A study published in the International Journal of Obesity suggests a possible link between the gut microbes along with high fat diet during pregnancy and increased body weight in the offspring.
That maternal diet during pregnancy and lactation influences the health of the offspring is already known. But there is lack of information on the impact of maternal high-fat diet and gut microbes on the body weight, fat deposition and gastrointestinal function in the offspring.
AdvertisementSo, researchers Frida Fak and her colleagues from Sweden investigated the effect of high fat diet plus Escherichia coli fed to female experimental animals (rats) during pregnancy and lactation on body weight and gut function of the 14-day-old male offspring.
They divided the experimental animals into three groups - the first group received high fat (HF) diet, the second group received HF diet plus drinking water containing E. coli bacteria (HF-EC group), and the third group received the standard low fat (LF) diet - during last two weeks of pregnancy and during lactation.
Results showed that -
-†No significant differences in body weight were observed between the three groups on day one offspring.
-†On the 14th day, the offspring from the HF diet group had significantly higher body weight as compared with those from the LF diet group.
-†On the 14th day, the offspring from the HF-EC group had even more increased body weight compared with the ones from HF diet group alone.
- The pH of the stomach was higher in LF group as compared with the HF and HF-EC group indicating that degree of stomach maturation is higher in LF group. But stomach weight was highest in HF-EC group followed by HF group and LF group.
-†Intestinal permeability is used as an indicator of small intestine maturation, which however, can also be affected by the diet, the gut flora and inflammatory provocations. The while the HF-EC group showed significantly higher intestinal permeability than the other two groups.
The researchers thus deduced that since the increase in body weight was seen on 14 day old offspring and not on day one of birth, it related to the suckling period indicating an increased fat content in the milk of the HF mothers.
Regarding the link between adiposity and gut flora, their research corroborated the results of another study in which E. coli numbers in pregnant women correlated positively with infant birth weight 'indicating that the maternal microbiota influences the body weight of the offspring' and earlier studies showing that gut microbes of obese individuals can harvest more energy from the diet.
Say the researchers, 'One potential mechanism that may explain why the addition of E. coli led to increased adiposity could be increased levels of endotoxin. It was recently shown that chronic infusion of low levels of lipopolysaccharides was sufficient to promote adiposity in mice'. What they are saying is that the increased permeability in the gut of the offspring from the HF-EC group might have led to increased transfer of endotoxins (endotoxins are lipopolysaccharide complexes that occur in the cell wall of bacteria) from the gut to the blood, leading to obesity.
They further reasoned - 'The addition of E. coli to the mothers' drinking water led to higher stomach and intestinal weights and increased protein concentration of the small intestine, along with higher disaccharidase activities. This indicates that the maternal E. coli feeding had stimulated the growth and functional adaptation of the gut in the offspring'. They however suggested that more studies are required to explain these effects.
The researchers concluded - 'The results point to a mechanistic link between the gut microbiota, increased intestinal permeability and metabolic endotoxemia, which appear to have led to increased adiposity in the young rats. This stresses the need for more extensive studies on the significance of the maternal diet and colonizing microflora in neonates'.
Reference: Fak F, Karlsson CL, Ahrnť S, Molin G, WestrŲm B. Effects of a high-fat diet during pregnancy and lactation are modulated by E. coli in rat offspring. Int J Obes (Lond). 2012 May;36(5):744-51.
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