Nicotinamide mononucleotide (NMN) supplementation ameliorates the impact of maternal obesity in mice: comparison with exercise

Nicotinamide mononucleotide (NMN) supplementation ameliorates the impact of maternal obesity in mice: comparison with exercise

Understanding the Impact of Maternal Obesity on Offspring Metabolism and Potential Interventions


  • Maternal overnutrition increases the risk of long-term metabolic dysfunction in offspring.
  • Exercise improves metabolism by upregulating mitochondrial biogenesis or function.
  • Nicotinamide mononucleotide (NMN), a precursor of nicotinamide adenine dinucleotide (NAD+), can reverse negative consequences of high fat diet (HFD) consumption.

Examining the Effects of Exercise and NMN in Offspring of Obese Mothers:

  • The study compared the effects of treadmill exercise and NMN injection in offspring of obese mothers.
  • Maternal obesity resulted in increased adiposity, liver triglycerides, decreased glucose tolerance, liver NAD+ levels, and citrate synthase activity in offspring.
  • Exercise and NMN interventions reduced adiposity and showed modest improvement in glucose tolerance and markers of mitochondrial function.
  • NMN appeared to have stronger effects on liver fat catabolism and synthesis compared to exercise.
  • The interventions were most effective in mice that were most metabolically challenged (HFD-consuming offspring of obese mothers).
  • Further study is needed to confirm the suitability of NMN for reversing metabolic dysfunction caused by maternal obesity.

Maternal Obesity and Offspring Health:

  • In the last three decades, the proportion of adults with a body mass index (BMI) greater than 25 has increased globally.
  • Maternal obesity is associated with increased birth weight, adiposity, and the risk of offspring developing obesity.
  • Developmental programming, shared environment, and genetics contribute to the association.
  • Childhood obesity increases the risk of metabolic disorders later in life.
  • Maternal obesity perpetuates the intergenerational cycle of obesity.
  • Lifestyle interventions in the mother can reduce weight, triglycerides, and insulin resistance in offspring.
  • Exercise during gestation protects against hepatic steatosis and glucose intolerance.
  • Pharmacological therapies in obese mothers have shown successful outcomes for offspring.
  • Interventions in the offspring themselves are still necessary.
  • Mitochondria play a critical role in obesity-related diseases and the mentioned interventions.
  • NAD+ levels are reduced in obesity and type 2 diabetes.
  • Physical activity increases NAD+ levels and improves mitochondrial function.
  • NAD+ precursors, such as NMN, are therapeutic targets for metabolic disorders and aging.
  • NMN supplementation increases NAD+ levels and improves metabolism in various conditions.

Investigating the Effects of NMN Supplementation on Offspring:

  • Maternal obesity affects offspring adiposity and involves alterations to oocyte state and the gestational milieu.
  • It is unknown whether NMN supplementation can reverse metabolic deficits initiated prior to birth.
  • The study aims to test NMN administration in female offspring consuming regular or high-fat diet after weaning.
  • The effects of exercise and NMN supplementation in female offspring will be compared.
  • Weight gain, adiposity, glucose tolerance, mitochondrial DNA copy number, triglyceride levels, liver NAD+ and NADH levels, citrate synthase activity, and mRNA levels of fat metabolism markers will be measured.

Experimental Protocol and Results:

  • Female mice were used in the experiment.
  • Mice were acclimatized to the diets before being assigned to control or HFD groups.
  • Pregnant mice were housed individually, and their diets were continued throughout pregnancy and lactation.
  • Offspring were weaned and distributed across the diet groups.
  • After post-weaning diet, offspring from HFD-fed mothers were further distributed into sedentary, exercise, or NMN groups.
  • Glucose tolerance tests were performed, samples were collected, and various measurements were conducted.
  • Maternal HFD increased pup body weight prior to weaning.
  • Maternal obesity and offspring HFD consumption had significant effects on body weight, organ weights, glucose tolerance, insulin levels, liver triglycerides, and gene expression.
  • Maternal obesity was associated with reduced NAD+ concentrations, but NMN supplementation increased NAD+ levels.
  • NMN and exercise reduced body weight and fat accumulation, with stronger effects in offspring consuming HFD.
  • NMN increased mitochondrial activity and beta-oxidation, reduced fat synthesis, and decreased fatty acid import.
  • Both NMN and exercise partially improved glucose tolerance and increased plasma insulin levels in offspring with post-weaning HFD.
  • NMN supplementation and exercise had similar effects in a mouse model of maternal obesity.
  • The interventions were most beneficial in the metabolically challenged offspring consuming HFD.


  • Maternal obesity during pregnancy can have long-term health risks for offspring.
  • Strategies like exercise and NMN supplementation can improve metabolism.
  • NMN treatment showed promising results in reversing negative effects of maternal obesity on offspring.
  • Further research is needed to explore the potential of NMN as a therapeutic option.

Title of paper: Nicotinamide mononucleotide (NMN) supplementation ameliorates the impact of maternal obesity in mice: comparison with exercise

Author(s): Uddin GM, Youngson NA, Doyle BM, Sinclair DA, Morris MJ.

Year published: 2017

Published in: Sci Rep

Original article can be found here.

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