Interestingly, both Lcn2Hep-/- and global Lcn2 knockout (Lcn2-/-)

Interestingly, both Lcn2Hep-/- and global Lcn2 knockout (Lcn2-/-) mice demonstrated comparable increases in susceptibility to infection MK-1775 with K. pneumoniae or E. coli. These mice also had increased enteric bacterial translocation from the

gut to the mesenteric lymph nodes and exhibited reduced liver regeneration after PHx. Treatment with IL-6 stimulated hepatocytes to produce LCN2 in vitro and in vivo. Hepatocyte-specific ablation of the IL-6 receptor or Stat3, a major downstream effector of IL-6, markedly abrogated LCN2 elevation in vivo. Furthermore, chromatin immunoprecipitation (ChIP) assay revealed that STAT3 was recruited to the promoter region of the Lcn2 Lumacaftor gene upon STAT3 activation by IL-6. In conclusion, hepatocytes are the major cell type responsible for LCN2 production after bacterial infection or PHx, and this response is dependent on IL-6 activation of the STAT3 signaling pathway. Thus, hepatocyte-derived LCN2 plays an important

role in inhibiting bacterial infection and promoting liver regeneration. (Hepatology 2014;) “
“I read with great interest the article by Guerrero et al.,1 who used a large population-based study and several spectroscopic and imaging methodologies to assess the contribution of body fat distribution to the differing rates of hepatic steatosis in the three major US ethnic groups (African American, Hispanic, and Caucasian). They suggested that the differing rates of hepatic steatosis among the

three ethnic groups are associated with similar differences in visceral adiposity. enough Interestingly, in comparison with either Hispanics or Caucasians, African Americans appear to be more resistant to the hypertriglyceridemia associated with insulin resistance despite their lower levels of intraperitoneal and liver fat.1 Here I propose hypovitaminosis D as a potential underlying mechanism for the high prevalence of insulin resistance in African Americans on the basis of the following findings. First, numerous studies have demonstrated that vitamin D insufficiency and hypovitaminosis D are more prevalent among African Americans than other Americans.2-6 This is primarily due to the fact that pigmentation reduces vitamin D production in the skin.2 A cross-sectional analysis of serum 25-hydroxyvitamin D levels showed that hypovitaminosis D was present in a substantial proportion of the studied African American population, even in the South and among those meeting recommended dietary guidelines.5 Moreover, no significant difference was found in the proportion of vitamin D insufficiency between obese and nonobese preadolescent African American children.6 Second, previous studies have established that vitamin D insufficiency and hypovitaminosis D are associated with insulin resistance.

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