease NPY & AgRP; decrease orexin Peptide YY (from ileum) - Increased Peptide YY = decrease NPY Insulin (from pancreas) = decreased NPY

What are the 2 hunger peptides influencing when we eat?

Ghrelin and Neuropeptide Y

Where is ghrelin released? When is it released? When would amounts of ghrelin rise? And what is ghrelin's role as a hunger peptide?

Ghrelin is released by the stomach in response to signal from the duodenum when empty. Duodenum empties on average of 4 hours. When duodenum empties, levels of ghrelin build up over the hours since you last ate a meal. Levels increase during fasting (highest before meal) Ghrelin results in perception of hunger (feeling hungry) and stimulates appetite Levels of ghrelin decrease during meal and are lowest after meal. The amount of decrease depends on size of the meal and the nutrient value (energy)). Regulates perception of reward. (stimulates dopamine) and increases pleasurable effects of eating.

(Fasting phase) What happens when there are low levels of insulin?

Glucose has difficulty entering most body cells, thus glucose stops being the body's primary fuel. In effect, this saves the body's glucose for the brain, because insulin is not required for glucose to enter most brain cells. The low levels of insulin also promote the conversion of glycogen and protein to glucose. (gluconeogenesis) The high levels of fasting-phase glucagon promote the release of free fatty acids from adipose tissue and their use as the body's primary fuel. The high glucagon levels also stimulate the conversion of free fatty acids into ketones, which are used by muscles as a source of energy during the fasting phase.

What activates NPY neurons?

Glucose-sensitive cells in medulla activate NPY neurons Glucoprivation (low glucose levels in cephalic phase) = activates neuropeptide Y neurons. Stimulation = increased appetite, hunger, eating behavior Orexin neurons have receptors NPY. NPY stimulates orexin. Orexin is released and triggers arousal system to activate.

What is glucostatic set point theory? What is the significance of glucose-sensitive cells?

Hunger waxes and wanes as a function of blood glucose levels. The lowest set point is when hunger levels reach their peak or are below the set point, so you eat in response. As blood glucose levels rise above set point, your hunger decreases. Medulla has glucose-sensitive cells to monitor blood-glucose levels. Glucose sensitive cells signal NPY neurons to be release. There is a connection to NPY neurons in the hypothalamus. When glucose levels decrease, those cells signal the hypothalamus, NPY neurons to release NPY.

(Cephalic phase) What does the body do in response to triggers? Why? (2)

In response to these triggers, insulin levels start to rise. We need higher levels of insulin to 1. Enable use of energy immediately from digested food and enable metabolism of glucose. 2. Excess food coming in and conversion of energy on chart.

Where are insulin and glucose released from? Summary of insulin and glucose levels across the 3 phases.

Insulin and glucose are released by the pancreas. Cephalic - insulin levels start to rise, low glucose Absorptive- high insulin levels, low glucose Fasting- high levels of glucagon, low levels of insulin

What are some issues with set point theories?

Issues with theory: Amount of energy reserves should hold us for 2-3 days. Evolution has proved otherwise in terms ofeating behaviors. Model does not account for social and environmental factors

According to the old view, what is the role of the lateral hypothalamus? What does stimulation and lesioning result in?

Lateral hypothalamus was the feeding center of the brain (stimulates perception of hunger and eating behaviors) Stimulation resulted in increased eating (hyperphasia) and drinking (hyperdipsia) Lesions resulted in: Aphagia (stop eating) Adipsia (stop drinking) Less arousal (lateral hypothalamus plays a role in arousal.)

What is leptin? Where is it secreted from? Where are the receptors for leptin located in the brain?

Leptin is a satiety peptide secreted by adipose cells in order to slow down the rate of eating for the next several hours. Leptin receptors are found on the arcuate nucleus. Leptin hyperpolarizes/inhibits the release on NPY neurons because there is no reason to eat if you have replenished fat stores. Leptin results in: - decreased eating, - increased metabolic rate and energy expenditure because you just replenished the energy stores - inhibition of orexin in the lateral hypothalamus (satiety signal) and inhibition of MCH. inhibition of orexin in release = decreased arousal.

Lipids and amino acids glucose are turned into what and stored where? And what are the percentages of lipids/amino acids/glycogen?

Lipids and fatty acids turned into triglyceride, stored in Adipose tissue under the skin. Visceral fat, type of Adipose tissue, is in the gut. About 85% of all energy storage is Triglyceride. Amino acids are combined into protein molecules. Proteins are typically stored in the muscles. (14.5%) Glycogen is stored primarily in the liver. Glycogen makes up .5% of energy reserve.

