Regulation internal milieu

Course Biological Psychology Atma Jaya 2011 Chapter 10, Kalat (9th ed), 3 modules

Gilles van Luijtelaar

Homeostasis
Maintenance of constant conditions in body and brain Corrections of deviations Negative feed-back loop

Critical for survival in mammals, Temp, glucose, hormones, emotions, pH, K+, etc etc

Why are weight loss programs not very successfull?

More Evidence in favor of setpoint for food intake

Setpoint increased in ventromedial hypothalamic lesioned rats: dynamic and static phase, food deprivation proves setpoint theory. Setpoint reduced in LH lesioned rats: aphagic and adipsia; slow recovery after tube feeding, only palatable food, later also some normal food. After recovery they keep low body weight.

What is controlled, what is the setpoint?

Setpoint in eating behaviour: body weight?
RdN, RZ Rat studies (LH and VMH) starvation programs in Africa weight loss programs are not very effective

but most people gain weight Setpoint in eating behaviour: glucose/insuline? Setpoint in drinking behaviour: Amount of water? Setpoint in thermoregulation: 37

Eating behaviour
Setpoint theory? We eat in order to avoid a shortage, the bodys energy sources are below an optimal level, a certain setpoint. But obesitas, A.N., learning, palatable food, migrating and hibernating animals

Control of body temperature: only homeostatic?

Body temp in mammals is not only controlled by a homeostatic principle, since anticipation takes place. Example: Emotional stim sympathetic activation of CNS, including GSR. Sweatening is thermoregulatory response, which induces cooling of the body. Not since it is necessary, but as an anticipation for putative behavioural reactions/actions.

Regulation of eating behaviour: determinants of meal size I

- Oral factors, taste, pleasure, nice to have things in mouth (gum, finger sucking), Taste preference for fat and sweet (high caloric input), avoidance of bitter (danger) - Smell cues - Social factors

Regulation of eating behaviour: determinants of meal size II

- Number of calories (rats adapt slowly after a period of high caloric food) - Full stomach, via nervus vagus. If food is put in stomach, eating behaviour stops, if food is removed, eating restarts. - Possibility to digest food

Determinants of meal size III

Time of day, circadian factors, expectations Cost factor (time/energy) Cholecystokinine is secreted by the small intestine if food has reached the small intestine. Eating behaviour is inhibited. CCK can be found in blood as well in the brain! If CCK is administered before a meal, little is eaten.

Glucose is the main body fuel

Digested food (mainly carbohydrates) is changed into glucose, the main source of energy of the brain cells (brain requires majority) [Glucose] determines eating behaviour, but not alone!

Role glucose in eating behaviour

Low [glucose] ==> eating behaviour increases High [glucose] ==> eating behaviour decreases But ...after food deprivation [glucose] is hardly changed.

Role of Insulin, Glucagon and eating behaviour

Insulin (pancreas, islets of Langerhans) fascilitates the utilization of blood glucose as a source of energy and converses excess glucose to glycogen and fat. Balance:
insulin

Glucose glycogen (liver), fats Amino Acids => proteins (energy for muscle)
glucagon

glycogen and fats glucose

Role insulin in eating behaviour

[Insulin] in blood: High [ ]: much conversion from glucose to fat little glucose left and .. ==> increase in eating behaviour, increase in body weight

Determinants of mealsize IV
Glucose Insulin Various NT and hormones (CCK) General metabolism

Reinterpretation of lesion studies

Obese rats: VHM lesion: there rats have increased insulin levels more conversion of glucose to glycogen little glucose available overeating. VMH setpoint for insulin. LH lesions:
lack of responses to all types of stimuli, also to food stimuli. problems with digesting food.

Factors that determine thirst: peripheral thirst theory

Cannons thirst theory was based on the feeling of being thirsty, mainly a dry throat. Evidence: 1) If saliva is no longer there dry mouth thirst 2) If feeling of thirst is blocked by local anesthetic in the throat, thirst is no longer experienced.

Evidence against the peripheral thirst theory

Removal of the saliva glands does not change to a large scale the amount of fluid that will be consumed. In case of a wet throat and the liquid does not enter the stomach, drinking behaviour is increased. Conclusion: other factors that dry/wet throat determine the amount of drinking behaviour.

