Mitochondria, Obesity and Metabolic Syndrome

Obesity is a complex disease involving an excessive amount of body fat.  Usually, obesity results from inherited, physiological and environmental factors, combined with diet, physical activity and exercise choices.  An increase in visceral adipose tissue deposition induces chronic local and systemic inflammation, which mediates most obesity-related complications.  The inflammation of the adipose tissue is characterized by the infiltration of activated M1 macrophages, leading to the production of reactive oxygen species (ROS) and release of pro-inflammatory cytokines.

An excess of macronutrients in the adipose tissues stimulates them to release the aforementioned inflammatory mediators resulting in a chronic metabolic inflammatory state, termed metaflammation. This chronic inflammation is an imbedded mechanism of developed diseases including obesity, metabolic syndrome, insulin resistance, and diabetes mellitus.

Recent publications from the laboratory of Dr. Lloyd, Luciole’s scientific co-founder, and his colleagues, have demonstrated that OGG1 plays a significant role in the prevention of obesity by increasing whole

body energy expenditure and increasing mitochondrial content and function in white adipose tissue.  Further studies indicate that expression of huOGG1 blunts adipogenesis (fat cell formation). 

These studies demonstrate the importance of mitochondrial OGG1 in preventing the chronic inflammation, obesity, dyslipidemia and insulin resistance that define metabolic syndrome.

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