Research

Hormonal

In the context of dietary obesity, activation of Hif1α in visceral white adipocytes suppresses fatty acid oxidation and energy expenditure by transcriptionally repressing Sirt2, thereby maintaining obesity and associated metabolic pathologies.

This research highlights that in states of severe obesity, visceral fat tissue can become hypoxic, triggering biological mechanisms (Hif1a/Sirt2) that actively suppress fat burning and maintain fat stores. This suggests that for some individuals, obesity is not just a passive accumulation of energy but an active biological state that may require addressing underlying tissue health or hypoxia, rather than just caloric restriction alone.

GoodSupportsHIGH confidence
Here we report that, in mice, Hif1a activation in visceral white adipocytes is critical to maintain dietary obesity and associated pathologies... This function of Hif1a is linked to its capacity to suppress b-oxidation, in part, through transcriptional repression of sirtuin 2 (Sirt2) NAD+-dependent deacetylase.
Jaya Krishnan et al. · Genes & Development · 2012

Why this rating

High-quality mechanistic evidence using genetically modified mouse models (adipocyte-specific knockout) and human tissue correlation, though not a human clinical trial.

Source

Dietary obesity-associated Hif1α activation in adipocytes restricts fatty acid oxidation and energy expenditure via suppression of the Sirt2-NAD<sup>+</sup> system

Jaya Krishnan et al. · Genes & Development · 2012

DOI 10.1101/gad.180406.111

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DOI resolved against Crossref · corpus check 2026-06-10

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