NESC 2470 Lecture Notes - Lecture 11: Thyroid-Stimulating Hormone, Catabolism, Paraventricular Nucleus Of Hypothalamus
10 May 2018
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Motivation I
o Discussing the length we will go to achieve something that you want
o What types of things motivate us? Different things, for different people
o On the surface, it looks like it difficult due to subjectivity. However we do have
many connections that motivate us
o Such as money, love (affiliation and relationships) and food
o Hunger is the basic motivation pathway
o Homeostasis is important because as mammals, we need to keep our body regulated
o Hypothalamus - there are non-hypothalamic regulations over homeostasis as well
o It is the part of the brain that tells you what to do when you don't have time
to think about it
o Neuronal response when
o Humoral response - some sort of event in the blood stream, usually the release of
hormones from the pituitary gland
o The hypothalamus has a direct anatomical connection the pituitary gland
o Visceromotor response - refers to effects of neurons on the autonomic nervous
system (fight or flight and rest and digest)
o Depending on conditions on the environment, sympathetic and
parasympathetic system will be activated
o Somatic Motor Response- what guides voluntary behaviour
o Responsible for seeking out goals in our motivation
o As mammals, we have the need for energy continuously, there is no point in the day
where your body doesn't need/use energy
o We eat intermittently which means that because we need energy all the time, if
this is going to work, we need storage
o Anabolism on the left - these are steroids
o Ana = building
o Intestines are full and then there is lots of nutrient absorption which get directed
to various areas
o Glycogen is a source of available glucose and is stored for times when we need
energy reasonable quickly. Found in the liver and some skeletal muscles
o Neurons will only utilize glucose as an energy fuel - they will not accept ketones
or fatty acids
o Catabolism on the right
o Cata = breaking down
o
o Evidence for set value comes from pushing metabolic conditions to the extreme in
animals
o They took a rat and starved it to forty days, when they are exposed to their
regular feeding schedule they return to their original weight. This works the
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other way around if they are force fed. They will gain the weight but then return
back to its set value, which in this case is 400g
o Glucostatic VS Lipostatic Theories
o Say the lipostatic theory states that we have a set point for fat, if there is a
deficiency, we will restore that by eating a meal and thus lead us to satiety which
means the feeling of fullness
o Set Point Theory Trashing
o Glucostatic and lipostatic theories do a poor job in explaining the current obesity
epidemic.
o If we have these set points and that we have the same set point and satiety,
shouldn't we all be the same weight?
o Evolutionarily, human beings didn't always live in a society of unlimited food.
Set points can't explain how our ancestors survived
o The physiological glucostatic and lipostatic theories don't explain feeding well. If
the set point theory is true, we should see that feeding follows changes in levels
of glucose and fat levels
o You need a large change in glucose to see changes in feeding
o The idea that we have a set point for fat has been around from 1953, Coleman's lab
made mice that lack a gene that codes for a protein called Leptin called an ob/ob
mouse
o The mouse in the centre is obviously a lot more chubby, so does this gene have
something to do with regulating satiety?
o Parabiosis is where you surgically alter organisms together
o Thus these two mice are now sharing the same blood flow
o When they did this, the obese mouse when hooked up to a normal mouse,
decreased the obesity
o The ob gene calls for a protein called Leptin that is a chemical messenger released in
fat cells
o The amount of leptin released is proportional to stored fat
o Leptin isn't important day to day influence of feeding, but it does set the overall tone
of feeding
o If leptin can reduce feeding, then there is a lot of medical interest in this in regards to
obesity
o Left mouse is ob/ob knockout mouse, but so is the right! However, the right mouse is
getting daily injections of leptin
o Essentially, they're both fat ass mice
o Looking at leptin depletion can allow us to look at adaptive responses to
starvation
o Are there leptin deficiencies in human obesity?
o This image is of a girl that does not produce leptin
o The image on the right is the results of her getting injections of leptin
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Document Summary
Different things, for different people: on the surface, it looks like it difficult due to subjectivity. Intestines are full and then there is lots of nutrient absorption which get directed to various areas: glycogen is a source of available glucose and is stored for times when we need energy reasonable quickly. This works the other way around if they are force fed. If we have these set points and that we have the same set point and satiety, shouldn"t we all be the same weight: evolutionarily, human beings didn"t always live in a society of unlimited food. Set points can"t explain how our ancestors survived: the physiological glucostatic and lipostatic theories don"t explain feeding well. If leptin can reduce feeding, then there is a lot of medical interest in this in regards to obesity: left mouse is ob/ob knockout mouse, but so is the right!
