Gestational low dietary protein induces intrauterine inflammation and alters the programming of adiposity and insulin sensitivity in the adult offspring.

Malnutrition associated with low dietary protein can induce gestational inflammation and sets a long-lasting metabolic impact on the offspring even after replenishment. The work investigated whether a low-protein diet (LPD) during pregnancy and lactation induces intrauterine inflammation and predisposes offspring to adiposity and insulin resistance in their adult life. Female Golden Syrian hamsters were fed LPD (10.0% energy from protein) or a control diet (CD, 20.0 % energy from protein) from preconception until lactation. All pups were switched to CD after lactation and continued until the end. Maternal LPD increased intrauterine inflammation by enhancing neutrophil infiltration, amniotic hsCRP, oxidative stress, and mRNA expression of NFκß, IL8, COX2, and TGFß in the chorioamniotic membrane (P<.05). The prepregnancy body weight, placental, and fetal weights, serum AST and ALT were decreased, while blood platelets, lymphocytes, insulin, and HDL were significantly increased in LPD-fed dams (P<.05). A postnatal switch to an adequate protein could not prevent hyperlipidemia in the 6-months LPD/CD offspring. The lipid profile and liver functions were restored over 10 months of protein feeding but failed to normalize fasting glucose and body fat accumulation compared to CD/CD. LPD/CD showed elevated GLUT4 expression & activated pIRS1 in the skeletal muscle and increased expression of IL6, IL1ß, and p65-NFκB proteins in the liver (P<.05). In conclusion, present data suggest that maternal protein restriction may induce intrauterine inflammation and affect liver inflammation in the adult offspring by an influx of fats from adipose that may alter lipid metabolism and reduce insulin sensitivity in skeletal muscle.

Fructooligosaccharide ameliorates high-fat induced intrauterine inflammation and improves lipid profile in the hamster offspring.

Maternal high-fat diet (HFD) often results in intrauterine and feto-placental inflammation, and increases the risks of fetal programming of metabolic diseases. Intake of prebiotic is reported beneficial. However, its effects on HFD during pregnancy and lactation is not known. We evaluated the maternal intake of fructooligosaccharide (FOS) and its impact on placental inflammation, offspring's adiposity, glucose, and lipid metabolism in their later life. Female Golden Syrian hamsters were fed with a control diet (CD, 26.4 % energy from fat) or HFD (60.7% energy from fat) in the presence or absence of FOS from preconception until lactation. All pups were switched over to CD after lactation and continued until the end. Placental inflammation was upregulated in HFD-fed dam, as measured by a high concentration of hsCRP in the serum and amniotic fluid. Neutrophil infiltration was significantly increased in the decidua through the chorionic layer of the placenta. The expression of pro-inflammatory cytokines such as COX2, NFκß, IL-8, TGFß mRNA was increased in the chorioamniotic membrane (P <.05). The HFD/CD hamsters had more adiposity, higher triglyceride, and low HDL at 12 months of age compared to CD/CD (P <.05). However, HFD+FOS/CD-fed hamsters prevented adverse effects such as placental inflammation, neutrophil infiltration, glucose, and lipid profiles in the offspring (P <.05). Anti-inflammatory and lipid-lowering effects of FOS may reduce placental inflammation by lowering neutrophil infiltration and decreasing the production of pro-inflammatory cytokines. Intake of FOS during pregnancy may be beneficial in maintaining lipid metabolism and preventing excess adiposity for mother and their offspring.

Semi-synthetic diet versus diet using natural ingredients-Comparative study in female Golden Syrian hamsters.

Semi-synthetic diets (SSD) are recommended and are widely used to carry out experiments in rodents. However, in our experiments planned to carry out generation studies in female Golden Syrian hamsters using semi-synthetic diets, it was observed that the hamsters did not conceive as a result of decreased food intake. In this paper, we present the effects of both semi-synthetic diets and natural source diets (NSD) on food intake, body weight and reproductive performance of this species. Four-week-old female hamsters were equally divided into 3 groups and initially acclimatized for 2 weeks on natural chow diet (NCD). Thereafter, they were fed either control diet, high fat diet (HFD) or low protein diet (LPD) based on semi-synthetic/natural source ingredients until 12 weeks. Daily food intake and weekly body weights were monitored. Hamsters were kept for mating for about 2 weeks from 10th week onwards, during which the pregnancy confirmation test was done using standard vaginal smear examination. In all the groups fed SSD, the food intake was very poor, hamsters lost body weight and did not conceive, thus preventing us from carrying out further experiments. Hamsters fed NCD/NSD ingested more than twice as much as hamsters fed SSD (7-8 g/day/hamster against 3 g/day/hamster on average respectively). Based on the results of the current research, we conclude that the routinely used semi-synthetic diet is not suitable for carrying out studies in female hamsters. We suggest that scientists must also consider the unusual biological characteristics of a given species besides other biological factors. It is therefore critical to select appropriate biological models and diets that provide optimal sensitivity and specificity to accomplish the research objectives.