Summary of amylin-related transgenic and knockout models
| Model | Genetic Background and Method | Reported Effects | Reference |
|---|---|---|---|
| Amylin gene deletion | 129Ola/B6 (coding sequence of exon 3) | Lower bone mass/increased osteoclasts | Gebre-Medhin et al., 1998a,b |
| Some reduced nociception | |||
| Increased insulin secretion/more rapid glucose elimination | |||
| Transient weight gain | |||
| Reduced sensitivity to anorexigenic effects of CCK | |||
| Above mice backcrossed onto C57/Bl6 | Transient increase in adiposity in females | Turek et al., 2010 | |
| Food intake, body weight unchanged (versus wild type) | |||
| Reduced sensitivity to endogenous leptin | |||
| Reduced hypothalamic leptin receptor mRNA | |||
| Amylin overexpression | FVB/n (pronuclear microinjection of construct into fertilized oocytes) | Diabetic | Wong et al., 2008 |
| Slight decrease in body weight (likely due to glycosuria, consequence of diabetes) | |||
| Calcitonin receptor deletion | Unclear. Deletion of exons 6 and 7 of calcr | High bone mass, increased bone formation (normal resorption) | Dacquin et al., 2004 |
| C57/Bl6. Cre-LoxP deletion of exons 13 and 14 | Food intake and body weight not well evaluated | Davey et al., 2008 | |
| C57/Bl6. Cre-LoxP deletion of exons 6 and 7 | Increased bone formation | Keller et al., 2014 | |
| RAMP2 and RAMP3 knockout models | RAMP2 deletion is lethal; haploinsufficiency results in defects in bone homeostasis | Dackor et al., 2007; Kadmiel et al., 2011 | |
| RAMP3 knockout models have reduced body weight with normal food intake | |||
| Neuronal RAMP1 overexpression | Multiple lines evaluated | Decreased body weight, adiposity and endogenous leptin | Zhang et al., 2011 |
| Increased energy expenditure and sympathetic tone | |||
| Increased BAT, UCP1, and UCP3 | |||
| Enhanced sensitivity to exogenous amylin |