Energy balance
Defective nitric oxide (NO) production and mitochondrial biogenesis are central mechanisms driving visceral adiposity, insulin resistance, and cardiovascular risk in the metabolic syndrome.
If you struggle with obesity and insulin resistance, standard calorie counting may fail because your body's energy sensors (mitochondria) are defective, signaling an 'energy emergency' that drives hunger and reduces energy expenditure. Addressing the root cause may require interventions that support mitochondrial health and nitric oxide production, rather than just focusing on willpower or simple caloric restriction, which might further suppress already defective lipid oxidation.
This suggests that mitochondrial function may be impaired in the metabolic syndrome and, thus, in the consequent cardiovascular disease. We have recently found that mitochondrial biogenesis and function are enhanced by nitric oxide in various cell types and tissues, including cardiac muscle. Increasing evidence suggests that this mediator acts as a metabolic sensor in cardiomyocytes. This implies that a defective production of nitric oxide might be linked to dysfunction of the cardiomyocyte metabolism.
Why this rating
The paper is a review of animal models (mice, rats) and in vitro studies; human data is observational or correlational, lacking direct interventional proof of causality in humans.
Source
Defective Mitochondrial Biogenesis
Enzo Nisoli et al. · Circulation Research · 2007
DOI 10.1161/01.res.0000259591.97107.6c
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