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Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes
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Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes

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Maternal High Fructose Intake Increases the Vulnerability to Post-Weaning High-Fat Diet-Induced Programmed

You-Lin Tain1,2, Wei-Chia Lee3, Kay L H Wu4

  • 1Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan. tainyl@hotmail.com.

Nutrients
|January 10, 2018
PubMed

Insights

Maternal high-fructose diet primes offspring for hypertension when exposed to high-fructose or high-fat diets later in life. This programming involves altered nutrient sensing, oxidative stress, and soluble epoxide hydrolase (SEH) pathways.

Area of Science:

  • Nutritional Programming
  • Developmental Origins of Health and Disease (DOHaD)
  • Cardiovascular Physiology

Background:

  • High-fructose and high-fat diets are linked to global hypertension epidemics.
  • Hypertension can originate from early-life nutritional insults, impacting long-term health.
  • Maternal diet during pregnancy and lactation significantly influences offspring's metabolic health.

Purpose of the Study:

  • To investigate if maternal high-fructose diet (HFR) increases offspring's susceptibility to hypertension induced by post-weaning high-fructose or high-fat diets (HFA).
  • To determine the underlying molecular mechanisms of this programmed hypertension.
  • To identify potential therapeutic targets for preventing diet-induced hypertension.

Main Methods:

  • Pregnant rats were fed either regular chow (ND) or a high-fructose diet (HFR).
  • Male offspring were fed ND, HFR, or HFA from weaning to 12 weeks, creating four groups: ND/ND, HFR/ND, HFR/HFR, and HFR/HFA.
  • Kidney gene expression (Sirt4, Prkaa2, Ppara, Nrf2, etc.), oxidative stress markers, and soluble epoxide hydrolase (SEH) levels were analyzed.

Main Results:

  • Maternal HFR exacerbated hypertension in offspring fed HFA post-weaning.
  • Both post-weaning HFR and HFA reduced key nutrient-sensing gene expression (Sirt4, Prkaa2, Ppara, Ppargc1a) in offspring kidneys exposed to maternal HFR.
  • HFA induced greater oxidative stress and reduced renal Ulk1, Atg5, and Nrf2 mRNA levels compared to HFR.
  • Maternal HFR increased renal SEH expression, which was normalized by post-weaning HFR/HFA diets.

Conclusions:

  • Maternal high-fructose intake programs male offspring for differential vulnerability to hypertension in response to post-weaning high-fructose or high-fat diets.
  • Targeting nutrient-sensing pathways, oxidative stress, and SEH may offer therapeutic strategies to prevent hypertension in at-risk populations.
  • Early-life nutrition plays a critical role in long-term cardiovascular health, highlighting the importance of maternal dietary choices.

Keywords:
developmental origins of health and disease (DOHaD)fructosehigh-fathypertensionnutrient sensing signaloxidative stresssoluble epoxide hydrolase

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