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Feeding 1: Neurobiology

Terms in this set (32)

Motivation to eat:
When food is plentiful:
We get hungry when stomach and upper intestine are empty (approx. 3 meals a day) Triggered by Ghrelin
But also by the sight and smell of food and even social cues

When food is scarce:
Hypoglycemia: low blood sugar
Can be mimicked by an insulin injection
Ghrelin: Circadian rhythm
Ghrelin increases with fasting

Decreases after a meal

Ghrelin antagonists inhibit feeding

Ghrelin increases before a meal suggesting a role in initiating eating

Ghrelin injections increase eating in humans and if given chronically can cause weight gain (inc. food, dec. metabolism)

Ghrelin injections also increase food imagery
Ghrelin in rats
Ghrelin is produced in the stomach and is released 1 - 2 hours before meals

Peripheral injections (systemic) or intracranial injections increase food intake (in animals)
Ghrelin in Humans
Subjects came into the lab early in the morning. They all ate the same breakfast, and then in the afternoon were presented with a free-choice buffet. On the test day with ghrelin administration, all subjects ate more than they had on the test with placebo, and reported greater subjective hunger.
Glucose levels: hypoglycemia
that the brain might starve
Neurons need glucose to function

The glucostatic theory suggests that low glucose levels trigger eating

Large injections of insulin cause hypoglycemia and glucoprivation
Insulin converts and stores glucose and allows non-neural cells to use it

Glucoprivation then stimulates eating
Cholecystokinin (CCK)
Short term control
Cholecystokinin (CCK) is released by the duodenum
It controls bile secretion and monitors the presence of fats

Injections of CCK suppress feeding and thus may act as a satiety signal

However mice with a targeted mutation of the gene producing CCK eat normally and do not become obese
PYY
Short term control
PYY Decreases Feeding:

Cholecystokinin (CCK) is released by the duodenum
It controls bile secretion and monitors the presence of fats

Injections of CCK suppress feeding and thus may act as a satiety signal

However mice with a targeted mutation of the gene producing CCK eat normally and do not become obese

Subjects presented with a buffet

Following peptide YY (PYY) administration, they ate less

PYY is a hormone released by the gut proportional to the amount of calories ingested

Subjects also reported less hunger after PYY

Effects were the same in lean and obese subjects

PYY levels have been shown to correlate with levels of satiety
Adipose Tissue: Leptin
Long term control

Body weight in most people seems to be regulated over the long-term

An animal fed a high or low calorie diet will adapt its intake to stay within a certain weight range
But what is the signal/detector?

Cutting the nerves from fat cells does not affect total body fat ( not a neural signal)

The ob mouse led to the discovery of leptin

Leptin is secreted by well nourished fat cells
More fat in fat cells more leptin signal

Fat cells of ob mice do not produce leptin

Daily injections of leptin rescue ob mice

The discovery of leptin raised exciting prospects for obesity treatments

Unfortunately it has had limited impact

However some very rare cases of human obesity are due to not producing leptin

High levels of leptin desensitize the brain to hunger signals

Low levels of leptin provide a stronger hunger signal than high levels provide one for satiety
Gut to Arcuate Nucleus (NPY, AgRP and POMC/CART Neurons)
Ghrelin stimulates Neuropeptide Y (NPY) and Agouti-Related Peptide (AgRP) release which stimulates feeding

PYY and leptin inhibit these same cells

Leptin (and insulin) also activate POMC/CART neurons which in turn stimulate the release of α-MSH, which inhibits feeding

-MSH receptor mutations might account for up to 5% of severe obesity cases
NPY
Neuropeptide Y (NPY) is an extremely potent feeding stimulator produced from neurons in the arcuate nucleus

Infusion of NPY into the hypothalamus produces ravenous/frantic eating

Rats infused with NPY will work very hard for food even if adulterated by quinine

They will drink milk paired with electric shock to the tongue

NPY secretion is sensitive to hunger/satiety signals, specifically glucoprivation and ghrelin
Hypothalamic Regions Implicated in Feeding
Lateral Hypothalamus (LH) stimulation produces eating and drinking
Lesions lead to adipsia and aphagia

Ventromedial Hypothalamus (VMH) stimulation suppresses eating
Lesions lead to obesity
appetitive mechanisms (External & Internal)
External:
appearance
smell & taste
variety
social factors

Internal:
time since last meal
size of last meal
time of day
physical activity
Mental (head) factors involved in feeding
Head factors refers to sets of receptors located in the eyes, nose, tongue and throat involved in feeding

They provide information about:
Appearance/odor/taste/texture/temperature
Most effects involve learning
Food is more filling swallowed than injected directly into the stomach
Sensory Specific Satiety
The quantity of food eaten by rats in two hours. In Phase I, they were fed four different diets, A, B, C, and D, on four successive days. In Phase II, either variety or no variety was provided on alternate days
Sensory-Specific Satiety: LH Cell Firing Response to Food Stimulus
The lateral hypothalamus (LH) is usually viewed as contributing homeostatic signals related to nutritional stores and energy needs.

However, LH firing seems to also depend on the satiation level of a particular type of food

Diversity promotes food intake
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