PPARγ Gene as a Possible Link between Acquired and Congenital Lipodystrophy and its Modulation by Dietary Fatty Acids

Lipodystrophy syndromes are rare diseases that could be of genetic or acquired origin. The main complication of lipodystrophy is the dysfunction of adipose tissue, which leads to an ectopic accumulation of triglycerides in tissues such as the liver, pancreas and skeletal muscle. This abnormal fat distribution is associated with hypertriglyceridemia, insulin resistance, liver steatosis, cardiomyopathies and chronic inflammation. Although the origin of acquired lipodystrophies remains unclear, patients show alterations in genes related to genetic lipodystrophy, suggesting that this disease could be improved or aggravated by orchestrating gene activity, for example by diet. Nowadays, the main reason for adipose tissue dysfunction is an imbalance in metabolism, caused in other pathologies associated with adipose tissue dysfunction by high-fat diets. However, not all dietary fats have the same health implications. Therefore, this article aims to summarize the main genes involved in the pathophysiology of lipodystrophy, identify connections between them and provide a systematic review of studies published between January 2017 and January 2022 of the dietary fats that can modulate the development of lipodystrophy through transcriptional regulation or the regulation of protein expression in adipocytes.

Automated summary

Lipodystrophy syndromes are rare diseases that result in dysfunction of adipose tissue and abnormal accumulation of triglycerides. Both genetic and acquired factors may contribute to the development of lipodystrophy, and dietary fats can modulate gene activity. This article summarizes the main genes involved in lipodystrophy and reviews the effects of dietary fats on its development.