| Background: The number of patients with diabetes complicating pregnancy and gestational diabetes has increased dramatically over the past three decades and the incidence of obesity and diabetes in children also showed continued growth state. Obesity generated in the childhood gathers a variety of risk factors which can make metabolic dysfunction syndrome. The etiology is related to more aspects of the interaction with the metabolic interactions, epigenetic and environmental factors. Some studies have shown that intrauterine hyperglycemia in mothers can produce glucose and lipid metabolism disorders in the offsprings and the difference in parents’ family history is more significant in the performance of the offspring female patients. Some animal experiments also showed that birth weight and glucose metabolism for first generation and second generation mice birthed in the high glucose intrauterine are abnormal. Parent-derived factor for first generation has played a leading role in the growth and glucose metabolism for second generation. Epigenetic mechanisms may also play an important role in metabolic diseases in offspring and grandparents. Ding et al also found that impaired glucose tolerance(IGT) is progressed more significantly in paternal offspring than maternal offspring. The Objective of this paper topic: Measuring body weight, blood glucose, insulin, triglycerides, leptin levels, methylation status, PPARGC1 A gene and m RNA expression in the pancreatic tissue for SD rats with diabetes complicating pregnancy group, gestational diabetes group and non-treated group. Discussing high glucose intrauterine environment has influence in the glucose and lipid metabolism for the offspring with diabetes complicating pregnancy gestational diabetes group, the differences are researched. Simultaneously the role of epigenetic play in this process is explored. Objective: To investigate the differences of glucose and lipid metabolism disorders in the SD rat offspring diabetes mellitus with pregnancy and gestational diabetes mellitus(GDM). Methods: SD rats were put by intraperitoneal injection of a small dose of STZ and was fed with STZ plus High glucose and lipid diet, then gestational diabetes mellilus and diabetes complicating pregnancy models were induced, F1 generation rats were gotten. They were hybridized with normal heterosexual rats at eight weeks old to produce the F2 rats and divided into five groups: Diabetes complicating pregnancy paternal group, Diabetes complicating pregnancy maternal group, GDM paternal group, GDM maternal group and non-treated group. body mass, blood glucose, insulin, triglyceride and leptin levels were measured for F2 generation SD rats. Results: Compared with GDM paternal group and GDM paternal group, at 0 weeks, body mass difference for GDM paternal group(6.01 ± 0.14) g and GDM maternal group(5.66 ± 0.14) g had statistical significance(P <0.05); at 8 weeks, body mass difference for GDM paternal group(233.12 ± 28.68) g and GDM maternal group(258.25 ± 54.49) g didn’t have statistical significance(P >0.05). Compared with diabetes complicating pregnancy paternal group and diabetes complicating pregnancy maternal group, at 0 weeks, body mass difference for diabetes complicating pregnancy paternal group(5.66 ± 0.14) g and diabetes complicating pregnancy maternal group(5.62 ± 0.10) g didn’t have statistical significance(P> 0.05); at 8 weeks, body mass difference for diabetes complicating pregnancy paternal group(284.37 ± 31.21) g and diabetes complicating pregnancy maternal group(210.37 ± 6.71) g had statistical significance(P <0.05). Compared with diabetes complicating pregnancy paternal group and maternal group, at 8 weeks, Insulin level difference for for diabetes complicating pregnancy paternal group(20.04±0.7) mμ/l and diabetes complicating pregnancy maternal group(20.04±2.5) mμ/l had statistical significance(P<0.05). Triglyceride level difference for for diabetes complicating pregnancy paternal group(1.87±0.24) mmol/L and diabetes complicating pregnancy maternal group(2.31±0.60) mmol/L had statistical significance(P<0.05). Empty stomach blood glucose level difference for diabetes complicating pregnancy paternal group(4.81±0.94)mmol/L and diabetes complicating pregnancy maternal group(5.53±0.64) mmol/L didn’t have statistical significance(P>0.05). Leptin level difference for diabetes complicating pregnancy paternal group(0.67±0.08) μg/ L and diabetes complicating pregnancy maternal group(0.79±0.13) μg/ L didn’t have statistical significance(P>0.05). Compared with GDM paternal group and maternal group, at 8 weeks, Insulin level difference for for GDM paternal group(22.80±3.3)m μ/l and GDM maternal group(19.49±0.9) m μ/l had statistical significance(P<0.05). Triglyceride level difference for for GDM paternal group(1.71±0.11) mmol/L and GDM maternal group(1.90±0.42)mmol/L had statistical significance(P<0.05). Empty stomach blood glucose level difference for GDM paternal group(4.76±0.39) mmol/L and GDM maternal group(5.04±0.57)mmol/L had statistical significance(P>0.05). Leptin level difference for GDM paternal group(0.78±0.11)μg/L and GDM maternal group(0.75±0.10)μg/ L didn’t have statistical significance(P>0.05). In the diabetes complicating pregnancy paternal group, PPARGC1 A gene methylation level for paternal group was(0.52 ± 0.02) and for maternal group was(0.45± 0.02), m RNA expression level for paternal group was(0.59± 0.04) and for maternal group is(0.73 ± 0.11). In the GDM group, PPARGC1 A gene methylation level for paternal group was(0.35± 0.03) and for maternal group was(0.22 ± 0.02), m RNA expression level for paternal group was(1.36 ± 0.18) and for maternal group is(1.67 ± 0.10). All the differences had statistical significance(P<0.05). Conclusion: The glucose and lipid metabolism disorders for offspring of diabetic rats may have differences between paternal and maternal, at the born period of GDM group and sexual maturity period of diabetes complicating pregnancy paternal group, the body mass differences for paternal groups were more significant than that for maternal groups, the triglyceride level metabolism disorder for diabetes complicating pregnancy maternal group and GDM maternal group were more significant than that for paternal groups. Metabolism disorders for offspring may be associated with intrauterine hyperglycemia environment. At the same time, metabolic abnormalities for offspring of diabetic rats during pregnancy may also be associated with high PPARGC1 A gene methylation, high PPARGC1 A gene methylation suppresses the m RNA expression, the metabolic regulation for offspring rats is affected, then causing metabolic abnormalities. |
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