title: Glucose intolerance associated with early-life exposure to maternal cafeteria feeding is dependent upon post-weaning diet.
abstract: In addition to being a risk factor for adverse outcomes of pregnancy, maternal obesity may play a role in determining the long-term disease patterns observed in the resulting offspring, with metabolic and dietary factors directly programming fetal development. The present study evaluated the potential for feeding rats an obesogenic cafeteria diet (O) pre-pregnancy, during pregnancy, during lactation and for the offspring post-weaning, to programme glucose tolerance. Early-life exposure to an O diet had no significant effect on offspring food intake. Early-life programming associated with O feeding to induce maternal obesity was associated with reduced adiposity in offspring weaned onto low-fat chow. Adult offspring exposed to an O diet in early life and weaned on a chow diet had low fasting glucose and insulin concentrations and appeared to be more sensitive to insulin during an intraperitoneal glucose tolerance test. When weaned on an O diet, male offspring were more prone to glucose intolerance than females. On the basis of the area under the glucose curve, maternal O feeding at any point from pre-mating to lactation was associated with impaired glucose tolerance. The mechanism for this was not identified, although increased hepatic expression of Akt2 may have indicated disturbance of insulin signalling pathways. The observations in the present study confirm that maternal overnutrition and obesity during pregnancy are risk factors for metabolic disturbance in the resulting offspring. Although the effects on glucose homeostasis were independent of offspring adiposity, the programming of a glucose-intolerant phenotype was only observed when offspring were weaned on a diet that induced greater fat deposition.
authors.affiliation: School of Biosciences, University of Nottingham, Sutton Bonington, Loughborough LE12 5RD, UK.
authors.forename: Asli
authors.initials: A
authors.lastname: Akyol
authors.forename: Sarah
authors.initials: S
authors.lastname: McMullen
authors.forename: Simon C
authors.initials: SC
authors.lastname: Langley-Evans
mesh_terms: D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D004032:Diet / Q000009:adverse effects*; D004195:Disease Models, Animal; D005260:Female; D018149:Glucose Intolerance / Q000209:etiology* / Q000235:genetics / Q000378:metabolism; D006801:Humans; D055504:Insulin Receptor Substrate Proteins / Q000235:genetics; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena; D009765:Obesity / Q000150:complications / Q000235:genetics / Q000378:metabolism; D044343:Overnutrition / Q000150:complications / Q000235:genetics / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012307:Risk Factors; D014886:Weaning
chemical_list: D055504:Insulin Receptor Substrate Proteins; C526299:Irs2 protein, rat; D012333:RNA, Messenger; C494923:Akt2 protein, rat; D051057:Proto-Oncogene Proteins c-akt