PTG gene deletion causes impaired glycogen synthesis and developmental insulin resistance
J. Clin. Invest. Sean M. Crosson, et al. 111:1423 doi:10.1172/JCI17975 [Go to this article.]

Figure 5
PTG+/– mice display glucose intolerance, moderate hyperinsulinemia, and insulin resistance with aging. (a) Fasting PTG+/– mice display the development of glucose intolerance with aging. Male animals fasted for 16 hours overnight were used for glucose tolerance experiments (n = 4–12 per group). Results are reported as mean ± SEM. (*P ≤ 0.05; **P ≤ 0.005; ***P ≤ 0.0002). Age of animals is shown at upper right of each graph. (b) Serum insulin levels of PTG+/– mice are elevated in the fasting state and in response to a glucose bolus during the intraperitoneal glucose tolerance test. Insulin levels were measured from additional sera collected at the time of the intraperitoneal glucose tolerance tests (n = 4–12 group). Results are reported as mean ± SEM (*P ≤ 0.05; **P ≤ 0.02; ***P ≤ 0.005). (c) Nonfasting PTG+/– mice display moderate insulin resistance at 12 months of age. Male animals in the nonfasting state were used for insulin tolerance experiments (n = 4–12 per group). Results are reported as mean ± SEM (*P ≤ 0.002; **P ≤ 0.001; ***P ≤ 0.0005).