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Appetite
| Question | Answer |
|---|---|
| Bagnol 1999 | In situ hybridisation of both AgRP and each of mc3r and mc4r separately. First shows colocalisation of POMC and AgRP. Shows that AgRP and POMC cells express mc3r but mc4r is not similarly localised |
| Graham 1997 | Overexpression of Agrp leads to obesity in transgenic mice |
| Huszar 1997 | Mc4r deficiency causes obesity as well as hyperphagia, hyperinsulinaemia and hyperglycaemia without any specific glucose challenge being applied |
| Butler 2000 | Mc3r deficiency causes increased adiposity with no weight gain indicating a role in metabolism rather than hunger. Incr adiposity more noticeable on a high fat diet while the rats also exercised less. Lee 2008 found role in hunger too so may involve both |
| Butler 2001 | Gave mice alternating access to low and high fat diets, weight fluctuations were greater in Mcr4 nulls. Mc4r- mice didnt reduce intake when food was more calorific, incr instead. Also mc4r- didnt incr thermogenesis on higher fat diet so no incr metabolism |
| Balthasar 2005 | selective re-expression of Mc4r, in all cells then in neurons by cre, then in PVH virally and using gene link (sim1). Caused less weight gain and food intake (to obese KOs). PVH re-express decr intake, but still obese due to poor metabolism. |
| Garza 2008 | Knocked down mc4r by viral shRNA, ordinary on normal diet but incr feeding on high fat. Balthasar found incr food intake on all diets but this prob due to the fact they knocked down in the amygdala too or maybe due to different animal housing conditions. |
| Lee 2008 | Selective Mc3r agonist induces hyperphagia centrally or peripherally, antagonist has converse effects. Mc3r thought to be autoinhibitory. Had to lower the antagonist dose due to presumed activity at Mc4rs. Agonists incr POMC and decr AGRP release |
| Lee 2002 | Mc3r human mutation: screened 41 obese children, found father and daughter heterozygotes. Less insulin resistance (contrast to mice) but v small sample. Whole family obese so poor reliability, girl failed with diet + exercise but father had more success. |
| Williams 2003 | Melanocortins given to rats. Used ribonuclease protection to show UCP-1 increase. Denervation prevents this increase although decerebration didnt, so presume action is in the brain stem |
| Nogueiras 2007 | Blockade of Mcrs rats causes 100% increase in adipose synthesis of triglycerides in an ex vivo assay. Incresae in WAT TAG persisted in pair fed groups (not intake). Beta AR KO removed effects on WAT. Treatment decreased UCP-1 and 2 |
| Zhang 1994 | Cloning of the leptin gene. Knew the region of mutation, cloned the whole area haplotypically linked to ob. Cut up using enzymes, screened fragments for possible exons, found 6 and screened these against adipose mRNA. Found to be absent in ob/ob mice. |
| Coleman 1978 | Summary of parabiosis experiments, suggestion of a humoural satiety factor causing death by starvation in normal/obese mice hooked up to a db |
| Rogers 1979 | Suggests that d-fenfluoramine causes a reduction in the speed of eating, cites evidence elsewhere of a reduction in meal-size |
| Garfield 2009 | Review of melanocortin signalling |
| Kelesidis 2010 | Review of leptin as a therapy |
| Marwaha 2012 | Review of links between alzheimers and leptin |
| Saller & Stricker 1976 | Intraventricular 5,7-DHT damaged all 5-HT neurons, NE would be damaged but protected by selective uptake inhibitor. Food intake decr 24-90% in first two days but in the long term incr beyond controls and hyperphagia evident (so long as NE protected). |
| Kennett 1988 | Anorexia caused by 5-HT2CR agonist m-chlorophenylpiperazine (mCPP) blocked by compounds with 5-HT2CR antagonist activity. First indicator of 5-HT2CR in feeding |
| Nonogaki et al 1998 | Back crossed mutant rats to reduce genetic variability surrounding a 5-HT2CR mutation and improve controls. When fed a high fat diet the mutant rats compensated far worse, continuing to eat and showed increased weight gain along with diabetes in old age. |
| Nonogaki 2003 | Mutations in the 5-HT2CR also caused incr activity, enhanced by food deprivation and therefore was not food-induced. This incr activity seems due to incr food seeking, despite activity energy spend was less causing obesity even with exercise |
| Dykens 2003 | Prader-willi associated with increased levels of compulsive behaviour (non-related to food) and SSRIs are beneficial. Also causes obesity |
| Kishore 2006 | SNORD115 deficiency has been shown to promote generation of alternatively spliced 5-HT2CR with reduced functionality. Incr SNORD115 incr exonVb expression, used a primer requiring complexation for detection |
| Heisler et al 2002 | Used Fos levels to measure activation after giving d-fen, found incr levels of fos activation in POMC (mRNA riboprobe) containing, a-MSH (immunoprobe) releasing neurons. MC3/4R agonists reduce impact of 5-HT2CR mutations, d-fen doesnt work if Agrp incr. |
| Heisler et al 2006 | mouse 5-HT1BR=human 5-HT1Dbeta. Agonists at 1BRs decr eating. 5-HT1B riboprobe showed 1/3 of 1BR+ves had AgRP (gene-link to GFP) & 1/6 of GFP+ had 1BR. 5-HT hyperpol POMC & AgRP neurons (electrophys). MC4R KO no response to 5-HT agonists, MC3R KO respond. |
| Tecott 2007 | Review of serotonin transmission |
Created by:
Jonmassie
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