Where is the arcuate nucleus located? What does the arcuate nucleus contain? What is AGRP release activated by? What does AGRP inhibit? What does stimulation or inhibition of AGRP result in?

Located in the hypothalamus. The arcuate nucleus contains 2 types of substances: Neuropeptide Y and AGRP neurons (agouti-related peptide) Neuropeptide Y stimulates orexin and melanin-concentrating hormone release from the lateral hypothalamus. - Higher levels of ghrelin (from stomach) lead to increased levels of neuropeptide Y (not eating=increased ghrelin levels=stimulation of neuropeptide y=hungry) AgRP release activated by calorie deficiency. - Stomach is empty and energy is being pulled out of storage. AgRP increases. Higher levels of AgRP are correlated with increased appetite and decrease in metabolism AgRP inhibits satiety melanocortin 4 receptor (MC4R receptors) neurons. - in paraventricular nucleus (of hypothalamus). MC4R receptors activate satiety. When inhibited, satiety is prevented from occurring. AgRP will override so you will keep eating and have more appetite

What are the 3 formats of energy being delivered? Where do they move from?

Moves from duodenum into bloodstream. Energy is delivered in 3 forms: - fats (lipids) - amino acids (proteins) - glucose (simple sugar)

In terms of looking at NPY neurons, how do people become overweight?

NPY neurons can stop responding to leptin after being overstimulated so much over time. Over long periods of time, the NPY neurons are abnormal and become the same level as people who are underweight

Where is NPY released? What is the role of Neuropeptide Y as a hunger peptide?

Neuropeptide Y is released by neurons in the hypothalamus, specifically the arcuate nucleus. When neuropeptide y are stimulated = increase in appetite Stimulates eating behavior Rats given high amounts of neuropeptide Y ate ravenously and consumed a lot of food. This study indicates the focus on eating behavior Increase in NPY occurs when we are deprived of food/in the fasting phase. After a meal, the levels decrease.

How do social factors impact satiety?

People consume 60% more when eating with others.

What is Peptide YY? Where is it secreted from and in response to what?

Peptide YY is a satiety peptide secreted by cells in the ileum. Secretion is proportional to the amount of calories in food. Eating more high calorie foods means that more peptide YY will be released. As food hits the ileum, gastric mobility is inhibited. Slows down so you can get all the nutrient value of the food you just ate. Increases water and electrolyte absorption by the colon. Food will stick along longer in the duodenum, resulting in longer absorption, and decreased eating. Overall, more satiety.

What are the 2 factors influencing when we eat?

Pre-meal hunger and conditioning of hunger

What role do vitamins and minerals play in food preferences?

Prefer foods that are good sources of vitamins and minerals, especially if there is a deficiency. During times of deficiency, we see more preference/choosing for this particular food. In experiment, rats would eat more of the food containing the nutrient they are deficient in.

What is the evolution of tastes?

Preferences for foods that have benefitted us over time. We prefer sweet, fatty, salty foods because they are higher in nutrient value (energy.) Salty foods are high in sodium, which is needed for electrolyte balance in the body. Prefer tastes of food with high nutrient value, avoid tastes that coincide with illness

What is the cephalic phase?

Preparatory phase for delivery of food Body starts preparing for delivery of food into digestive systems in reaction to various triggers (smelling food, initiated by sight.) Ends when the food starts to absorbed into the bloodstream.

What does insulin do? (3)

Promotes the use of glucose as the primary source of energy by the body. Promotes the conversion of bloodborne fuels to forms that can be stored. (ex. glucose to glycogen, fat and amino acids to proteins) Promotes the storage of glycogen in liver and muscle, fat in adipose tissue, and proteins in muscle. - The function of insulin during the cephalic phase is to lower the levels of bloodborne fuels, primarily glucose, in anticipation of the impeding influx. - The function of insulin during the absorptive phase is to minimize the increasing levels of bloodborne fuels by utilizing and storing them.

What do the fasting phases promote and inhibit?

Promotes: - conversion of fats to free fatty acids and utilization of free fatty acids for energy - conversion of glycogen to glucose, free fatty acids to ketones, and protein to glucose Inhibits: - utilization of glucose by the body ( but not by the brain) - conversion of glucose to glycogen & fat and amino acids to protein - storage of fat in adipose tissue

What do the cephalic and absorptive phases promote and inhibit?

Promotes: - utilization of blood glucose for energy -conversion of excess glucose to glycogen and fat - storage of glycogen in liver and muscle, fat in adipose tissue, and protein in muscle Inhibits: - conversion of fat reserves into readily available fuels

What is pre-meal hunger?

Relates to the times you typically eat meals. Body kicks into cephalic phase. Sudden spike in insulin and drop in blood sugar = hunger feeling.

