Temperature control, eating, and drinking

What is the motivation? How is consumption regulated? What goes wrong?

Homeostasis maintains internal states within a critical range.

Homeostatic mechanisms are redundant Feedback

Set

point Set zone

Set points/zones can change

Temperature regulation is critical

Endotherms (Isothermic,warm-blooded) Ectotherms (poikilothermic, cold-blooded)

Behavioral

mechanisms Location choice Physiological mechanisms

Control metabolism Brown adipose tissue thermogenesis

BAT surrounds vital organs and C1-T12 of spinal cord

Juvenile mammals
Link to penguin shuffle Huddling of rat pups

Move

to periphery of huddle when hot, to center when cold

Neural centers control temperature

Location: POA and lateral hypothalamus

Lateral hypothalamus controls behavioral thermoregulation POA controls physiological thermoregulation Homeostatic redundancy

Receptors are in the skin, body core, and hypothalamus Spinal or body centers control temperature in a broad range (2 -3 degrees C); hypothalamus controls temperature in a narrow range, and appears to affect the activity of the other systems.

Thirst and drinking

Water transporting channels: aquaporins Cellular dehydration or osmometric thirst: Salt makes ECF hypertonic, drawing water from cells and dehydrating them. Hypovolemic or volumetric thirst: loss of blood volume, detected by atrial baroreceptors and kidney blood-flow detectors

Reactions to thirst

Osmometric thirst triggers receptors in:

AV3V supraoptic nucleus organum vasculosum of the lamina terminalis (OVLT), and possibly the lateral POA

What happens when osmosensory neurons are stimulated?

These cells stretch and contract in response to osmolality, thus opening and closing ion channels: mechanically gated channels. Receptor activity neurally activates the experience of thirst, and cause the posterior pituitary to release ADH Drinking behavior is also triggered, and stops when enough water has entered the gi tract.

How do we respond to hypovolemic thirst?

Hypovolemic thirst baroreceptors trigger ADH (vasopressin) release from posterior pituitary
Absence

of ADH production diabetes insipidus

Blood flow receptors affect kidney action directly We experience thirst and salt hunger SNS activity constricts blood vessels

Kidney action is organizational

Similar effects of hypovolemis thirst come from the renin-angiotensin system

Renin converts angiotensis I angiotensis II

Angiotensis II constricts blood vessels Increases secretion of ADH/vasopressin and aldosterone Acts on hypothalamus to trigger drinking behavior Acts on cirumventricular organs:

Sense level of angiotensis II through leaky BBB Subfornical organ increases activity in response to angiotensis II

Note the redundant systems

Kidney to brain
ADH => Renin => Angiotensin II => constriction of peripheral blood vessels and release of aldosterone => sodium retention Angiotensin II also acts on the subfornical organ (SFO), which is outside the BBB, to trigger drinking. Angiotensin II is also manufactured in the brain, and can trigger thirst without SFO activity.

Why drink if you are not thirsty?

Positive incentive theory

Taste:

Bad tasting water decreases drinking, sweet taste increases drinking Eating increases drinking: Dry and protein-rich foods induce hypovolemic thirst, but drinking increases with any food. Insulin may be a trigger. Anticipation or learned drinking

Satiety for drink

Sham drinking studies show that drinking is proportional to the length of time since the last drink, suggesting oral factors in satiety. Injected water reduces deprivation-induced drinking only moderately. Sensory-specific satiety: Rats drink more saccharin flavored water, especially after being deprived of it for awhile. They drink even more if the flavor changes frequently.

Review the processes of digestion

Digestion: Energy and nutrients Forms of energy delivery

Lipids,

amino acids, and glucose

Forms of energy storage

Fats,

glycogen, and proteins absorptive, and fasting

Phases of energy metabolism

Cephalic,

Brain has first dibs on glucose, but will use ketones if fasting is prolonged.

Pancreatic hormones

Insulin
Helps

us use glucose energy first (cephalic) Helps store energy by conversion of unused glucose to glycogen and fat, and amino acids to proteins (absorptive and cephalic) Helps store converted energy in appropriate places (absorptive and cephalic)

Glucagon in fasting phase helps convert stored fat energy to free fatty acids and ketones

What controls eating behavior?

Set-point theories
Homeostatic

mechanisms and negative feedback loops Glucostatic and lipostatic theories: Short- and long-term homeostasis But why does weight increase long-term? Set-point theories ignore other influences

Positive incentive theory

Items in positive incentive theory

Species-specific preferences and aversions Learned preferences and aversions

Conditioning

and cultural exposure: Fufu Deficiency selection: Sodium salt preference Deficiency selection: Aversion to low-nutrient tastes; overcome in humans by food preparation and by variety of choices of foods: Confusion.

Timing factors: Social influence, anticipatory insulin release, conditioning

More incentives...
Satiety, learned knowledge of the effects of a familiar food; decreased with novel foods in sham-eating studies Lower nutritive density, to a point Appetizer effect: Anticipation raises hunger Social influence: Group eating suppresses satiety Cafeteria effect: Variety of good-tasting foods increases consumption and compensates for sensory-specific satiety

Regulation of food consumption

Blood glucose levels Hypothalamic mechanisms

Ventromedial

hypothalamus (VMH) and satiety Lateral hypothalamus (LH) and eating Paraventricular nuclei

Gastrointestinal sensations GI peptides: cholecystokinin, bombesin, glucagon, somatostatin; CSF insulin levels

Regulating body weight

Set point theory Thermogenesis Settling point theory: Six factors in the leaky barrel model.

Amount of available food Incentive value of available food Amount of consumed energy Level of body fat Amount of energy expended Strength of the satiety signal

Disorders
Obesity Anorexia nervosa

Social

influence Dieting trigger Increased cephalic phase insulin response, even when protesting no feelings of hunger. Binging and purging may cancel the incentive value of food, by associating food with vomit.

Bulimia nervosa