Abstract
Thyroid hormones control lipid metabolism by exhibiting specific effects on the liver and adipose tissue in a coordinated manner. Different diseases of the thyroid gland can result in hypothyroidism. Hypothyroidism is frequently associated with dyslipidemia. Hypothyroidism-associated dyslipidemia subsequently results in intrahepatic accumulation of fat, leading to nonalcoholic fatty liver disease (NAFLD), which leads to the development of hepatic insulin resistance. The prevalence of NAFLD in the western world is increasing, and evidence of its association with hypothyroidism is accumulating. Since hypothyroidism has been identified as a modifiable risk factor of NAFLD and recent data provides evidence that selective thyroid hormone receptor β (THR-β) agonists are effective in the treatment of dyslipidemia and NAFLD, interest in potential therapeutic options for NAFLD targeting these receptors is growing. In this review, we summarize current knowledge regarding clinical and molecular data exploring the association of hypothyroidism, dyslipidemia and NAFLD.
Highlights
Nonalcoholic fatty liver disease (NAFLD) is the most important chronic liver disease in the western world, affecting almost 30% of the general population
We summarize current knowledge regarding clinical and molecular data exploring the association of hypothyroidism, dyslipidemia and NAFLD
Hypothyroidism was independently associated with nonalcoholic steatohepatitis (NASH)
Summary
Nonalcoholic fatty liver disease (NAFLD) is the most important chronic liver disease in the western world, affecting almost 30% of the general population. The prevalence of NAFLD can be higher in type 2 diabetic patients and obese patients, affecting up to 90% of people with a body mass index higher than 40 kg/m2. NAFLD is the most rapidly increasing cause of hepatic cirrhosis requiring hepatic transplantation in the future. The pathophysiology of NAFLD is complex and involves multiple hits, but the principal contributing factor to its development is hepatic lipid accumulation, which leads to hepatic insulin resistance [1]. All lipids are not equivalent in terms of their association with the development of insulin resistance. Triglycerides are usually considered inert, whereas diacylglycerols and ceramides can alter insulin signaling [2]
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