Journal
CELL METABOLISM
Volume 6, Issue 1, Pages 69-78Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2007.05.005
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Funding
- NCRR NIH HHS [C06-RR018928] Funding Source: Medline
- NIA NIH HHS [AG028716] Funding Source: Medline
- NIDDK NIH HHS [R01 DK065969, R01-DK065599, DK58398, K01-DK60484, R01 DK065599] Funding Source: Medline
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Hepatic steatosis, the accumulation of lipids; in the liver, is widely believed to result in insulin resistance. To test the causal relationship between hepatic steatosis and insulin resistance, we generated mice that overexpress acylCoA:diacylglycerol acyltransferase 2 (DGAT2), which catalyzes the final step of triacylglycerol (TG) biosynthesis, in the liver (Liv-DGAT2 mice). Liv-DGAT2 mice developed hepatic steatosis, with increased amounts of TG, diacylglycerol, ceramides, and unsaturated long-chain fatty acyl-CoAs in the liver. However, they had no abnormalities in plasma glucose and insulin levels, glucose and insulin tolerance, rates of glucose infusion and hepatic glucose production during hyperinsulinemic-euglycemic clamp studies, or activities of insulin-stimulated signaling proteins in the liver. DGAT1 overexpression in the liver also failed to induce glucose or insulin intolerance. Our results indicate that DGAT-mediated lipid accumulation in the liver is insufficient to cause insulin resistance and show that hepatic steatosis can occur independently of insulin resistance.
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