INSR and SHORT syndrome: First, the fact that low liver fat, normal lipid profile, and nearly undetectable hepatic de novo lipogenesis were still seen in P1 despite concomitant genetic suppression of adiponectin argues that the apparent protection from these components of the metabolic syndrome in SHORT syndrome — and probably by extension also in insulin receptor defects — is not accounted for by the preserved or elevated plasma adiponectin seen in these forms of severe insulin resistance.