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. 2021 Mar 5;24(4):102265. doi: 10.1016/j.isci.2021.102265

Figure 1.

Figure 1

Progressively impaired glucose homeostasis and islet dysfunction of HFD mice both in vivo and in vitro

(A) Schematic of the experimental design.

(B–D) Weekly monitored body weight (N ≥ 16 mice/group) (B), morning ad libitum blood glucose (N ≥ 14 mice/group) (C), and caloric intake (N ≥ 4 cages/group) (D).

(E and F) Blood glucose (E) and the corresponding plasma insulin concentration (F) during IPGTT (2 g/kg glucose) (N ≥ 6 mice/group). The ratios of AUC for HFD versus CD are presented at the top of each graph.

(G and H) AUC calculation for glucose (G) and insulin (H) during IPGTT.

(I) First-phase insulin secretion defect in HFD mice indicated by fold change of insulin level at 5 min with respect to 0 min.

(J–L) Insulin (J), glucagon (K), and somatostatin (L) secretion in islets isolated from HFD and CD mice after 4, 12, and 24 weeks of diet (N = 4–5 mice/group).

All data are expressed as mean ± standard error of mean (SEM) and analyzed using unpaired two-tailed t test. ∗p < 0.05, ∗∗p < 0.01. See also Figure S1.