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. 2020 May 7;5(9):e135236. doi: 10.1172/jci.insight.135236

Figure 3. Short-term T2D, but not HFD alone, causes deterioration of bone microarchitecture.

Figure 3

(A) Schematic of the study design depicting male C57BL/6 mice randomized to either LFD (10% kcal from fat) or HFD (60% kcal from fat) for 1 month (lead-in phase) followed by treatment (at baseline) with either VEH or STZ and follow-up for 3 months (experimental phase) out to 7 months of age (endpoint): LFD/VEH, HFD/VEH, HFD/STZ (n = 10/group). (B–C) Quantification of μCT-derived BV/TV (%) assessed ex vivo at the lumbar spine and tibia metaphysis at study endpoint. (D) Percentage change (% Δ) in trabecular BV/TV at the tibia metaphysis assessed by longitudinal in vivo μCT analysis (at baseline and endpoint). Longitudinal percentage changes in (E) cortical volumetric bone mineral density (Ct.vBMD, mg/cm3), (F) cortical thickness (Ct.Th, mm), (G) endocortical circumference (EC, mm), (H) periosteal circumference (PC, mm), and (I) μFEA-derived failure load (N, Newton, an index of bone strength) at the tibia metaphysis. Longitudinal percentage changes in (J) Ct.vBMD (mg/cm3), (K) Ct.Th (mm), (L) EC (mm), (M) PC (mm), and (N) μFEA-derived failure load (N) at the tibia diaphysis. For all analyses, n = 10/group. Data represent mean ± SEM (error bars). ns, P ≥ 0.10; †P < 0.10; *P < 0.05; **P < 0.01; ***P < 0.001 (1-way ANOVA with post hoc Tukey’s correction for multiple comparisons). HFD, high-fat diet; STZ, streptozotocin; T2D, type 2 diabetes; LFD, low-fat diet; VEH, vehicle.