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Maternal endotoxemia results in obesity and insulin resistance in adult male offspring.

Artikel i vetenskaplig tidskrift
Författare Cecilia Nilsson
Britt-Mari Larsson
Eva Jennische
Elias Eriksson
Per Björntorp
D A York
Agneta Holmäng
Publicerad i Endocrinology
Volym 142
Nummer/häfte 6
Sidor 2622-30
ISSN 0013-7227
Publiceringsår 2001
Publicerad vid Hjärt-kärlinstitutionen
Institutionen för anatomi och cellbiologi
Institutionen för fysiologi och farmakologi, Avdelningen för farmakologi
Sidor 2622-30
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Adipose Tissue, Animals, Blood Glucose, analysis, Body Composition, Brain Chemistry, Carrier Proteins, analysis, Corticosterone, secretion, Endotoxemia, complications, Estradiol, blood, Fatty Acids, Nonesterified, blood, Female, Glucose Clamp Technique, Glycerol, blood, Insulin, blood, Insulin Resistance, Leptin, analysis, Male, Obesity, etiology, Organ Size, Pregnancy, Pregnancy Complications, Prenatal Exposure Delayed Effects, Progesterone, blood, RNA, Messenger, analysis, Rats, Rats, Wistar, Receptors, Cell Surface, Receptors, Glucocorticoid, analysis, genetics, Receptors, Leptin, Stress, Physiological, Testosterone, blood
Ämneskategorier Farmakologi och toxikologi


Events in utero appear to be important factors contributing to the development of somatic disorders at adult age. The aim of this study was to examine whether maternal immune challenge would be followed at adult age by metabolic and endocrine abnormalities in the offspring. Pregnant rats were given injections of either endotoxin (Escherichia coli lipopolysaccharide; 0.79 mg/kg, ip) or vehicle on days 8, 10, and 12 of gestation. Adult male offspring to lipopolysaccharide-exposed dams were heavier than controls (P < 0.05) and showed increased adipose tissue weights (P < 0.05), elevated food intake (P < 0.05), and increased circulating leptin (P < 0.01). The effect of insulin on glucose uptake was reduced, as measured by an euglycemic hyperinsulinemic clamp technique (P < 0.05). Serum levels of 17beta-estradiol and progesterone were elevated (P < 0.01 and P < 0.05, respectively). Baseline levels of corticosterone were normal, but the corticosterone response to stress was attenuated (P < 0.05), and hippocampal glucocorticoid receptor protein was up-regulated (P < 0.05). Female offspring were uninfluenced, except for increased testosterone levels (P < 0.05), increased baseline corticosterone levels (P < 0.05), and enlargement of heart and adrenals (P < 0.05). The results indicate that maternal endotoxemia leads to obesity, insulin resistance, and high serum levels of leptin in the adult male offspring. This study reports a novel animal model of obesity with features of the metabolic syndrome.

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