Alternatgive: Homeostatic control of water balance

The concentration of all dissolved substances in the body fluids must be kept constant (setpoint). Osmosis is the proces in which a disturbed water balance is restored. At locations with an increase of the concentration [many molecules, little water], water moves from neighboring structures (read cells), in order to equalize the concentrations.

Thirst, how is it elicited? I

Disturbance of fluid balance may occur through loss of water or after eating/drinking salty food, this increases the extracellular concentration Water is transported from intracellulair sources and the result is a shortage of intracellular water: OSMOTIC thirst.

Osmosis

Osmotic thirst arises through

loss of water or Salty/spicy food In both cases there is an increase in the extracellulair concentration. Neural structure involved in detecting osmotic thirst is the OVLT (leaky BB), lateral preoptic nucleus produces drinking behavior OVTL=organum vasculosum laminea terminalis

Role preoptic area of the hypothalamus in osmotic thirst

- After administration of salt in the preoptic area drinking behaviour increases, after administration of distilled water the animal stops drinking water - After injection of salt into the blood, drinking behaviour increases, after lesioning in preoptic area the response to injection of salt is reduced.

Two types of thirst

HYPOVOLEMIC thirst I
As a consequence of low blood pressure (large wound) there is a shortage of water and solved substances low volume of body fluids, hypovolemic thirst. Consequence: to few possibilities for transport of oxygen and glucose. Hypovolemic thirst is relieved by drinking water with solvents, isotonic drink.

Hypovolemic thirst II
Is detected by: - baro (bloodpressure) receptors in large blood vessels - Kidneys detect low volume, indirectly a hormone is released (angiotensine II) ==> vasoconstriction (to compensate for low blood pressure)

Neural structure involved in control of hypovolemic thirst

Structure involved in detecting hypovolemic thirst is the area around the 3e ventricle subfornical organ Evidence:
Application of angiotensin II around preoptic area stimulates drinking behaviour Inactivation of angiotensin II inhibits drink ing behaviour.

Hypothalam ische kernen

Temperature control:
Neural structure involved in control of body temperature is the lateral preoptic area of the hypothalamus (similar to osmotic thirst). Both brain temperature (preoptic area) as temparature of the skin determine the control of Temp.

Final remarks concerning eating and drinking behaviour :

Is a homeostatic model sufficient to explain all aspects of eating, drinking and thermoregulation? What is the setpoint? Are there other processes involved in eating behaviour than control and correction? Over eating, anticipation, learning processes (obesitas). Can this be explained by a homeostatic model? Complex control of eating behaviour! Why?

Clinical eating disturbances

Anorexia Nervosa Bulimia Nervosa Obesitas

Anorexia nervosa
Primary somatic disease but a morbide (=ill) mental condition (Gull, 1874) History of dieting, Females, young (14-25) Extreme loss of body weight Intens efforts to loose body weight Mentally and Physically active Additional hairgrowth Denial of illness Disturbances in perception of own body image (thights, stomach) Menstruation (Amenorrhea) and Ovulation disappear before the full stage have developed.

Is the disappearance of Menstruation the cause of body weight loss?

F in concentration camps: 60% lost Menstruation (M) before food problems occured stress is the cause AN: 38% professional dancers, no or less stress When body weight increases M and Ovulation return and fertility returns. Weightloss and Stress are both inducing factors

A.N.: Disturbances in pituitary?

No Menstruation Cyclicity looks like a prepuberal girl Stimulation of hypothalamus (LH and FSH) normilizes M, other symptoms do not normalise. Not cause of pituitary or ovarian hormones

Bulimia nervosa
Young high achievers, Females Middle-Higher class Keep their bunge eating attacks secret Ashamed Purging, laxating, till 30 p/d Wrong perception of own body image

Three theories on Obesitas

Learning theory: all Emotions are conditioned with eating B every E elicits eating B

Perception: disturbed perception of internal stimuli. O pay less attention on internal ques than non O, a satiety signal is not well recognized.
After depr: O eat less than non-O O eat more if you inform them wrongly about the time of day

Psychobiological theory Hirsch

Set point: number of bodyfat cells Reduce body weight is difficult, to keep the new body weight is impossible
Body weight reduction does nor reduce the number of fat cells Only liposuction reduces setpoint