Chapter 10. Internal Regulation
Essay questions:
1. Describe the internal reflexive thermoregulatory responses of homeotherms
2. Why does an injection of sodium chloride produce thirst?
3. Describe the compensatory physiological reactions to hypovolemia
4. List the components of digestive system and describe the major functions of insulin and glucagons
5. Describe the interrelations of glucose, insulin and glucagon, and LH and VMH for eating and satiety
Chapter 10. Internal Regulation
1. Temperature regulation
1.1. Homeotherms = warm blooded = gentlemen
Mammals and birds are homeotherms, they remain an almost constant body temperature, range of 36 - 37.2 C degree. Their blood must keep warm in order to perform biochemical reaction
1.2. Poikilotherms = cold blooded animals = ruthless killers???
Fish, amphibians, and reptiles are poikilotherms, their body temperature is the same as the temperature of their environment
1.3. Heat gain: through metabolism
Metabolism: utilization of stored food in the body releases heat, so all living tissues produce heat
Carbohydrates per gram produce 4 Kilocalories
Protein .. .. .. 4 .. ..
Fat .. .. .. 9 .. ..
Alcohol .. .. .. 7 .. ..
Note: 1 kilocalories = enough heat to raise the temperature of 1000 grams of water 1 degree C.
1.4. Internal reflexive thermoregulatory response of homeotherms
See Transparency
(1). Warming responses (when exposing to cold environment)
1). By shivering the muscles to generate heat
2). Peripheral vasoconstriction decreases heat loss from skin
3). The release of thyroxine increases the metabolic rate and thus generates more heat
(2). Cooling responses (when exposing to hot environment)
1). Increased respiration (panting) increases heat loss from lungs. Dogs, cats, and rats have no sweat glands, so they pant to evaporate moisture
2). Perspiration increases heat loss from the skin (evaporation). Humans, horses, cattles, sweating helps to prevent overheating.
3). Peripheral vasodilation increases heat loss from the skin. Rabbits has two large ears to increase the area of blood vasodilation (it will not work in desert if the temperature is over 100 C)
1.5. Neural control of thermoregulation
See Transparency 51
(1). Thermodetectors in various parts of the body
(2). They send signals to Preoptic area of the hypothalamus (POAH), the thermoregulatory center
(3). The set-point temperature is 37 degree in the preoptic area.
If the temperature is below 37 degrees (set-point), the neurons in the preoptic area will generate warming responses
If the temperature is higher than 37 degree, the neurons in the preoptic area will generate cooling responses
See Transparency Figure 12-18
1.6. Fever
Fever is induced by pyrogen which travels through the blood to the CNS (in the preoptic area of hypothalamus), cause the set-point reach to 38-40 degrees.
Pyrogens: bacteria, virus, inflammation, cancer
Leukocytes (white blood cells)
The release of interleukin-1
Prostaglanding E1 and prostaglanding E2
Activation of neurons in the preoptic area of hypothalamus
Three phases of fever:
Chill phase - as the temperature increases, feel cold
Plateau phase - feel hot, dry skin, high body temperature
Sweating phase (defervescence phase: to cool off) - the set-point returns to normal, the body rids itself of excessive heat by profuse sweating
Question: sweating first or recovering first?
Note: Heating a feverish patient to induce sweating is very dangerous, causing overheat and brain damage
1.7. Hypothermia
See Transparency Table 12-2
Note: Cooled tissue use little oxygen, patients who have drowned in ice water can be revived many minutes after they stopped breathing and suffer little brain damage. It is possible for storing fertilized eggs or overies for many years for future use. However, we cannot ice a man for years, because we can not revive the body without causing body tissue damages.
2. Thirst
2.1. Distribution of fluid in the body
(1). Solute: a substance which is dissolved in a solution, such
as, sugar in the water, salt in the water
(2). Isotonic: two solutions are said to be isotonic if they contain the same concentration of solutes
(3). Hypotonic: less concentrated (less solutes) than the reference solution
(4). Hypertonic: more concentrated (more solutes)
(5). Osmotic pressure: the pressure that draws water from a hypotonic solution to a hypertonic solution
(6). Osmoreceptors: receptors sensitive to dehydration
(7). Distribution of fluid in the body
66% within cell bodies: intracellular fluid
34% is outside of the cell body: extracellular fluid
26% between cell bodies: interstitial fluid
7% in blood
1% is cerebralspinal fluid
(8). Normally, the concentration of solutes in the fluids of intracellular and extracellular compartments is the same, they are isotonic in humans
2.2. Osmotic thirst: more solutes in extracellular compartments: caused by intaking too much salt or sweating
(1). Question: why does an injection of sodium chloride produce thirst?
Answer: If solutes in the extracellular compartment increased, such as, eat too much salt in diet, or the injection of sodium into blood, (makes that) extracellular compartment becomes hypertonic (because the sodium can not pass into the inside of the body cells), which draw water from intracellular compartment into extracellular compartment. As a result of this, the cellular dehydration follows, people feel thirsty.
