title: [Expression of glucagon in gestational and diet-induced hyperlipidemic gestational rats].
abstract: OBJECTIVE
  To observe the difference in the expression of glucagon in normal and in diet-induced hyperlipidemic gestational rats.
  
  
  METHODS
  Thirty-two female SD rats were divided into control group, hyperlipidemia group, gestation group and hyperlipidemic-gestation group. Fourteen days after gestation, real-time quantitative PCR was performed to detect the expression of preglucagon mRNA and Western blot was employed to detect the expression of glucagon in pancreas in different groups.
  
  
  RESULTS
  The glucose peak of OGTT was 30 minutes after glucose load in all the rats. The insulin peak of OGTT was 15 minutes after glucose load in controls, while the insulin peak was 30 minutes after glucose load in other groups. Fasting insulin in both gestation rats and hyperlipidemic-gestation rats was higher than that in controls(21.68+/-2.55 vs 14.35+/-0.86 mIU/L, P<0.05; 25.76+/-3.31 vs 14.35+/-0.86 mIU/L, P<0.01). Insulin AUC in both hyperlipidemic-gestation rats and hyperlipidemia rats was also higher than that in controls(204.60+/-79.06 vs 129.71+/-11.33 mIU/L, P<0.05; 230.25+/-13.19 vs 129.71+/-11.33 mIU/L, P<0.05). PG relative mRNA levels in gestation rats and in hyperlipidemic-gestation rats were respectively 1.46 fold and 1.77 fold higher than that in controls (P<0.05 and P<0.01)and 1.54 fold higher than that in hyperlipidemia rats (P=0.01). Glucagon in gestation rats and hyperlipidemic-gestation rats was respectively 2.57 fold and 3.44 fold higher than that in controls (both P<0.01)and 2.9 fold higher than that in hyperlipidemia rats(P<0.01).
  
  
  CONCLUSIONS
  Both hyperlipidemia and gestation may delay the releasing peak of insulin after glucose load. In normal gestation it is mainly reflected by fasting insulin resistance and in hyperlipidemic-gestation it is reflected by both fasting and glucose load insulin resistance. The rising pancreatic glucagons may partly lead to the increased gestational insulin resistance.
authors.affiliation: Department of Endocrinology and Metabolism, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. jiangn@fmmu.edu.cn
authors.forename: Li
authors.initials: L
authors.lastname: Wang
authors.forename: Hong-wei
authors.initials: HW
authors.lastname: Cao
authors.forename: Jing
authors.initials: J
authors.lastname: Zhang
authors.forename: Chao-wu
authors.initials: CW
authors.lastname: Tang
authors.forename: Qiu-he
authors.initials: QH
authors.lastname: Ji
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004032:Diet / Q000009:adverse effects*; D005260:Female; D005786:Gene Expression Regulation; D005934:Glucagon / Q000235:genetics*; D005951:Glucose Tolerance Test; D006949:Hyperlipidemias / Q000097:blood / Q000139:chemically induced / Q000235:genetics*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D010179:Pancreas / Q000378:metabolism; D016133:Polymerase Chain Reaction; D011247:Pregnancy; D011248:Pregnancy Complications / Q000097:blood / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats
chemical_list: D001786:Blood Glucose; D007328:Insulin; D012333:RNA, Messenger; D005934:Glucagon