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. 2018 Nov 9;7:e38472. doi: 10.7554/eLife.38472

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© 2018, Riahi et al

This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

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Figure 10. — (a–b) IPGTT at P30-35: glucose (1 g/kg) was injected IP after an overnight fast; (a) heterozygous Tsc1 knockout Akita mice (RIP-Cre:Tsc1^flox/+:Akita (Akita, βTsc1^+/-) and matched controls: Tsc1^flox/+ mice (Tsc1^+/+), RIP-Cre:Tsc1^flox/+ mice (βTsc1^+/-), and Tsc1^flox/+:Akita (Akita) (n = 3–5 mice in each group); (b) homozygous Tsc1 knockout Akita mice (RIP-Cre:Tsc1^flox/flox:Akita (Akita, βTsc1^-/-) and matched controls: Tsc1^flox/flox mice (Tsc^+/+), RIP-Cre:Tsc1^flox/flox mice (βTsc1^-/-), and Tsc1^flox/flox:Akita (Akita) (n = 3–5 in each group); (c–d) pancreatic insulin content of heterozygous and homozygous Tsc1 knockout Akita mice and matched controls at P30-35 (WT (n = 7), Akita (n = 11), Akita, βTsc1^+/- (n = 3) and Akita, βTsc1^-/- (n = 4); (e) islet insulin content. (f–g) Effects of mTORC1 activation in neonate Akita β-cells on insulin secretion in vivo and ex vivo. (f) insulin secretion in response to IP glucose injection (n = 6 mice in each group); (g) islets were isolated from Tsc1^flox/+ WT mice (WT), Tsc1^flox/+:Akita (Akita) and RIP-Cre:Tsc1^flox/+:Akita (Akita, βTsc1^+/-) mice and insulin secretion assessed following static incubations at basal (3.3 mmol/l) and stimulated (16.7) mmol/l glucose. (h) a model of the pathophysiology of permanent neonatal diabetes. *p<0.05 **, p<0.01, ***, p<0.001****, p<0.0001.

Figure 10—figure supplement 1. — (a–b) IPGTT at P30-35: glucose (1 g/kg) was injected IP after an overnight fast; (a) heterozygous Tsc1 knockout Akita mice (RIP-Cre:Tsc1^flox/+:Akita (Akita, βTsc1^+/-) and matched controls: Tsc1^flox/+ mice (Tsc1^+/+), RIP-Cre:Tsc1^flox/+ mice (βTsc1^+/-), and Tsc1^flox/+:Akita (Akita) (n = 3–5 mice in each group); (b) homozygous Tsc1 knockout Akita mice (RIP-Cre:Tsc1^flox/flox:Akita (Akita, βTsc1^-/-) and matched controls: Tsc1^flox/flox mice (Tsc^+/+), RIP-Cre:Tsc1^flox/flox mice (βTsc1^-/-), and Tsc1^flox/flox:Akita (Akita) (n = 3–5 in each group); (c–d) pancreatic insulin content of heterozygous and homozygous Tsc1 knockout Akita mice and matched controls at P30-35 (WT (n = 7), Akita (n = 11), Akita, βTsc1^+/- (n = 3) and Akita, βTsc1^-/- (n = 4); (e) islet insulin content. (f–g) Effects of mTORC1 activation in neonate Akita β-cells on insulin secretion in vivo and ex vivo. (f) insulin secretion in response to IP glucose injection (n = 6 mice in each group); (g) islets were isolated from Tsc1^flox/+ WT mice (WT), Tsc1^flox/+:Akita (Akita) and RIP-Cre:Tsc1^flox/+:Akita (Akita, βTsc1^+/-) mice and insulin secretion assessed following static incubations at basal (3.3 mmol/l) and stimulated (16.7) mmol/l glucose. (h) a model of the pathophysiology of permanent neonatal diabetes. *p<0.05 **, p<0.01, ***, p<0.001****, p<0.0001.