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Transcranial direct current stimulation (tDCS) has beneficial effects on liver lipid accumulation and hepatic inflammatory parameter – Click Here

Regulation of liver regeneration by growth factors and ……

National Center for Biotechnology Information

by F Böhm – ‎2010 – ‎Cited by 74 – ‎Related articles

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Am. J. Physiol. Gastrointest. Liver Physiol.

Am J Physiol Gastrointest Liver Physiol 2016 Mar 3:ajpgi.00056.2016. Epub 2016 Mar 3.

Laurie D DeLeveXiangdong WangLei Wang

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In liver injury, recruitment of bone marrow progenitors of liver sinusoidal endothelial cells (now named sprocs) is necessary for normal liver regeneration. Hepatic VEGF is a central regulator of the recruitment process. Here we examine whether stromal cell derived factor-1 (sdf-1 or CXCL-12) acts downstream from VEGF to mediate recruitment of bone marrow sprocs, what the sdf-1 receptor type (CXCR4 or CXCR7) is on sprocs, and whether sdf-1 signaling is required for normal liver regeneration.

Studies were performed in the rat partial hepatectomy model. Tracking studies of bone marrow sprocs were performed in wild type Lewis rats that had undergone bone marrow transplantation from transgenic EGFP+ Lewis rats. Knockdown studies were performed using anti-sense oligonucleotides.

Expression of sdf-1 doubles in liver and in LSECs after partial hepatectomy. The upregulation of sdf-1 expression increases proliferation of sprocs in the bone marrow, mobilization of CXCR7+ bone marrow sprocs to the circulation, and engraftment of CXCR7+ bone marrow sprocs in the liver, and promotes liver regeneration. Knockdown of hepatic VEGF with anti-sense oligonucleotides decreases hepatic sdf-1 expression and plasma sdf-1 levels. When the effect of VEGF knockdown on sdf-1 is offset by infusion of sdf-1, VEGF knockdown-induced impairment of BM sproc recruitment after partial hepatectomy is completely attenuated and liver regeneration is normalized.

These data demonstrate that the VEGF-sdf-1 pathway regulates recruitment of CXCR7+ bone marrow sprocs to the hepatic sinusoid after partial hepatectomy and is required for normal liver regeneration.


University of Southern California Keck School of Medicine.


Signals and Cells Involved in Regulating Liver Regeneration


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Signals and Cells Involved in Regulating Liver Regeneration

Bone marrow stem cells and liver disease


  1. SDF-1/CXCR4 signaling central to BMSC homing to liver
  2. BMSCs support liver repair through the delivery of growth factors that promote liver regeneration, fibrosis resolution or new blood vessel formation
    • Of specific interest, BMSCs upregulate HGF which may play a role in diminishing fibrosis

Growth inhibition and apoptosis in liver myofibroblasts promoted by hepatocyte growth factor leads to resolution from liver cirrhosis

Effects of transcutaneous electrical stimulation of lower limb … – NCBI

by BM El-Kafoury – ‎2016 – ‎Cited by 1 – ‎Related articles

Apr 5, 2016 – Effects of transcutaneous electrical stimulation of lower limb muscles on experimental fatty liver. El-Kafoury BM(1), Seif AA(2), El-Aziz Abd …

 2016 Mar;17(1):20-8. doi: 10.1016/j.ajg.2016.03.004. Epub 2016 Apr 5.

Effects of transcutaneous electrical stimulation of lower limb muscles on experimental fatty liver.



Although the beneficial effects of exercise on fatty liver have been described, a previous study conducted at our department showed that transcutaneous electrical muscle stimulation (TEMS) of lower abdominal muscles aggravated fatty liver. The present study aims to evaluate the ability of TEMS of the lower limb muscles to improve fatty liver infiltration.


Thirty male Wistar rats were randomly allocated into three groups: control; fructose-fed (F), fed fructose-enriched diet for 6weeks; and fructose-fed with transcutaneous electrical muscle stimulation (F+TEMS), fed fructose-enriched diet for 6weeks and lower limb muscles subjected to TEMS during the last 3weeks of feeding, five sessions/week. Body weight, length, body mass index (BMI), and abdominal and lower limb circumferences were all recorded. Fasting blood glucose, serum insulin, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), total protein, serum albumin, high density lipoprotein cholesterol (HDL-C), triglyceride (TG), and total cholesterol (TC) levels were measured. LDL cholesterol (LDL-C) and the atherogenic index (AI) were calculated. Absolute and relative hepatic weights as well as histological examination of the liver were assessed.


Final body weight, abdominal and lower limb circumferences, absolute liver weight, homoeostasis model assessment (HOMA) score, and TG, LDL-C, AI, serum ALT, and AST levels were all significantly reduced in the (F+TEMS) group compared to the (F) group. There was a significant increase in GPx and HDL-C levels, HDL/LDL ratio, and total protein and serum albumin content in (F+TEMS) rats compared to (F) rats. Histologically, hepatic tissue from (F+TEMS) rats had minimal steatotic changes that were restricted to zone 1 and less marked inflammatory cell infiltration compared to (F) rats.


TEMS was able to reverse steatosis, hyperglycaemia, insulin resistance, dyslipidaemia, and fatty liver caused by fructose feeding. The study confirmed that the variation in the anatomical site of skeletal muscle contraction affects fatty liver in different ways.