(2). Question: where are the receptors that detect cellular dehydration and mediate thirst?
Answer: osmotic receptors are located in OVLT (organum vaculosum laminae terminalis)
See Transparency 52
Procedures: thirsty - the activation of neurons in OVLT - OVLT relays information to supraoptic nucleus and paraventricular nucleus - these nuclei control the rate of vasopressin release by anterior pituitary
Evidence: microinjection of hypertonic saline in these areas induce drinking
Sodium intake was suppressed by bilateral microinjection of water into these areas
2.3. Hypovolemia (hypovolemic thirst)
See Transparency 89, 90, 91, 92
(1). Definition: a reduction of blood volume caused by blood loss (Both water and solutes are lost in both extra - and intracellular compartments)
(2). Compensatory physiological reactions to hypovolemia
Withdrawing blood from blood vessels (accident)
hypovolemia
reduces blood flow reduces blood pressure
activates blood flow activates baroreceptors
detectors in the kidneys in the heart
causes kidneys release renin causes posterior pituitary release antidiuretic hormone
Formation of angiotensin I & II (ADH)
constriction of kidneys increase kidneys increase
peripheral blood reabsorption of reabsorption of
vessels sodium from urine water from urine
compensated blood volume and blood pressure increase
(3). Question: where does angiotensin II act to mediate hypovolemic drinking?
See Transparency 52
Answer: subfornial organ (SFO) is a midline structure just beneath the fornix on the roof of the their ventricle between the openings to the two lateral ventricles as the site of angiotensin action. Evidences: Microinjection of angiotensin II into SFO induced drinking
3. Hunger
3.1. The components of digestive system
See Transparency Figure 10.10
(1). Mouth: eating food
(2). Salivary glands: food mixed with saliva to break down carbohydrates
(3). Esophagus: moves food and drinks to the stomach
(4). Stomach: food is mixed with hydrochloric acid and enzymes: digestion of proteins. Surgically removal is not fatal
(5). Liver: release enzymes
(6). Gall bladder: secrete bile
(7). Pancreas: secrete insulin and glucagons
(8). Duodenum: connects stomach through pyloric sphincter
(9). Small intestine: contain large number of enzymes: digests fats, proteins, and carbohydrates. It is the main site for the absorption of digested food nutrition.
The surgical removal of small intestine can cause malnutrition
(10). Large intestine: absorbs water and minerals and lubricates the remaining materials to pass them as feces
Questions: for hunger strikers, who can live longer? Fat or thin people?
Answer: fat can be converted into glucose as body's primary fuel
(11). Lactase (enzyme) and consumption of dairy products
Milk contains lactase. Lactase is necessary to metabolize lactose. About two-thirds Asians have very low level of lactase, so they cannot drink milk. Intestine lactase level declines after certain age. Using my own example.
3.2. Physiological mechanisms of hunger and satiety
(1). Oral factors: See Transparency
Sham feeding: cues from mouth are insufficient for satiety
Introgastric feeding: cues from mouth are not necessary for feeding
(2). Stomach distention See Transparency 61
When the stomach contracts, feel hunger
When the stomach is fulled with air, feel satiety
(3). The duodenum and hormone CCK See Transparency
CCK (cholecystokinin) is released by the duodenum and plays an important role in satiety
Ex: when food is injected into the stomach
CCK is released
Pyloric sphincter (muscles) closes
Stomach emptying retards
Further food intake stops
(4). Digestion and energy flow (See Transparency 94)
1). The food is breaking down fat, glucose, and amino acids to provide energy
2). Most of the body's energies are stored as fats, glycogen, and protein
3). Three phases of energy metabolism
a. Cephalic phase: preparatory phase, which is initiated by the sight, smell, or expectation of food.
b. Absorptive phase: nutrients from a meal meeting the body's immediate energy requirements, with the excel being stored
c. Fasting phase: energy being withdrawn from stores to meet the body's immediate needs.
(5). Blood glucose regulation
Digested food enters the blood stream in the form of glucose, fat, and amino acids.
Under normal conditions, blood glucose levels fluctuate very little.
They are controlled by two pancreatic hormones, insulin and glucagon
1). Functions of Insulin: Facilitates the entry of glucose into cells, the conversion of excess glucose to fat and glycogen, and the convertion of amino acids to proteins
2). Functions of glucagon: promotes the conversion of glycogen to glucose, the utilization of fat by the body, and the conversion of protein to glucose
3). When food is in stomach: insulin is released and glucagon is inhibited. Some of the secreted insulin reaches the brain and acts as a satiety hormone to decrease hunger
4). When the stomach is empty: blood glucose level falls, glucagon is released and insulin is inhibited
5). Diabetes:
Pathology: lack adequate insulin in the blood
Causes: unknown
Consequences: glucose cannot be metabolized by the body cells and therefore causes high levels of glucose in the blood
Symptoms: Blood vessels be damaged
Hungary
Excessive sugar is excreted in the urine, causing patient frequent urination and dehydration
Treatment: injection of insulin daily
6). Why do untreated diabetic people eat so much but lose weight?
