Eating and Obesity Flashcards
Lecture 7 (26 cards)
Body Stores
energy stores: fat in adipose tissue 85%, protein in muscle 14.5%, glycogen in liver 0.5% - glycogen is straight conversion from glucose (main energy used by body) but 1g fat stores 2x amount of glucose than 1g glycogen - glycogen holds water so if all energy stored as glycogen body weight would be 40 stone
Metabolism definition
chemical reactions in body
Respiration definition
breakdown of glucose making energy available to the organism
Energy for Cells
Cells use blood glucose as energy
levels of glucose in blood affected by two hormones: insulin and glucagon
glucose can’t enter cells without insulin, a peptide hormone produced by pancreas
insulin changes glucose into glycogen stored in liver, so it reduces blood glucose by putting it into cells where it’s changed to energy, or into liver where it’s changed into glycogen
glucagon stimulates glycogen into glucose to increase blood glucose levels
Role of Hormones in Metabolism
glucose (simple sugar) is converted into glycogen (complex, insoluble carbohydrate) by insulin (created by pancreas), and vice versa by glucagon
Metabolism 3 Phases
Cephalic phase = preparatory phase set off by sight or expectation of food
Absorptive phase = meeting of body’s immediate energy requirements
Fasting Phase = energy withdrawn from stores - promotes fat to fatty acids and inhibits glucose to energy except by brain, stores fat
Cephalic and Absorptive Phase associated with high insulin and low glucagon and promotes glucose to energy (respiration) and excess glucose converts to fat that is stored. Fat in these phases converted to utilisable fuels
In fasting phase, high levels of glucagon release high levels of blood glucose from liver but low levels of insulin mean only brain cells use energy
glucagon also promotes release of fatty acids and ketones
Define homeostatic system and function in eating
Starts and stops a meal
body wants to stay the same
What starts a meal - previous thoughts
energy set-point view = energy reserves drop and we get hungry in a cycle
Campfield and Smith show 8% drop in blood glucose just before meal time
BUT Le Mangen shows blood glucose levels don’t normally vary even under prolonged period of fasting
AND diabetics remain hungry with high blood glucose levels
What starts a meal? Ghrelin
Ghrelin is a peptide hormone released by stomach that increases eating and blood levels of ghrelin increase shortly before each meal
Ghrelin stimulates food intake and food thoughts
Schmid et al found single intravenous injection of ghrelin enhanced appetite and elicited vivid images of liked foods
When animal eats/experimenter infuses food into animal’s stomach, ghrelin secretion suppresses
Injection of nutrients into blood however, don’t suppress ghrelin secretion so hormone release is controlled by digestive system contents not by whats happening in your blood
Ghrelin Critique
Can’t be only hunger signal as people who have undergone gastric bypass surgery have no levels of ghrelin in blood - they eat less and stop eating
What starts a meal? External Factors
Learning - Pavlov trained dogs to salivate to sound of bell - Weingarten paired buzzer with food and bell with inter-meal times so started pressing level for food when they heard buzzer but not bell - Birch did similar study with children
What stops a meal?
Body fat levels in adipose tissue
Wilson et al found force feeding increases weight and decreases voluntary eating
Campfield et al Obese mice don’t produce leptin
Kahler et al found injecting leptin in normal mice stops eating - leptin reduces size of meals animals eat -
What stops a meal? Stomach and Duodenum
Cannon and Washburn found swallowing balloons and inflating when in stomach meant less hunger - vagus nerve records stretch of stomach and stops hunger when more stretched
Greenberg et al found entry of a fat emulsion into duodenum inhibited feeding - AND Gonzalez removed nutrient content and replaced with water in stomach and rats kept eating until nutrient level was restored, splanchnic nerves convey info to brain about nutrient content of stomach
Glucose infused to duodenum caused satiation, glucose infused to blood did not
entry of food into duodenum causes duodenum to release cholecystokinin hormone, decreasing size of meal by closing pyloric sphincter causing stomach to fill faster also acts as neurotransmitter in brain to decrease eating
What stops a meal? Hormones
Signals are sent by Stomach and Duodenum
Entry of food stimulates release of Cholecystokinin
CCK injections suppress feeding
Peptide YY released by stomach after meal in proportion to calories consumed
Injections of PYY inhibits size of meals
Cannon and Washburn (1912) = Washburn swallowed balloon and contractions coincided with hunger pains but people without stomach still have hunger pains?
