Under insulinopenic conditions, the hormone adiponectin is essential for lipid uptake specifically in subcutaneous white adipose tissue, and is sufficient to ameliorate islet lipotoxicity.
Silencing the acyl-coA synthethase ACSL1 protects against saturated fat lipotoxicity by preventing the degradation of polyunsaturated fatty acids, allowing them to be incorporated into phospholipids and improves membrane fluidity.
The activation of beige adipocyte thermogenesis by cold temperatures and β3-adrenergic receptor agonists induce beige adipocyte formation, function and perdurance.
Specific human mitofusin 2 mutations induce selective upper body obesity with suppressed leptin expression and severe adipose mitochondrial dysfunction.
A single mutation in acetyl-CoA carboxylase blocking AMPK regulation inhibits food intake in mice in response to cold exposure or fasting causing them to lose weight.
Genetic inactivation of the transcription factor, Zfp423, in visceral white adipocyte precursors leads to the formation of thermogenic adipocytes in visceral fat depots and improves insulin sensitivity in obese mice.
A large-scale transcription factor screen reveals over twenty novel adipogenic regulators: most notably ZEB1, which exerts essential transcriptional control of fat cell differentiation.