Hunger
Eating
Blood glucose increases but insulin level is low
Glucose does not enter cells
Glucose leaves in urine and feces
Hunger remains high
Blood glucose levels stay high
But cells are starving (need glucose)
Hunger
(6). Brain mechanisms in hunger and satiety
1). The lateral hypothalamus and hunger (LH)
See Transparency 53 91, 54
a. Large bilateral lesions of the LH induced rats aphagic and adipsic
b. Stimulation of LH elicited feeding in the satiated rats
c. After damage to LH, animal has low levels of insulin
d. Pathways from LH to other brain structures in regulating eating
2). How does the lateral hypothalamus (LH) contribute to eating?
a. Axons from LH to NTS (nucleus of the tractus solitarius): increase the taste sensation
b. Some LH cells increase pituitary gland's secretion of hormones, which, in turn, increase insulin secretion
c. Axons from LH to forebrain structures: increase eating responses to taste, smell, or sight of the food
d. Dopamine-containing axons that pass through LH initiates and reinforce learned eating behaviors
e. LH sends axons to spinal cord: increase digestive secretion
3). The ventromedial hypothalamus (VMH) and satiety
(VMH also includes nearby meida; hypothalamic cells and axons)
a. Large bilateral lesions of the VMH produced hyperphagia and gross obesity
See Transparency 71, Extra
b. Electrical stimulation of VMH caused hungary rats to stop eating
c. Damage to the VMH leads to a lasting increase of insulin
d. Damage to the ventral noradrenergic bundle leads to overeating and weight gain
4). Paraventricular nucleus (PVN) of the hypothalamus: damage to PVN causes the animal eat larger meals: overeating
5). Interrelations of glucose, insulin and glucagon, and LH and VMH for eating and satiety:
Hunger - eating - insulin release - increase in blood glucose - inhiting LH and Exciting VMH - feel satiety - stop eating - glucagon release - decrease in blood glucose - exciting LH and inhibiting VMH - feel hunger
(7). Social and cultural influence
1). People eat more when they are with other people
See Transparency Figure 12.21
2). Americans eat more on weekends
See Transparency Figure 12.22
3). People eat more in the evening than at noon
4). People eat more when food tastes good
5). People eat the same amount as usual when people drink an alcohol beverage with a meal
(8). Genetic, metabolic rate, and body weight
Weight is the outcome of both the amount of food consumed and the amount of energy used
1). The efficiency of energy utilization
Body responds to energy shortage and excesses by increasing or decreasing the efficiency of energy utilization
2). The metabolic rate difference is largely inherited
Ex: my son eats a lot but he is OK shape, he has a very high metabolic rate.
See Transparency 9
Overweighted people have low metabolic rate
3). Dieting may not work, because the dieters may lower their metabolic rate during dieting
See Transparency Extra
4). Conclusion: losing body weight is difficult
(9). Body fat and puberty
High level of body fat induces early arrival of puberty
Low level of body fat delays puberty
(10). Relationships among Leptin (peptide), NPY (neuropeptide Y), and PVN (Paraventricular nucleus of the hypothalamus)
For normal body weight people: body fat produces leptin
--- Leptin inhibits the release of NPY
--- NPY inhibits the activity of PVN of the hypothalamus
--- Body weight maintains a normal range
For obese people: obese gene makes leptin fails to inhibit NPY secretion
--- The activity of PVN increases
--- overeating and obesity
(11). Weight-loss technique
(1). Incresed exercise
(2). Decresed eating
(3). Not overeating when the food tastes good
(4). Select low-calarie recipes
(4). Using appetite-suppressant drugs:
a. Fenfluramine: increases the release of serotonin and blocks its reuptake.
(has severe side effects)
b. Phentermine: blocks reuptake of norepinepherine and dopamine
c. The combination of the two drugs produces brain effects similar to theose of a completed meal
d. Sibutramine (Meridia): blocks reuptake of bothe serotonin and norepinepherine
e. Xenical: inhibits the absorption of dietary fat into the intestines
4. Eating disorders
4.1. Obesity
(1). Biological factors:
If neither of your parents is obese, 10% chance of obese
.. one .. .. .. .. .. , 40% .. ..
.. both .. .. .. .. .. 70% .. ..
(2). Psychological factors: depression causes overeating
(3). Behavioral factors: reduced exercises
4.2. Anorexia: self-starvation and extreme weight loss
(1). 2.5% of the North American student population has the disorder
(2). Majority of patients are female
(3). Health-threatening weight loss: a loss of 20 to 25% of original body weight
(4). About half of patients with anorexia have a binge eating followed by purging by vomiting or laxatives
(5). Causes: it is a psychiatric disorder
See Transparency A
4.3. Bulimia: intense, recurring episodes of binge eating followed by efforts to avoid weight gain, such as vomiting and using laxatives in the absence of extreme weight loss
See Transparency Table 12.12
Causes are more psychological and social factors