Figure 2: TBP-2 deficiency ameliorates insulin resistance and increase Akt signalling.
From: Disruption of TBP-2 ameliorates insulin sensitivity and secretion without affecting obesity
(a–f) Fat and muscle content. Body weight (a), total fat (b), internal fat (c), hypodermic fat (d), fat rate (e), muscle (f) in male WT (WT), TBP-2−/− (KO), ob/ob (ob/ob) and ob/ob·TBP-2−/− (ob/ko) mice calculated from computed tomography scan data are shown for 15 weeks aged mice, N≥4. (g, h) Serum physiological parameters. Free fatty acid (g) and MCP-1 (h) were measured in 15 weeks aged mice, N≥7. (i) Blood adiponectin concentration was measured in 6, 10 and 15 weeks aged mice, n=≥5. (j) Distribution of adipocyte size in white adipose from 10 weeks aged WT (black closed rectangle), TBP-2−/− (blue open rectangle), ob/ob (green closed circle) and ob/ob·TBP-2−/− (red open circle) mice (left panel). The right panel shows histological analyses of haematoxylin and eosin (HE)-stained white adipose sections in these mice. Scale bar indicates 100 μm. (k–m) Immuno blotting (IB) analyses of ser473-phospholylated Akt (pAkt), ser256-phospholylated FoxO1 (pFoxO1) and total Akt in response to insulin (2 U kg−1) in skeletal muscle (k), heart (l) and liver (m). Densitometric quantification of pAkt/Akt ratios in skeletal muscle (n), heart (o) and liver (p). Open and closed bar represents without or with insulin stimulation, respectively. (q) Loss of endogenous TBP-2 mRNA in MEFs. (r) IB analyses. TBP-2 deficiency enhances insulin/Akt signalling in primary MEFs. MEFs were serum starved for 12 h and then stimulated with insulin (100 nM) for different times. Data are presented as mean±s.d. *P< 0.05, **P< 0.01, versus control (t-test).
