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Dietary fat overload reprograms brown fat mitochondria.

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Area of Science:

  • Metabolic physiology
  • Mitochondrial biology
  • Nutritional science

Background:

  • Chronic nutrient overload accelerates aging and related diseases.
  • Mechanisms of overnutrition on tissue metabolism are known, but its effect on brown adipose tissue (BAT) physiology remains unclear.
  • BAT plays a crucial role in energy expenditure and thermogenesis.

Purpose of the Study:

  • To investigate the impact of high-fat diet (HFD) on BAT mitochondrial responses across different life stages in female mice.
  • To explore the effects of maternal HFD during pregnancy and lactation on offspring BAT physiology.
  • To understand the role of mitochondrial dynamics and transcription factors in HFD-induced BAT dysfunction.

Main Methods:

  • Mice were exposed to a high-fat diet (HFD) at different life stages (adults, pregnant/lactating mothers, and offspring).
  • Mitochondrial respiration, oxidative phosphorylation (OxPHOS) subunits, mitochondrial mass, and dynamics (Drp1) were assessed in BAT.
  • FoxO1 transcription factor activity and thermogenic responses to cold exposure were evaluated.

Main Results:

  • Adult mice on HFD showed altered mitochondrial respiration and OxPHOS, despite unchanged mitochondrial amount.
  • Offspring exposed to maternal HFD exhibited reduced mitochondrial mass but high oxidative efficiency, leading to increased BAT bioenergetics.
  • HFD induced decreased Drp1 content, linked to FoxO1 inactivation, and impaired thermogenic activation in offspring, with only partial recovery after weaning to a normal diet.

Conclusions:

  • Maternal dietary fat overload irreversibly affects offspring BAT mitochondrial function and thermogenic capacity.
  • Early-life HFD exposure leads to BAT unresponsiveness to cold stimuli, potentially impacting metabolic health and lifespan.
  • Maternal nutrition during critical developmental windows significantly influences offspring's long-term metabolic programming and health outcomes.