Term
| Hypothalamus - endocrine role |
|
Definition
- Corrects deviations from given set point (measures current value, comparison to correct value, adjustments made through effectors)
- Used in the maintainence of blood osmolarity (ADH release through OVLT and SFO stretch gated neurons), metabolism rate (corticotrophin releasing hormone, thyrotropin releasing hormone), hormone levels (negative feedback from pituitary hormones)
|
|
|
Term
| Hypothalamus - non endocrine |
|
Definition
- Food intake - Lateral hypothalamic area (feeding area) recieves inputs from medial forebrain bundle, ventromedial nucleus (satiety centre) receptors for glucose and fatty acids, arcuate nucleus - receptors for leptin and insuline
- Drink intake - subfornical organ contains osmosensitive neuorons, projects to PVN, SON and POA to stimulate drinking behaviour
- Thermoregulation - anterior/posterior hypothalamic area endogenous temperature sensor - stimulation of thermogenesis (shivering, piloerection, skin vasoconstriction and behaviour) and heat loss (sweating, vasodilation and behaviour) as well as controlled elevation of temperature in fever
- Suprachiasmatic nucleus - sleep wake cycles, direct inputs from ganglion cells
- Mamillary bodies - effect in memory formation and possible in behaviour
|
|
|
Term
| Effect of hypothalamus on ANS |
|
Definition
|
|
Term
| Hypothalamus and response to stress |
|
Definition
- Acute stress reaction - sympathetic nerve activation increase circulating catecholamines
- Prolonged stress - upregulation of of hypothalamic release of CRH, pituitary ACTH and adrenal cortex cortisol
- Hypothalamus receives input from amygdala, brainstem and hippocampus to induce stress response
|
|
|
Term
| Hormonal control of energy metabolism |
|
Definition
- IGF-1 - primary mediator of growth hormone release - growth promoting effects in most cells by binding to IGF1R and triggering AKT signalling (tyrosine kinase)
- IGF-2 - growth promoting hormone during gestation - creation of thecal cells and cellular proliferation furing menstrual cycle
- Insulin - increases cellular intake of glucose, DNA replication and protein synthesis, increased glycogen synthesis, increased lipid synthesis and modification of numerous enzymes
|
|
|
Term
| Crucial neurons in food intake regulation |
|
Definition
- In arcuate nucleus - POMC/CART neurons. Express pro-opiomelanocortin and cocaine- and amphetamine-regulated transcript (CART) - POMC converted into α-MSH which is released onto neurons in PVN expressing MC4R (stimulatory) as well as the DMN, LHA and VMN to decrease food intake (satiety) and increase TRH release (PVN)
- In arcuate nucleus - NPY, AgRP neurons expressing neuropeptide Y and agouti-regulated peptide release onto neurons expressing MC4R in PVN - inhibition. Activation of YR, as well as projecting to DMN, VMN and LHA (contain YR) to stimulate food intake and decrease TRH release (PVN)
|
|
|
Term
| Appetite hormones from adipose tissue |
|
Definition
- Leptin produced by adipose tissue and circulating levels mirror body adipose mass. Acts on tyrosine kinase receptor RbR - expressed on POMC/CART neurons (stimulates to decrease food intake) and NPY/AgRP neurons (inhibits)
- In VMN, SF-1 neurons express leptin receptors to decrease food intake
|
|
|
Term
| Appetite hormones from pancreas |
|
Definition
- Insulin - circulating levels are proportional to body adipose mass
- Similar action to leptin - stimulation of POMC/CART neurons and inhibition of NPY/AgRP neurons
- Pancreatic polypeptide - released from pancreatic PP cells (proportional to calorific intake) and binds to Y4 receptors (GPCR) in NTS of brainstem and Arc, PVN of hypothalamus to reduce food intake
|
|
|
Term
| Appetite hormones from GI tract |
|
Definition
- Ghrelin - only GI messenger that increases food intake. Rises before meal and decreases on feeding. Receptor on NPY/AgRP neurons in arcuate to stimulate NPY/AgRP neurons and therefore inhibit POMC/CART neurons (through GABAergic connections)
- Peptide tyrosin tyrosin (PYY) - produced in ileum in response to food intake (mainly fat), binds to Y receptors in arcuate nucleus and brainstem to decrease food intake
- Cholecystokinin - increases after meal and action to elicit satiety through vagal inputs
|
|
|
Term
| Nutrients implicated in appetite |
|
Definition
- Glucose - metabolism of glucose to produce ATP, which closes KATP and depolarises cells, or through AMPK activation when AMP/ATP increases
- Glucose excited cells - require KTPATP inhibition so cell firing initiates satiety response, while glucose inhibited cells stop firing action potential when glucose rises (through inhibiton of AMPK?)
- Glucose sensing in Arc, as well as LHA, VMN and NTS
- Free fatty acids - diffuse across BBB and into cells - converted into acyl-CoA to modulate conductance of ion channels (chloride, potassium, calcium etc.)
- Amino acids - essential AAs reflect food intake, e.g. leucine selectively activated mTOR
- mTOR stimulation reduces food intake, also implicated in leptin and insulin pathway, while inhibited directly by ghrelin, and indirectly on low glucose and ghrelin activity on AMPK
|
|
|
Term
| Other areas involved in appetite regulation |
|
Definition
- Solitary nucleus - leptin receptors (decrease food intake), ghrelin receptors (increase intake), PYY3-36 receptors (decrease food intake), glucose sensing neurons (decrease food intake), gastic distention detected through vagal nerve (decrease intake) and reciprocal projections to ArcN
|
|
|
