2.12. Mitochondria and lipodystrophy: Proceedings of the annual meeting of the European Consortium of Lipodystrophies (ECLip)

Mitochondria play central roles in cellular energy production through oxidative phosphorylation, calcium homeostasis, regulation of apoptosis, and the control of glucose and lipid metabolism. Lipodystrophies belong to a group of disorders characterized by abnormal fat distribution and alterations of mitochondrial function. An early link between mitochondria and lipodystrophies refers to the putative effects of “highly active antiretroviral therapy” (HAART), a combination of potent antiretroviral drugs such as viral protease inhibitors or nucleoside-analogue reverse-transcriptase inhibitors that has been associated with lipodystrophy by altering mitochondrial DNA and mitochondria function.
We will thus discuss how mitochondrial dysfunction could be linked to lipodystrophies by affecting/altering adipogenesis, oxidative stress, and lipid metabolism. This dysfunction can lead to a vicious cycle in which disrupted mitochondrial function exacerbates metabolic abnormalities and vice versa. We will discuss how the inhibition of mitochondria electron transport chain but not uncoupling is able to trigger triglyceride accumulation in murine preadipocytes but also how mitochondria uncoupling leads to reduce triglyceride content in these cells. Eventually, we will also present preliminary data on adipose stem cells (ASCs) derived from pathological human adipose tissue of lipedema patients showing that their mitoproteome is different than ASCs isolated from subcutaneous of “healthy” abdominal fat pads.
In conclusion, research on the intersection of mitochondrial biology and lipodystrophies is now crucial for understanding the underlying mechanisms of these disorders.