Heme oxygenase-1 drives metaflammation and insulin resistance in mouse and man

Cell. 2014 Jul 3;158(1):25-40. doi: 10.1016/j.cell.2014.04.043.

Abstract

Obesity and diabetes affect more than half a billion individuals worldwide. Interestingly, the two conditions do not always coincide and the molecular determinants of "healthy" versus "unhealthy" obesity remain ill-defined. Chronic metabolic inflammation (metaflammation) is believed to be pivotal. Here, we tested a hypothesized anti-inflammatory role for heme oxygenase-1 (HO-1) in the development of metabolic disease. Surprisingly, in matched biopsies from "healthy" versus insulin-resistant obese subjects we find HO-1 to be among the strongest positive predictors of metabolic disease in humans. We find that hepatocyte and macrophage conditional HO-1 deletion in mice evokes resistance to diet-induced insulin resistance and inflammation, dramatically reducing secondary disease such as steatosis and liver toxicity. Intriguingly, cellular assays show that HO-1 defines prestimulation thresholds for inflammatory skewing and NF-κB amplification in macrophages and for insulin signaling in hepatocytes. These findings identify HO-1 inhibition as a potential therapeutic strategy for metabolic disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / metabolism
  • Animals
  • Diet, High-Fat
  • Heme Oxygenase-1 / metabolism*
  • Hepatocytes / metabolism
  • Humans
  • Inflammation / metabolism
  • Insulin Resistance*
  • Liver / metabolism
  • Macrophages / metabolism
  • Membrane Proteins / metabolism*
  • Metabolic Diseases / metabolism
  • Metabolic Diseases / physiopathology
  • Mice
  • Mice, Knockout
  • Obesity / complications*
  • Obesity / physiopathology
  • Reactive Oxygen Species / metabolism

Substances

  • Membrane Proteins
  • Reactive Oxygen Species
  • HMOX1 protein, human
  • Heme Oxygenase-1
  • Hmox1 protein, mouse