BACKGROUNDPrenatal hyperglycaemia may increase metabolic syndrome susceptibility of the offspring. An underlying component of the development of these morbidities is hepatic gluconeogenic molecular dysfunction. We hypothesized that maternal hyperglycaemia will influence her offsprings hepatic peroxisome proliferator-activated receptor coactivator-1α (PGC-1α) expression, a key regulator of glucose production in hepatocytes.

METHODWe established maternal hyperglycaemia by streptozotocin injection to induce the maternal hyperglycaemic Wistar rat model. Offspring from the severe hyperglycemia group (SDO) and control group (CO) were monitored until 180 days after birth. Blood pressure, lipid metabolism indicators and insulin resistance (IR) were measured. Hepatic PGC-1α expression was analyzed by reverse transcription polymerase chain reaction and Western blotting. mRNA expression of two key enzymes in gluconeogenesis, glucose-6-phosphatase (G-6-Pase) and phosphoenolpyruvate carboxykinase (PEPCK), were analyzed and compared.

RESULTSIn the SDO group, PGC-1α expression at protein and mRNA levels were increased, so were expression of G-6-Pase and PEPCK (P < 0.05). The above effects were seen prior to the onset of IR.

CONCLUSIONThe hepatic gluconeogenic molecular dysfunction may contribute to the metabolic morbidities experienced by this population.

Animals ; Female ; Hyperglycemia ; chemically induced ; physiopathology ; Insulin Resistance ; physiology ; Liver ; metabolism ; Male ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Peroxisome Proliferator-Activated Receptors ; metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects ; RNA-Binding Proteins ; Rats ; Rats, Wistar ; Streptozocin ; toxicity ; Transcription Factors

Background Prenatal hyperglycaemia may increase metabolic syndrome susceptibility of the offspring.An underlying component of the development of these morbidities is hepatic gluconeogenic molecular dysfunction.We hypothesized that maternal hyperglycaemia will influence her offsprings hepatic peroxisome proliferator-activated receptor coactivator-1α (PGC-1α) expression,a key regulator of glucose production in hepatocytes.@@Method We established maternal hyperglycaemia by streptozotocin injection to induce the maternal hyperglycaemic Wistar rat model.Offspring from the severe hyperglycemia group (SDO) and control group (CO) were monitored until 180 days after birth.Blood pressure,lipid metabolism indicators and insulin resistance (IR) were measured.Hepatic PGC-1α expression was analyzed by reverse transcription polymerase chain reaction and Western blotting.mRNA expression of two key enzymes in gluconeogenesis,glucose-6-phospha-tase (G-6-Pase) and phosphoenolpyruvate carboxykinase (PEPCK),were analyzed and compared.@@Results In the SDO group,PGC-1α expression at protein and mRNA levels were increased,so were expression of G-6-Pase and PEPCK (P<0.05).The above effects were seen prior to the onset of IR.@@Conclusion The hepatic gluconeogenic molecular dysfunction may contribute to the metabolic morbidities experienced by this population.

Objective To observe the clinical effect of pelma massage collaborating with lactulose in the treatment of constipation of pregnancy.Methods Totals of 80 patients with constipation of pregnancy were divided into observation group and control group randomly.The control group was only given a pelma massage therapy,while the observation group was given pelma massage plus oral lactulose therapy.Then,the clinical effects were compared between the two groups.Results By rank sum test,the healing rate of observation group (95％) was higher than that of the control group (65％),and the difference was statistically significant (U =322.0,P ＜ 0.01).Conclusions Lactulose collaborating with pelma massage has better clinical effect than pelma massage only in the treatment of constipation of pregnancy.