What stops a meal? External Factors
LEARNING:
Weingarten and Kulikovsky - Sham feeding studies show amount eaten based on previous experience
CAFETERIA DIET:
Rolls et al - if you have new food all the time you increase eating
SOCIAL:
Polivy et al = four female participants and one accomplice, a model, ate a meal together and half of them told she was on a diet and all ate much less
Redd and DeCastro = people eat 60% more when more people present, diaries kept
Berry et al - males eat more lasagne in groups
What in the brain responds to signals of hunger and satiation?
The Arcuate Nucleus = aggregation of neurons in mediobasal hypothalamus responding to Ghrelin released by stomach
Arcuate Nucleus secretes Neuropeptide Y as a response to Ghrelin
Infusion of NPY into other areas of hypothalamus leads to ravenous hunger
Neural mechanisms controlling hunger
‘Feeding Centre’
Lateral hypothalamus
Electrical stimulation to LH elicited eating
Lesions on LH caused no eating
NPY (in Arcuate Nucleus) stimulates activity of Melanin-concentrating hormone (MCH) and orexin in response to Ghrelin
MCH and orexin are produced by neurons in LH and stimulate hunger and decrease metabolic rate, increasing and preserving the body’s energy stores
Neural mechanisms controlling satiation
Leptin binds with leptin receptors on neurons in arcuate nucleus
Arcuate nucleus also has receptors for PYY secreted by stomach after a meal
PYY and Leptin inhibit release of NPY in Arcuate Nucleus
Arcuate Nucleus releases peptides CART/alpha-MSH (known as anorexigens)
Leptin activates these neurons which inhibit MCH and orexin neurons in LH and prevent their appetite stimulation
Obesity: Current Scene
In USA 67% of men and 62% of women are overweight
In past 20 years incidence of obesity in adolescents has tripled
Over 10 year period incedence in young urban children in China has increased by a factor of 8
Obesity: Health Hazards
cardiovascular disease
diabetes
stroke
arthritis
some cancers
Obesity: Why’s it getting worse?
DIET:
Ravussin et al found populations of similar genetic backgrounds but located in US and Mexico with diff jobs and diets show different incidence of obesity
Snack Food containing High Fructose Corn syrup - Fructose doesn’t stimulate insulin or leptin production
ACTIVITY LEVELS:
Levine, Eberhardt and Jensen found overweight people remained seated 2.5 hours per day more than lean people - diff in energy expenditure is 350kcal per day
Obesity: Genetic Predisposition
Sims and Horton found same food and same sedentary lifestyle but increase in calorie intake only affected some prisoners
Bouchard et al = twins put on weight in same place
Price and Gottesman = 85% heredity between twins
Stunkard et al = adopted children far more like biological parents in weight than adopted parents
Obesity: Leptin
Licinio et al = some populations of people don’t produce leptin (leptin deficiency) - families with this deficiency who had leptin injections lost weight
Schwartz et al = plasma levels of leptin is correlated with total body fat in both control and obese people
Caro et al = leptin levels are higher in blood plasma of obese people than controls
BUT not much higher in cerebrospinal fluid of obese people
Leptin is a peptide so can’t cross blood brain barrier without active transport process - is this not present in obese people?
Obesity: Leptin Receptors
mutations in genes controlling activation of receptors in Hypothalamus found in overweight Labradors (this gene is found in 1/4 pet Labradors)
If receptors in hypothalamus aren’t activated then signals of satiation won’t be effective
Comparative genomics identified canine obesity genes associated with human obesity
