title: Fructose only in pregnancy provokes hyperinsulinemia, hypoadiponectinemia, and impaired insulin signaling in adult male, but not female, progeny.
abstract: OBJECTIVE
  Fructose intake from added sugars correlates with the epidemic rise in metabolic syndrome and cardiovascular diseases. However, consumption of beverages containing fructose is allowed during gestation. Recently, we found that an intake of fructose (10 % wt/vol) throughout gestation produces impaired fetal leptin signaling and hepatic steatosis. Therefore, we have investigated whether fructose intake during pregnancy produces subsequent changes in the progeny, when adult.
  
  
  METHODS
  Fed 261-day-old male and female descendants from fructose-fed, control or glucose-fed mothers were used. Plasma was used to analyze glucose, insulin, leptin, and adiponectin. Hepatic expression of proteins related to insulin signaling was determined.
  
  
  RESULTS
  Fructose intake throughout pregnancy did not produce alterations in the body weight of the progeny. Adult male progeny of fructose-fed mothers had elevated levels of insulin without a parallel increase in phosphorylation of protein kinase B. However, they displayed an augmented serine phosphorylation of insulin receptor substrate-2, indicating reduced insulin signal transduction. In agreement, adiponectin levels, which have been positively related to insulin sensitivity, were lower in male descendants from fructose-fed mothers than in the other two groups. Furthermore, mRNA levels for insulin-responsive genes were not affected (phosphoenolpyruvate carboxykinase, glucose-6-phosphatase) or they were decreased (sterol response element-binding protein-1c) in the livers of male progeny from fructose-supplemented rats. On the contrary, adult female rats from fructose-fed mothers did not exhibit any of these disturbances.
  
  
  CONCLUSIONS
  Maternal fructose, but not glucose, intake confined to the prenatal stage provokes impaired insulin signal transduction, hyperinsulinemia, and hypoadiponectinemia in adult male, but not female, progeny.
authors: Facultad de Farmacia, Universidad San Pablo-CEU, Urbanización Montepríncipe, 28668, Boadilla del Monte, Madrid, Spain.
authors: Lourdes
authors: L
authors: Rodríguez
authors: Facultad de Farmacia, Universidad San Pablo-CEU, Urbanización Montepríncipe, 28668, Boadilla del Monte, Madrid, Spain.
authors: María I
authors: MI
authors: Panadero
authors: Facultad de Farmacia, Universidad de Barcelona, CIBERobn, Barcelona, Spain.
authors: Núria
authors: N
authors: Roglans
authors: Facultad de Farmacia, Universidad San Pablo-CEU, Urbanización Montepríncipe, 28668, Boadilla del Monte, Madrid, Spain.
authors: Paola
authors: P
authors: Otero
authors: Facultad de Farmacia, Universidad San Pablo-CEU, Urbanización Montepríncipe, 28668, Boadilla del Monte, Madrid, Spain.
authors: Silvia
authors: S
authors: Rodrigo
authors: CQS Lab, Madrid, Spain.
authors: Juan J
authors: JJ
authors: Álvarez-Millán
authors: Facultad de Farmacia, Universidad de Barcelona, CIBERobn, Barcelona, Spain.
authors: Juan C
authors: JC
authors: Laguna
authors: Facultad de Farmacia, Universidad San Pablo-CEU, Urbanización Montepríncipe, 28668, Boadilla del Monte, Madrid, Spain. carbocos@ceu.es.
authors: Carlos
authors: C
authors: Bocos
mesh_terms: D052242:Adiponectin / Q000097:blood / Q000172:deficiency*; D000818:Animals; D000831:Animals, Newborn; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D005234:Fatty Liver / Q000097:blood / Q000209:etiology; D005260:Female; D005333:Fetus / Q000187:drug effects / Q000378:metabolism; D005632:Fructose / Q000008:administration & dosage / Q000009:adverse effects*; D005952:Glucose-6-Phosphatase / Q000235:genetics / Q000378:metabolism; D006946:Hyperinsulinism / Q000097:blood / Q000209:etiology*; D007328:Insulin / Q000097:blood; D055504:Insulin Receptor Substrate Proteins / Q000235:genetics / Q000378:metabolism; D007333:Insulin Resistance; D020738:Leptin / Q000097:blood; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D039382:Maternal Nutritional Physiological Phenomena; D008661:Metabolism, Inborn Errors / Q000097:blood / Q000209:etiology*; D019764:Phosphoenolpyruvate Carboxykinase (ATP) / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics / Q000378:metabolism
chemical_list: D052242:Adiponectin; D001786:Blood Glucose; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D020738:Leptin; D012333:RNA, Messenger; D051780:Sterol Regulatory Element Binding Protein 1; D005632:Fructose; D051057:Proto-Oncogene Proteins c-akt; D005952:Glucose-6-Phosphatase; D019764:Phosphoenolpyruvate Carboxykinase (ATP)
keywords: Fetal programming; Fructose; Metabolic syndrome; Pregnancy