Figure 3.

Deregulation of TSC22D1 in conditions of metabolic dysfunction. (A) Quantitative PCR analysis of hepatic TSC22D1 expression of db/db or ob/ob mice compared to wild-type control (wt) or mice fed a high-fat diet (HFD) compared to control mice on a low-fat diet (LFD). (B) Western blot of liver extracts from representative mice fed a high-fat diet (HFD) compared to control mice on a low-fat diet (LFD), using TSC22D1 (D1) or actin specific antibodies. (C) Quantitative PCR analysis of TSC22D1 expression in primary hepatocytes stimulated with 10 ng of human recombinant TGFβ1 or PBS for the indicated time (means±SEM, n=3). (D) Quantitative PCR analysis of hepatic TSC22D1 expression in C57Bl/6 mice treated with PBS or 5 µg human recombinant TGFβ1 for the indicated time points (means±SEM, n=4). (E) Quantitative PCR analysis of hepatic TSC22D1 expression in pancreatic cancer patients with or without cachexia (means±SEM, n=5). (F) Quantitative PCR analysis of hepatic TSC22D1 expression in Balb/C mice treated with PBS or 1.5×10⁶ colon 26 (C26) cells over 3 weeks (means±SEM, n=6). (G) Western blot of liver extracts from representative mice as in (e), using TSC22D1 (D1) or actin specific antibodies. (H) Quantitative PCR analysis of hepatic TSC22D1 in mice fed a choline deficient diet (MCD) or a corresponding control diet for 4 weeks (means±SEM, n=5). (I) Quantitative PCR analysis of TSC22D1 expression levels in LDL-receptor knockout (LDLRKO) mice without or with streptozotocin treatment (STZ). (means±SEM, n=5). (J) Correlation of TSC22D1 RNA expression and lesion size in LDL-receptor knockout (LDLRKO) mice without or with streptozotocin treatment (STZ). The surface lesion area was quantified with ImageJ software and is presented in arbitrary units (n=10). Statistical test for (a)–(h): students t-test, ^⁎, p<0.05, ^⁎⁎, p<0.01, ^⁎⁎⁎, p<0.001, for (i) Pearson correlation coefficient, F-test to determine significance.