Hormonal
Deficiency or inhibition of the nuclear receptor RORα protects against diet- and age-induced obesity, hepatosteatosis, and insulin resistance by increasing energy expenditure and suppressing pro-inflammatory gene expression in adipose tissue.
This research highlights RORα as a critical regulator of metabolism. While you cannot change your genetics, the discovery of RORα antagonists suggests that future pharmaceutical interventions could potentially mimic the protective effects seen in RORα-deficient mice, such as improved insulin sensitivity and reduced fat storage, by targeting this specific receptor pathway.
RORα-deficient mice are protected against age- and diet-induced obesity, hepatosteatosis, and insulin resistance... The resistance to hepatosteatosis in RORα-deficient mice is related to the reduced expression of several genes regulating lipid synthesis, transport, and storage. Adipose tissue-associated inflammation... is considerably diminished in RORα-deficient mice... Indirect calorimetric analysis showed that VO2, VCO2, and heat generation were significantly enhanced in RORαsg/sg mice on a HFD.
Why this rating
Evidence is derived from multiple mouse models (RORα-deficient, Staggerer) and human genetic association studies, but no human clinical trials are reported.
Source
Retinoic acid-related orphan receptors α and γ: key regulators of lipid/glucose metabolism, inflammation, and insulin sensitivity
Anton M. Jetten et al. · Frontiers in Endocrinology · 2013
DOI 10.3389/fendo.2013.00001
More from this paper
- Deficiency or inhibition of the nuclear receptor RORγ1 protects against diet-induced insulin resistance and improves glucose tolerance, potentially through mechanisms distinct from RORα.Moderate
- RORs (RORα and RORγ) function as intermediaries linking the circadian clock machinery to the regulation of lipid and glucose metabolism, suggesting that circadian disruption may contribute to metabolic syndrome.Moderate
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