Eating and Metabolism

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Eating and Metabolism
eating is more than just acquiring calories- it
includes social, physical, and behaviors to go
along with the calories cells require energy to
continue to survive, and it gets stored in cells
and in the body, unlike oxygen brain requires
large amounts of glucose for continued
functioning even though other chemicals like
lipids and amino acids can be used prandial
newly fed state fasted no new energy
absorbed energy is always carried in blood
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Eating and Metabolism
insulin is a key hormone regulated by glucose
levels in the blood secreted from pancreatic
islet b cells activated by cholinergic
neurons inhibited by adrenergic neurons
stimulates the storage of glucose as
glycogen sight, aroma, etc of food stimulates
insulin production through the vagus nerve
from the hypothalamus also stimulated by
gastrointestinal hormones and absorbed
glucose insulin levels and sensitivity to
insulin are linked to maintain a balance
between storage and utilization of glucose
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Eating and Metabolism
meals are not constant, therefore eating is based
on more than just energy requirements in
mice, meal sizes were unpredictable as were the
intervals what WAS linked was that larger
meals led to larger intervals between
meals stomach has stretch receptors to determine
fullness gastric distension sent through the
vagus nerve to brainstem, hypothalamus, then
cortex cholecystokinin (CCK) intestinal hormone
strengthinging fullness signal leptin and
glucagon also signal fullness nausea
(illness) can also signal food aversion
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Eating and Metabolism
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Eating and Metabolism
after periods of extended fasting or overeating,
meal sizes tend to increase or decrease,
respectively, to maintain a constant
adiposity leptin is a key hormone signaling
adiposity, or body weight more leptin hormone
causes an animal to eat less leptin receptor
has been found in the hypothalamus works
cooperatively with insulin signals obese
individuals are desensitized or habituated to
higher levels of insulin and leptin loss of
insulin response can lead to diabetes only 1
leptin receptor splicing isoform signals to
the nucleus (longest form)
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CNS Control of Food
lesions in the ventromedial hypothalamus (VMH)
cause marked obesity lesions in ventrolateral
hypothalamus (VLH) caused starvation led to
the idea of a satiation (VMH) and hunger (VLH)
brain center however, that argument is too
simplistic VMH lesions don't change meal size
rather it increases frequency after periods of
starvation, VMH lesioned animals eat more to
become obese again- returns to a higher set
point of adiposity VMH lesions increase fat
storage by chronic insulin secretion VLH lesions
cause loss of drinking and movement and
sensory response overall hunger centers are more
complex
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CNS Control of Food
neuropeptides seem to play a major role in food
intake anabolic peptides cause increased
eating catabolic peptides decrease it arctate
nucleus of the hypothalamus has both leptin and
insulin receptors makes a-melanocyte
stimulating hormone (a-MSH) and cocaine-
amphetamine related transcript (CART), both
catabolic peptides VMH and VLH both have a-MSH
receptors which cause obesity when
mutated neuropeptide Y and agouti related
peptide (AgRP) are made in different neurons
of the arctate nucleus- strong anabolic
peptides and inhibited by insulin/leptin
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CNS Control of Food
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CNS Control of Food
NPY is most effective in the PVN (paraventricular
nucleus) of the hypothalamus PVN levels of
NPY peak around dusk when rats eat their largest
meal AgRP antagonizes a-MSH receptors, promoting
food intake orexin A and melanin-concentrating
hormone (MCH) are made in the VLM and are
strong catabolic peptides, increasing
eating oxytocin made in the PVN acts in the
cortex to reduce eating stress also releases the
PVN hormone corticotropin releasing hormone
(CRH) reducing food intake
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CNS Control of Food
nucleus of the solitary tract (NST) in the
brainstem receives vagus nerve and gustatory
signals from nose and throat, stomach, intestine
and liver the NST projects to the hypothalamus,
amygdala, and thalamus where it can stimulate
the peptide neurons reciprocal connections can
regulate emotional and cognitive eating cutting
hypothalmic connections blocks intentional
feeding but does not prevent swallowing
unless the stomach senses fullness meal size and
frequency mediated by combined hormone effects
along with sensory neurons through the
vagus nerve and NST