In type 2 diabetics, insulin fails to suppress blood sugar production by the liver while paradoxically allowing the production of hepatic triglycerides.
This combination results in multiple health risks, including high blood sugar and fatty liver disease.
For years, to gain insight into this phenomenon, researchers focused on the role of altered insulin action in the liver in the production of triglycerides.
Yale University researchers tested a theory that triglycerides formed in the liver were more dependent on the delivery of fatty acids to the liver than on insulin action.
They found that in all of the animals tested increased triglyceride production was primarily dependent on fatty acid delivery and not on insulin action in the liver.
The findings also explain the long-standing paradox of why insulin therapy does not exacerbate, but instead reduces, fatty liver disease in patients with type 2 diabetes.
Shulman and his team plan to apply similar methodology to translate their findings to insulin-resistant patients with type 2 diabetes, hyperlipidemia, and fatty liver disease.
The study was published in the journal PNAS.
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