Different evidence supports an important role for maternal obesity in the development of childhood obesity and subsequent adult disease. This study is addressed to investigate if and to which extend maternal high fat feeding would induce compensatory and adaptative responses in gut predisposing to the eventual development of paediatric obesity. Adult female mice were divided into two groups fed with i) high fat (HF) diet and ii) standard chow (SC)diet, during pregnancy and lactation. HF mothers showed a significant weight gain, higher levels of blood glucose and an abnormal glucose tolerance compared to SC mother, indicating the establishment of metabolic syndrome. Then, offspring subdivided according to maternal diet, O-SC pups birthed from mothers fed SC, whereas O-HF pups birthed from mothers fed HF diet, and morphological and functional experiments were performed in the small intestine 2 developmental ages, early suckling (P2) and late suckling (P15 ) to evaluate the contribute of maternal milk in the development of obesity.O-HF at P2 and P15 did not show significant changes in the morphology of the small intestinal wall (villus height, depth of the crypt, villus width near the crypt and thickness of the muscular layer) compared to O-SC. Moreover in agreement with morphological data, no difference has been found in the amplitude and frequency of the intestinal spontaneous mechanical activity from O-HF compared to O-SC. The contractile and relaxant responses to well know drugs as the muscarinic receptor agonist, carbachol, and the b-adrenergic receptor agonist, isoproterenol, were similar in both groups of animal. This study suggested that during lactation, maternal high fat feeding did not induce any compensatory and adaptative responses in gut that could suggest a predisposition to the development of pediatric obesity. Further experiments at later ages are currently in progress.
|Number of pages||1|
|Publication status||Published - 2015|