. Author manuscript; available in PMC: 2007 Oct 15.

Published in final edited form as: Biochim Biophys Acta. 2007 Mar 27;1771(8):999–1013. doi: 10.1016/j.bbalip.2007.03.006

Table 3.

A comparison of PPARγ knockout models specific to other tissues.

Targeted tissue (Cre promoter)	Main phenotypic characteristics
Vasculature, endothelial cells (Tie2)[103]	Normal plasma profile Blood pressure normal on chow, increased on high-fat diet Hypertension unresponsive to rosiglitazone on high-fat diet
Heart, cardiomyocytes (αMHC)[105]	Normal body weight and plasma glucose Cardiac hypertrophy but normal (or slightly improved) systolic function
Kidney, collecting ducts (Aq2)[106,107]	Protection from thiazolidinedione-induced edema
Lung, conducting airway epithelium (CC10)[109]	Impaired lung maturation (non-progressive condition)
Mammary epithelium (WAP, MMTV)[112]	Normal mammary function No differences in tumorigenesis
B- and T-cells, and ovaries (MMTV)[112]	Normal B- and T-cell production Partial to complete infertility (due to impaired implantation?)
Intestine (Villin)[117] (on ApcMin/+ background)	Normal body weight Enhanced intestinal tumorigenesis (some gender differences)
Colon, epidermal cells (Villin)[119]	Sensitization to experimental inflammatory bowel disease with similar relative protection by rosiglitazone
Epidermis (K14)[123]	Normal skin function

αMHC, alpha myosin heavy chain; Aq2, aquaporin 2; WAP, whey acidic protein; MMTV, mouse mammary tumor virus; Apc, adenomatosis polyposis coli; K14, keratin 14.