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. Author manuscript; available in PMC: 2015 Mar 1.
Published in final edited form as: Rev Endocr Metab Disord. 2014 Mar;15(1):21–29. doi: 10.1007/s11154-013-9273-5

Table 1.

Glucose homeostasis and insulin sensitivity phenotypes of PGC-1 gain- and loss-of-function genetic mouse models. See text for details.

Tissue Genetic
Model
PGC-1α PGC-1β PGC-1α/β PRC
Whole body Transgenic Increased Insulin sensitivity; Glucose tolerance [75] n/d n/d n/d
Knock-out Insulin sensitive; lean and hyperactive [22] No apparent phenotype [23] n/d Implantation Lethal [46]
Hypomorphic knockout Insulin sensitive and glucose tolerant (HFD only) [24] No apparent phenotype [25] Perinatal Lethal [77]
Muscle Transgenic Insulin resistant (HFD only) [33]; Increased Insulin sensitivity and glucose tolerant (aged and exercised animals)[34]; glucose tolerant (α4 isoform with cancer cachexia)[40] Not reported[43] Not reported [78] n/d
Knock-out Glucose intolerant (HFD) [41] No apparent phenotype[44] No apparent phenotype [44] and not reported [45] n/d
Liver Transgenic n/d Not reported[57] n/d
Knock-out Insulin resistant (heterozygote) [53] Insulin resistant [56] n/d n/d
Adipose Transgenic n/d n/d n/d n/d
Knock-out Insulin resistance and glucose intolerance (HFD) [61] n/d n/d n/d
Brain Transgenic Not reported[71] n/d n/d n/d
Knock-out No phenotype [69] n/d n/d n/d
Pancreas Transgenic Glucose intolerance [73] n/d n/d n/d
Knock-out n/d n/d n/d n/d