>>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.

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4 thoughts on “Human Physiology – Regulation of Food Intake”

  1. This is very good, but I just couldn’t help but got distracted by her pronunciations, satiety? Duodenum? Anyhow, still very good.

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