Sentence examples for livers when challenged from inspiring English sources

Although mTORC1 has been implicated in de novo lipogenesis in cells [10], the lack of TG accumulation in the Tsc1-null livers when challenged with HFD suggests that mTORC1 is not the primary 'driver' of steatosis in vivo.

To our surprise, liver-specific Tsc1−/− mice not only failed to show evidence of steatosis, but also were resistant to triglyceride accumulation in the liver when challenged with a high-fat diet.

These in vitro findings are concordant with in vivo observations that adiponectin-null mice developed exaggerated liver fibrosis when challenged with thioacetamide [ 54, 55].

While other factors such as TG export may influence hepatic lipid accumulation, we did not find a significant difference in the expression of hepatic microsomal triglyceride transfer protein (Mttp) between the groups although ApoB expression in the wild-type livers was significantly reduced when challenged with the HFD, a response not seen in the Tsc1−/− mice (Figure 9B).

In these animals, histological liver damage was less evident than in control mice when challenged with ConA.

When challenged with a high-fat diet, liver-specific Sirt1 knockout (KO) mice develop hepatic steatosis, hepatic inflammation, and endoplasmic reticulum stress [ 5].

When challenged, he vanished.

When challenged with an intraperitoneal (i.p).

PD-L1-deficient mice accumulate CD8+ T cells in the liver that could cause enhanced autoimmune hepatitis when experimentally challenged, but did not develop spontaneous liver disease [ 27].

Accept when challenges come your way.

When we challenged FHL2-deficient mice with CCl4, we observed that FHL2-deficient mice displayed aggravated liver fibrosis compared to wt mice as indicated by morphometric analysis of Sirius Red-stained histological slides and direct measurement of hepatic hydroxyproline content in liver protein extracts that is indicative for deposited collagen.