Fig 1: Neutrophil elastase deficiency improves HFD-induced glucose intolerance and insulin resistance in male, but not female mice.a–d Body weight of male and female neutrophil elastase deficient (Elane−/−; purple circle for male, blue triangle for female) mice or wild-type (WT; green circle for male, ivory triangle for female) littermates fed a high-fat diet for 8 weeks. Corresponding weight gains are depicted. e–h Blood glucose levels during an IPGTT in mice with the indicated genotypes and sex. Corresponding areas under the curve (AUCs) are depicted. i–n Plasma insulin levels during 0 min and 15 min time points of IPGTT in mice with the indicated genotypes and sex. Corresponding changes in plasma insulin post-glucose are depicted. HOMA-IR measure of insulin sensitivity are depicted. o–r Blood glucose levels during insulin tolerance test (ITT) in mice with the indicated genotypes and sex. Glucose decay rate during the ITT (kITTs) are depicted. Data are presented as mean (dashed line) -/+ SD (dotted line). Male WT n = 7, male Elane−/− n = 7, female WT n = 5, female Elane−/− n = 9. Data analysed by RM two-way ANOVA with Sidak post-hoc tests (a, c, e, g, i, l, o, q), or two-tailed unpaired t-tests (b, d, f, h, j, k, m, n, p, r). *P < 0.05, **P < 0.01.
Fig 2: HFD-fed male Elane−/− mice display reduced glucocorticoid action in visceral adipose tissue.a–d, Serum glucocorticoid parameters in male Elane−/− (purple circle) and WT (green circle) mice after 8 weeks of HFD, including total corticosterone (a), free corticosterone (b), percent free corticosterone (c), and CBG binding capacity (d). e Tissue weights as % body weight for the indicated genotypes. f, Serum triglyceride levels (WT n = 7, Elane−/− n = 5). g Representative H& E images of gonadal adipose (gWAT), scale bar = 100 µm. h quantification of adipocyte size for the indicated genotypes. i, j gWAT corticosterone levels and transcript expression for the indicated genotypes. k, l Representative H&E images of liver (scale bar = 100 µm) and quantification of lipid accumulation for the indicated genotypes. m, n Liver corticosterone levels and transcript expression for the indicated genotypes. Data are presented as mean (dashed line) -/+ SD (dotted line). Male WT n = 7, male Elane−/− n = 7 unless otherwise stated. Data analysed by two-tailed unpaired t-tests. *P < 0.05, **P < 0.01, ***P < 0.001.
Fig 3: The improved metabolic phenotype of male Elane−/− mice is adrenal-dependent.a, b Body weight of male neutrophil elastase deficient (Elane−/−; purple symbols) mice or wild-type (WT; green symbols) littermates who underwent bilateral adrenalectomy (ADX; white-filled symbols) or sham-surgery (Sham; colour-filled symbols) prior to 8-week HFD. Corresponding weight gains are depicted. c, d Blood glucose levels during an IPGTT in mice with the indicated genotypes and surgery. Corresponding areas under the curve (AUCs) are depicted. e Plasma insulin levels during 0 min and 15 min time points of IPGTT in mice with the indicated genotypes and surgery. f HOMA-IR measure of insulin sensitivity with the indicated genotypes and surgery. Data are presented as mean (dashed line) -/+ SD (dotted line). WT: Sham n = 7, Elane−/−: Sham n = 7, WT: ADX n = 7, Elane−/−: ADX n = 6. Data analysed by RM two-way ANOVA (a, c, e) or two-way ANOVA with Sidak’s post-hoc tests (b, d, f). ANOVA results are indicated beside graphs. *P < 0.05, **P < 0.01, ***P < 0.001. ns = not significant.
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