Thyroid hormone analogues and derivatives: Actions in fatty liver

Figure 1 Hepatic lipid partitioning and liver and systemic metabolic damages in nonalcoholic fatty liver disease (A) and a schematic representation of the anti-steatotic effect of 3,3’,5-triiodo-L-thyronine (B). A: Hepatic lipid partitioning and liver and systemic metabolic damages in nonalcoholic fatty liver disease. Chronic overnutrition/hyperlipidemic feeding causes fat retention in hepatocytes that, in turn, results in alteration of fat uptake, de novo synthesis (lipogenesis) and oxidation with a significant imbalance of lipid homeostasis. This can subsequently induce insulin-resistance, metabolic syndrome and cardiovascular diseases; B: A schematic representation of the anti-steatotic effect of T3: An update. T3-administration associated adverse effects are also highlighted (for details see the text). T3: 3,3’,5-triiodo-L-thyronine; TRs: Thyroid hormone receptor isoforms; FFA: Free fatty acid; TG: Triglyceride; L-FABP: Liver-type fatty acid-binding protein; COX2: Cyclooxygenase 2; JNK: c-Jun N-terminal kinases; STAT3: Signal transducer and activator of transcription 3.