Selective depletion of hepatic Kupffer cells significantly alleviated hepatosteatosis and intrahepatic inflammation induced by high fat diet

Hepatogastroenterology. 2012 Jun;59(116):1208-12. doi: 10.5754/hge11903.

Abstract

Background/aims: To address the impact of Kupffer cell ablation via intraperitoneal injection of gadolinium chloride (GdCl3) on hepatosteatosis, intrahepatic inflammation and other metabolic derangements induced by high-fat diet (HFD).

Methodology: C57/BCL male mice were fed with either standard normal diet or HFD. Meanwhile, mice received an intraperitoneal injection of either natural saline (5mL/kg) or 0.2% GdCl3 solution (10mg/kg) twice a week. After 8 weeks, intraperitoneal glucose tolerance test (IPGTT) was performed. F4/80 expression was quantified by immunohistochemistry, immunofluorescence and quantitative (q) RT-PCR. Adipokines in liver were detected via qRT-PCR.

Results: HFD led to clear Kupffer cell infiltration and migration into areas surrounding the hepatic central vein. Both F4/80 expression and F4/80-positive cells in the liver were significantly reduced after GdCl3 administration (both p<0.01). Liver triglyceride and cholesterol deposition decreased dramatically after GdCl3 administration (p<0.01, p<0.05, respectively). TNF-a and IL-6 expression in mouse liver decreased significantly after Kupffer cell depletion (both p<0.01). Daily diet amount, weight and the area under IPGTT curve of the mice fed with HFD were clearly decreased after Kupffer cell depletion, though not statistically significant (all p>0.05).

Conclusions: Selective depletion of hepatic Kupffer cells significantly alleviated hepatosteatosis and intrahepatic inflammation induced by HFD.

MeSH terms

  • Animals
  • Antigens, Differentiation / analysis
  • Blood Glucose / analysis
  • Diet, High-Fat
  • Fatty Liver / prevention & control*
  • Gadolinium / toxicity
  • Inflammation / prevention & control*
  • Insulin Resistance
  • Interleukin-6 / genetics
  • Kupffer Cells / physiology*
  • Liver / metabolism
  • Liver / pathology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Antigens, Differentiation
  • Blood Glucose
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • monocyte-macrophage differentiation antigen
  • Gadolinium
  • gadolinium chloride