>>Dr. Ketchum: So we’re going to go ahead and pick up where we left off with the regulation
of food intake. So there’s satiety factors that are involved in both short-term and long-term.
If it’s long-term, that’s going to involve leptin. If it’s short-term, it’s going
to involve insulin, CCK, and then some neural input from your chemo- and mechanoreceptors.
And then in terms of the feeding behavior, in other words, why do you eat? There’s
also short-term regulation and long-term regulation for those as well. Both of these involve orexigenic
factors. Ghrelin—this hormone here—is also an orexigenic factor as well. All right,
so we’re going to be going through each one of these. So this, again, is just sort
of a—a recap of what we’re going to be discussing. So let’s take a closer look
at leptin. So once again, leptin is a hormone that is synthesized and secreted by the adipose
tissue. So leptin then, since it’s a hormone, right, it goes into the blood stream, and
then it targets the hypothalamus. So once it targets the hypothalamus, the hypothalamus
then is going to synthesize and secrete two satiety factors. Those are alpha-MSH. Alpha-MSH
is alpha-Melanocyte-stimulating hormone. Okay, then the other one is called CART, C-A-R-T.
So what this stands for is cocaine- and amphetamine-related transcript. And so what those are going to
do then is they’re going to target another part of the hypothalamus called the paraventricular
nucleus. And the paraventricular nucleus is the one responsible for synthesizing and secreting
corticotropin-releasing hormone, CRH, and thyrotropin-releasing hormone. Remember that
once they’re released, they travel through a portal vein to get to the anterior pituitary.
Once they’re in the anterior pituitary, it’s going to synthesize and secrete its
respective hormone. So remember corticotropin-releasing hormone will cause the synthesis and
secretion of ACTH from the anterior pituitary, and thyrotropin-releasing hormone will cause the synthesis
and secretion of thyroid stimulation hormone from the anterior pituitary. So these two hormones, then, will
go off to their targets. So ACTH, as you know, will target the adrenal cortex, and that will
cause the synthesis and secretion of cortisol. TSH, as we know, targets the thyroid gland.
The thyroid gland will then synthesize and secrete thyroid hormone. So now we have both
cortisol and thyroid hormone in the blood, and we know that cortisol and thyroid hormone
both impact metabolism. So they’re going to increase metabolism. So all of this is
happening because of leptin. Remember that leptin is the hormone that makes you feel
full; it’s a satiety factor for long term.
Okay, so here are some other factors then that are going to contribute to satiety.
All right, and again, these are suppressing your hunger. If you feel full, you’re going to
suppress your hunger. So in short-term regulation, you have insulin. And so we know that the
pancreas—specifically, what cells of the pancreas—are going to synthesize and secrete
insulin? The correct answer are the beta cells, and the beta cells are going to synthesize
and secrete insulin under what conditions? Remember that they’ll synthe—the pancreas
or the beta cells will synthesize and secrete insulin when there’s a high blood glucose
level and high amino acid levels in the blood as well. Okay, so the thing about insulin,
though, is that insulin is going to act on the hypothalamus. So start tying in the hypothalamus
to these feelings of fullness or feelings of hunger; the hypothalamus is responsible
for those. So insulin then, once it’s synthesized and secreted because of those conditions,
it will go up to the hypothalamus, and then the hypothalamus will trigger satiety. Okay,
then there’s the hormone CCK that we’re going to talk a lot more about. But for now,
CCK is synthesized and secreted when there’s a presence of food in the duodenum. So that
can lead to this feeling of being full as well. And then also you have neural input
from mechanoreceptors. So think about the gut being full, it’s distended, right, so
mechanoreceptors are going to detect the distension, and therefore you’ll feel full. And then
you’re also going to have the chemoreceptors that are going to detect products of digestion.
And that will trigger satiety as well. So those are short-term mechanisms. Now, so those
are things that suppress your hunger, but what promotes eating? So first off, let’s
look at the long-term factors. So this is the long-term, everything on the slide. So
you have these orexigenic factors. There’s what’s called neuropeptide Y and agouti-related
peptide. So what these things are going to do. Do you think that they’re going to increase
parasympathetic activity or sympathetic activity? Again, the goal is to promote eating;
it’s going to cause you to eat. So the correct answer is that these factors here are going
to cause an increase in parasympathetic activity, and then do you think these factors are going
to inhibit ACTH and TSH, or stimulate them? They’re actually going to inhibit the production
of ACT and TSH, and that way you do not produce cortisol and you don’t produce thyroid hormone
either. Then there’s also the short-term regulation of feeding behavior. So in other
words, why do you eat? Okay, what causes you to eat? And that’s this hormone called ghrelin.
This is a gastric hormone, so it’s released by the stomach, and it’s released by the
stomach when the stomach is empty. And so when you think about the short-term regulation,
also think about, okay, well the food smells good, you know it tastes good. It looks good.
It’s a social activity, and so on. Those things may all cause feeding behavior to occur.
Okay, so that concludes this segment.