Figure 8: Loss-of-function of fly Ck1alpha homologue (CSNK1a1) in mouse adipose tissue progenitors induces hyperglycaemia. | Nature Communications

Figure 8: Loss-of-function of fly Ck1alpha homologue (CSNK1a1) in mouse adipose tissue progenitors induces hyperglycaemia.

From: Drosophila glucome screening identifies Ck1alpha as a regulator of mammalian glucose metabolism

Figure 8

(a) Plots show weights and per cent fat content (NMR spectrometry) of 3.5-month-old control and mutant mice fed standard chow. n=4 each. (b) Fed and fasted glucose was measured in control, and homozygous and heterozygous PPARγ-CSNK1a1 knockouts. n=4 each. (c,d) Fasted plasma triglycerides (c), and insulin levels (d) detected in control and mutant mice. n=3 each. (e) GTT was performed on 3.5-month-old control and mutant mice. n=4 each. (f,g) Blood glucose was measured in 5-week (f) and 10-week-(g) old control and PPARγ-CSNK1a1 mutant mice. n=6 each. Error bars indicate s.e.m.. Statistical significance was assessed by two-tailed Student’s t-test, *P<0.05, **P<0.01. Data shown for male mice; phenotype was less pronounced in females.

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