L3.1 - control of food intake (III)

a mutation in the leptin gene or a mutated downstream gene can lead to leptin deficiency and resistance

a high fat diet in pregnancy can lead to inflammation in the child hypothalamus making it less responsive to leptin

insulin, GLP-1 and leptin inhibit AMPK signalling that there is enough ATP in the body reducing food intake

the hypothalamus contains a region called the arcuate nucleus which contains orexigenic neurons that promote food intake (NPY-AgRP neurons) and anorexigenic neurons that inhibit food intake (POMC/CART neurons). AgRP neurons act on the ventromedial nucleus in the hypothalamus inhibiting it which stops it from suppressing food intake. NPY neurons stimulate the lateral hypothalamus which promotes food intake. both of these pathways promote hunger. POMC neurons act on the ventromedial nucleus stimulating it which suppresses food intake and the CART neurons send inhibitory signals to the lateral hypothalamus inhibiting food intake. both of these pathways promote satiety. the paraventricular nucleus integrates signals from other hypothalamic nuclei and modulates the release of hormones that influence appetite.

Ghrelin: - ghrelin is produced by the stomach when the stomach is empty. - ghrelin acts on the arcuate nucleus to activate NPY and AgRP to increase food intake. - ghrelin activates AMPK to raise energy levels in the body. - ghrelin acts on the PVN to reduce energy expenditure. Leptin: - leptin is released by adipose tissue. - high leptin levels activate POMC/CART neurons and inhibit AgRP and NPY production and decreasing food intake. - leptin inhibits AMPK. insulin: - insulin is released after meals by the pancreas when blood glucose is high and suppresses food intake by inhibiting NPY/AgRP and activating POMC/CART reducing apetite

• CCK, PYY and GLP-1 inhibit AgRP/NPY suppressing food intake
• GLP-1 enhances insulin secretion and promotes satiety
• the vagus nerve transmits signals from the gut to the brainstem and hypothalamus

• when food tastes bad, this generates satiety signals in the hypothalamus.
• when food tastes good this activates the reward system and dopamine and endogenous opiates are released.
• the reward system(dopamine and endogenous opiates)blocks the effects of CCK, GLP-1 and Leptin so food intake doesn't stop