Fig. 3: Adipocyte CI deficiency limits adipose expansion and impairs systemic glucose homeostasis.
From: Adipocyte NADH dehydrogenase reverses circadian and diet-induced metabolic syndrome

a, Body weight of control (Ndufs2loxP/loxP) and Ndufs2 KO (Adipoq-cre; Ndufs2loxP/loxP) mice at 4 months of age on a chow diet (n = 7 control and n = 5 Ndufs2 KO). b, Tissue weights of control and Ndufs2 KO mice at 4 months of age (n = 7 control and n = 5 Ndufs2 KO). c, Representative images of H&E staining of gWAT and liver at 4 months of age (×10 magnification). d, Oral GTT and insulin during the GTT at 4 months of age (n = 7 control and n = 5 Ndufs2 KO). e, Serum non-esterified fatty acid (NEFA) in control and Ndufs2 KO mice at 4 months of age (n = 7 control and n = 5 Ndufs2 KO). f, KEGG pathway analysis of downregulated (top) and upregulated (bottom) genes in Ndufs2 KO versus control adipocytes (n = 4). g, RNA-seq was performed on fractionated adipocytes from the gWAT of control (Ndufs2loxP/loxP), Ndufs2 KO (Adipoq-cre;Ndufs2loxP/loxP) and Bmal1 KO (Adipoq-cre; Bmal1loxP/loxP) mice. Pathway analysis of Gene Ontology biological process terms with highlighted genes among differentially expressed genes in Ndufs2 KO versus control and Bmal1 KO versus control fractionated adipocytes. h, Motif analysis of downregulated genes in Ndufs2 KO versus control and Bmal1 KO versus control fractionated adipocytes. Data are presented as the mean ± s.e.m. a,e, Statistical significance was calculated using an unpaired two-sided t-test. b,d, A two-way ANOVA followed by multiple comparisons test was used. h, A two-sided hypergeometric test with Benjamini–Hochberg correction for multiple testing was used. *P < 0.05, **P < 0.01, ***P < 0.001. Panel g includes elements created in BioRender; M, B. https://BioRender.com/s27y548 (2025).