Summary of amylin-related transgenic and knockout models

ModelGenetic Background and MethodReported EffectsReference
Amylin gene deletion129Ola/B6 (coding sequence of exon 3)Lower bone mass/increased osteoclastsGebre-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/Bl6Transient increase in adiposity in femalesTurek et al., 2010
Food intake, body weight unchanged (versus wild type)
Reduced sensitivity to endogenous leptin
Reduced hypothalamic leptin receptor mRNA
Amylin overexpressionFVB/n (pronuclear microinjection of construct into fertilized oocytes)DiabeticWong et al., 2008
Slight decrease in body weight (likely due to glycosuria, consequence of diabetes)
Calcitonin receptor deletionUnclear. Deletion of exons 6 and 7 of calcrHigh bone mass, increased bone formation (normal resorption)Dacquin et al., 2004
C57/Bl6. Cre-LoxP deletion of exons 13 and 14Food intake and body weight not well evaluatedDavey et al., 2008
C57/Bl6. Cre-LoxP deletion of exons 6 and 7Increased bone formationKeller et al., 2014
RAMP2 and RAMP3 knockout modelsRAMP2 deletion is lethal; haploinsufficiency results in defects in bone homeostasisDackor et al., 2007; Kadmiel et al., 2011
RAMP3 knockout models have reduced body weight with normal food intake
Neuronal RAMP1 overexpressionMultiple lines evaluatedDecreased body weight, adiposity and endogenous leptinZhang et al., 2011
Increased energy expenditure and sympathetic tone
Increased BAT, UCP1, and UCP3
Enhanced sensitivity to exogenous amylin