Nancy Solís

Learn More
Hepatocyte gap junction proteins, connexins (Cxs) 26 and 32, are downregulated during obstructive cholestasis (OC) and lipopolysaccharide hepatocellular cholestasis (LPS-HC). We investigated rat hepatic Cxs during ethynylestradiol hepatocellular cholestasis (EE-HC) and choledochocaval fistula (CCF) and compared them with OC and LPS-HC. Levels(More)
Bile acids or its derivatives may influence non-alcoholic fatty liver disease development through multiple mechanisms. Intestinal L-cells secrete glucagon-like peptide-1 (GLP-1) and can be activated by bile acids (BA) influencing insulin resistance and hepatic steatosis development and progression. The aim of the present study was to assess the effects of(More)
Hepatocyte gap junction proteins, connexins (Cxs) 26 and 32, are down regulated during obstructive cholestasis (OC) and lipopolysaccharide hepatocellular cholestasis (LPS-HC). We investigated rat hepatic Cxs during ethynylestradiol hepatocellular cholestasis (EE-HC) and choledochocaval fistula (CCF) and compared them with OC and LPS-HC. Levels(More)
published 12 times a year (monthly) by the American Physiological Society, 9650 Rockville Pike, Bethesda MD involving normal or abnormal function of the gastrointestinal tract, hepatobiliary system, and pancreas. It is publishes original articles pertaining to all aspects of research AJP-Gastrointestinal and Liver Physiology
  • 1