What are some factors playing a role in how much we eat?

Satiety signals Social Factors Sensory Specific Satiety

What is serotonin? What does it do? What do serotonin agonists do in humans? How does it affect NPY neurons?

Serotonin is a neurotransmitter for satiety. It appears to increase short-term satiety with a meal. Results in: - better resistance to eating high-calorie food - reduced amount of food consumed - food preferance shifts away from fatty foods Serotonin agonists like fenfluramine and dexfenfluramine (appetite suppressants) have been shown to reduce hunger, eating, and body weight. Serotonin has inhibitory effect on NPY receptors. Receptors are not reacting to NPY (hunger peptide) as they should. By not allowing NPY to have its effect, there is a decrease in hunger and eating behavior.

What leads to breakdown of triglycerides? When would protein be used?

Signals for energy leads to breakdown of triglycerides. Glycogen basically buys time until triglyceride can be converted. Protein is not used until other stores of food are used up. Once triglycerides can no longer be converted to energy, breakdown of muscle cells begin.

How do you end up at a new settling point?

Smaller lifestyle changes over a long period of time allows the body weight to come off slowly. The homeostatic balances balance out and over the course of a few years, you may end up at a new settling point. If diets are maintained, body weight eventually stabilizes at a new level.

What is the role of the paraventricular nucleus? What signals does the PVN detect? What does the PVN inhibit? What happens when the PVN is damaged?

The PVN controls both appetite and endocrine function. It detects and integrates NPY and AGRP signals. The PVN inhibits orexin and melanin-contentrating hormone. When the PVN is damaged, inhibition stops occuring. Therefore, orexin and MCH levels rise. Hunger levels rise and is linked to obesity.

According to the old view, what is the role of the ventromedial hypothalamus? (VMH) What are the results of lesioning the VMH? What happens after 20 days?

The VMH was the satiety center of the brain. Lesioning resulted in hyperphagia (eating all the time), increased meal frequency, and high insulin levels. After 20 days, food intake dips a bit and stabilizes. The initial high rate of consumption does not continue they end up eating less than they had before, but weight gain continues and they're still maintaining a higher weight level.

What is digestion?

The gastrointestinal process of breaking down food and absorbing its constituents into the body. The purpose of eating is to provide the body with molecular building blocks and energy

What is the arcuate nucleus?

The main center for hunger and eating, located in the hypothalamus.

What is sensory-specific satiety?

The number of different tastes available at each meal has a major effect on meal size. A cafeteria diet (varied diet of highly palatable foods) results in an increase in caloric intake. Satiety occurs when you eat the same types of food or limited foods within a meal, not a lot of variety. You are more likely to get tired of the taste and the sensation of the food you're eating here. Makes you less likely to eat what's in front of you if there's one type of food. Eating one food at a time brings you to the satiety level faster than if you were rotating through foods. Switching between multiples types of food fights against the sensory specific satiety.

What is the fasting phase?

The period during which all of the unstored energy from the previous meal has been used and the body is withdrawing energy from reserves to meet its immediate energy requirements. Glucagon levels are rising, and insulin levels are lowering. Don't need as much insulin because there is no excess energy needing to be converted. Occurs when food has moved through the intestines. Because no more energy is coming in, we have to tap into energy reserves and turn into glucose by glycogen. As adipose reserves become depleted, our body shifts from using glucose and gives it to the brain for utilization. The longer we are in the fasting phase, the more we are using reserves.

What has new research found about the Ventral noradrenergic bundle? What happened with lesioning?

The ventral noradrenergic bundle is close to the VMH and is damaged with VMH lesions **satiety** It was found that perhaps it was not the VMH that was damaged, but rather the VNA bundle . Lesions through the VNA bundle only = increased appetite When offered highly palatable food, rats ate more Increase in norepinephrine linked to increase in appetite

What happens if you don't maintain the diet? (Graph) what do the levels of food incentive value and energy expenditure look like?

Weight loss occurs rapidly at beginning Weight comes back on quickly until original settling point is regained High incentive value and low level of energy leakage/expenditure

What is the settling point model?

Weight tends to drift around a natural settling point The settling point is a level at which the various factors that affect body weight reach equilibrium Mechanisms will kick in to keep you from maintaining or gaining weight. It's difficult to maintain a change over time.

What is the absorptive phase?

When you start to eat food. The period during which the energy absorbed into the bloodstream from the meal is meeting the body's immediate energy needs. No conversion of glucose (energy taken out of storage.) insulin promotes storage of glucose, therefore glucagon levels are low. Glucagon's job is to convert the storage into glucose.