Dr Clare Reynolds is a scientist from the Liggins Institute at the University of Auckland, New Zealand. Clare is a research fellow within the Developmental Programming Research Group at the Liggins Institute, investigating maternal programming-induced metabolic inflammation. She is looking to answer questions like: Is inflammation set in motion by the maternal dietary environment? Can early-life stressors set us on the path to immunological dysfunction eventually culminating in type 2 diabetes and cardiovascular disease? Can early-life anti-inflammatory strategies reverse programmed immuno-metabolism?


There are many myths and old wives tales which relate to pregnancy, perhaps one of the most common is the misconception that pregnant women should be “eating for two”. There is much conflicting advice when it comes to food consumption and exercise during pregnancy, however one thing has become very clear, gaining too much or too little weight can be detrimental for both mother and child. While increased caloric intake is important for the health of the growing baby, the average woman requires only 300 extra calories (this amounts to a small sandwich or glass of full-fat milk) and even less for overweight/obese women. It is also important to note that the quality and not the quantity of food consumed during pregnancy is key to maintaining the health of both mother and child and women must be sensitive in their approach to the increased energy demands which result during pregnancy. Overconsumption and increased weight gain during pregnancy can have serious effects which include increased risk of C-section and preterm birth along with altered metabolic state in the mother resulting in dangerously increased blood pressure (preeclampsia) and glucose intolerance (gestational diabetes). Unfortunately, these direct effects are not where the story ends. Evidence gathered from both human and animal studies over the past two decades have shown that increased maternal obesity and food intake results in higher risk for development of obesity, heart disease and type 2 diabetes in the child. This DOHaD, or developmental origins of health and disease, concept has played a huge part in revolutionising our view of how early life in the womb adversely affects future disease risk, however, the precise mechanisms which govern these effects are still uncertain.    

There has been a huge increase in overweight/obesity rates worldwide, particularly where a “westernised” diet is the norm. These diets are typically highly processed and rich in saturated fatty acids, salt and sugar. The effects of high-fat diet are continuing to be examined in both human and animal studies; our particular focus in the current study was to examine maternal metabolic inflammation. We know that obesity is associated with a consistent level of low-grade inflammation and we were interested to see if this could alter maternal metabolism and offspring inflammatory profiles. The contribution of maternal high salt is less clear in terms of developmental programming. As with most nutrients, sodium is required in larger amounts during pregnancy, but excessive intake is associated with negative effects on fetal kidney development, altered fluid balance (oedema) and high blood pressure (preeclampsia). In our current study we examined the impact of high fat and high salt alone and in combination on maternal metabolic and inflammatory profiles and the effects on offspring body weight in a rat model of pregnancy.

Why rats? Rodents represent a useful model of the DOHaD theory for several distinct reasons. Logistically, they have relatively short lifespans enabling us to examine a system from pre-pregnancy, to pregnancy (about 22 days) in the mother to adulthood in the offspring in a relatively short period of time (approximately a year, as opposed to 30-40years in humans). However it is important that model systems are also scientifically appropriate. As opposed to some of the large ruminant animal models that are used to study the DOHaD paradigm, rats have a similar metabolic system to humans which make them ideal for analysing the contribution of dietary nutrients to pregnancy progression and indeed long-term metabolic effects in offspring. While it can be argued that the reproductive system of rats is not comparable to humans given their ability to produce litters (one pregnancy can give rise to upwards of 12 pups), they have similar placental structure (haemochorial or highly invasive placentas). This makes the rat an ideal model of feto-placental development.

In our recent study we fed rats one of four diets (low-fat/low-salt, low-fat/high salt, high fat/low-salt and high-fat/high salt) before pregnancy (3 weeks) and during pregnancy and lactation. Rats on a high-fat diet ate roughly the same amount of food but consumed more calories and were therefore heavier during pregnancy thus underscoring the importance of food quality during pregnancy. We examined metabolic and inflammatory markers in our pregnant mothers (day 18 of pregnancy) and saw that despite no increase in body weight, the high-salt fed animals displayed increased inflammation both in the blood and in the fatty tissue (adipose tissue), this was accompanied by enhanced uptake of fat in the adipose tissue along with evidence of glucose intolerance and fat mass expansion, all hallmarks of pre-diabetes, indicating that excessive salt consumption may initiate the path to type 2 diabetes in these mothers. We also see increased inflammation in high-fat animals and in addition to increased metabolic disturbance in the adipose tissue there is increased fat uptake by the liver, this may represent a worrying prelude to fatty liver disease and type 2 diabetes.

Salt and fat clearly have negative effects in the mother but does this extend to the offspring? Salt appears to have limited effects in terms of the fetal to weanling growth trajectory and weanling fat mass in both male and female offspring. However in the case of offspring exposed to high fat diets there is considerable evidence of fetal growth restriction followed by increased “catch-up” growth and fat mass by weaning. This increase in adiposity (larger fat mass) at such a young age is typical of the pattern of events which is associated with the DOHaD phenomenon. 

At this point there are no clear answers as to why we do not see an overt DOHaD effect in our salt-exposed offspring despite a clear detrimental effect on mothers. However it is obvious that high-fat exposure has disruptive effects which may be important for development of obesity, heart disease and diabetes in offspring during adulthood and indeed the metabolic effects in the mother post-partum. Our next step is to examine offspring long term to determine if salt induces a hypertensive effect in the absence of obesity. Overall it is important to understand the processes behind the physiological effects which we see in animals, by doing this we can develop targeted approaches very early in the life course of the individual and therefore prevent the onset of maternal diet-induced programming of obesity and disease in the next generation. Either way it is very clear that a healthy diet is paramount during pregnancy and “eating for two” is certainly a myth which has been debunked.

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