Hormonal
Silencing or deficiency of the mitochondrial Complex IV subunit COX5B in white adipose tissue drives intracellular lipid accumulation and adipocyte enlargement, whereas restoring COX5B expression counteracts age-dependent obesity.
This research suggests that age-related weight gain is driven by a specific decline in mitochondrial efficiency (Complex IV) in fat cells, regulated by the HIF1A protein. While you cannot directly 'dose' COX5B, the findings imply that strategies supporting mitochondrial health and reducing chronic hypoxic stress in adipose tissue may help prevent age-related fat accumulation. For humans, higher COX5B levels are associated with better weight loss outcomes after bariatric surgery, suggesting this biomarker has prognostic value.
Silencing of Cox5b decreased fatty acid oxidation and promoted intracellular lipid accumulation. Moreover, local in vivo Cox5b silencing in WAT of young mice increased the size of adipocytes, whereas restoration of COX5B expression in aging mice counteracted adipocyte enlargement.
Why this rating
Strong mechanistic evidence in mice (knockout, silencing, restoration) and correlational human data, but lacks direct human interventional trials.
Source
Role of Mitochondrial Complex IV in Age-Dependent Obesity
Inés Soro-Arnáiz et al. · Cell Reports · 2016
DOI 10.1016/j.celrep.2016.08.041
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