Programmed regulation of rat offspring adipogenic transcription factor (PPARγ) by maternal nutrition

Area of Science:

• Endocrinology
• Developmental Biology
• Nutritional Science

Background:

• Maternal nutrition during gestation and lactation significantly influences offspring's metabolic health and long-term obesity risk.
• Peroxisome proliferator-activated receptor gamma (PPARγ) is a key regulator of adipogenesis and energy homeostasis.
• Dysregulation of PPARγ and its co-regulators is implicated in the development of obesity.

Purpose of the Study:

• To investigate the protein expression of PPARγ and its co-regulator complexes in the adipose tissue of offspring exposed to maternal nutritional programming.
• To determine how maternal high-fat diet (Mat-OB) or intrauterine growth restriction (IUGR) affects PPARγ and its co-regulators in offspring at different life stages.

Main Methods:

• Female rats were fed either a high-fat (60% kcal) or control (10% kcal) diet before and during gestation/lactation (Mat-OB).
• A subset of dams underwent 50% food restriction from day 10 of gestation to term, inducing IUGR.
• Protein expression of PPARγ, co-repressors, and co-activators was analyzed in adipose tissue of newborn and adult male offspring.

Main Results:

• Newborn offspring from both Mat-OB and IUGR groups exhibited upregulated PPARγ with varied changes in co-regulators.
• Adult obese offspring (Mat-OB and IUGR) showed increased PPARγ expression.
• In adult offspring, co-repressor expression decreased, while co-activator expression increased, alongside elevated PPARγ.

Conclusions:

• Nutritional programming in utero leads to increased PPARγ expression in offspring.
• Altered expression of PPARγ co-regulators is associated with PPARγ changes in offspring exposed to maternal malnutrition.
• Further functional studies on PPARγ co-regulators are essential to elucidate their role in programmed obesity.