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Weight loss itself was suggested to significantly contribute to blood pressure, lipid levels, and liver function changes
These have argued for insulin-independent lipid synthesis [61, 62], or hepatic / adipose selective sensitivity to insulin [63, 64], or extrahepatic insulin effects (hypothalamic, adipose, pancreatic alpha-cell) [65], or selective / differential activity of Akt in phosphorylating its downstream substrates [66], or hepatic zone specificity of carbo-lipid metabolism [67]
This longevity of research interest is itself informative: compounds that fail to replicate across independent laboratories typically disappear from the literature within a decade
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