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Obesity plays a crucial role in the development of non-alcoholic fatty liver disease (NAFLD). However, the
underlying mechanism for the pathogenesis of obesity-driven NAFLD remains largely obscure. Although the
芒??multiple hit芒?聺 theory provides a more accurate explanation of NAFLD pathogenesis, it still cannot fully explain
precisely how obesity causes NAFLD. The liver is the key integrator of the body芒??s energy needs, receiving input
from multiple metabolically active organs. Thus, recent studies have advocated the 芒??multiple crosstalk芒?聺 hypothesis,
highlighting that obesity-related hepatic steatosis may be the result of dysregulated 芒??crosstalk芒?聺 among multiple
extra-hepatic organs and the liver in obesity. A wide variety of circulating endocrine hormones work together
to orchestrate this 芒??crosstalk芒?聺. Of note, with deepening understanding of the endocrine system, the perception of
hormones has gradually risen from the narrow sense (i.e. traditional hormones) to the broad sense of hormones as
organokines and exosomes. In this review, we focus on the perspective of classic endocrine hormones (traditional
hormones), organic endocrine hormones (organokines), and molecular endocrine hormones (exosomes),
summarizing systematically how the three types of hormones mediate the dialogue between extra-hepatic organs
and liver in the pathogenesis of obesity-related NAFLD.
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