Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add filters








Type of study
Year range
1.
Acta Laboratorium Animalis Scientia Sinica ; (6): 6-11, 2014.
Article in Chinese | WPRIM | ID: wpr-455986

ABSTRACT

Objective Maternal dietary modifications determine the susceptibility to metabolic diseases in adult life.However, whether maternal high-fat diet can induce early-onset aberrant glucose and lipid metabolism in offspring mice is less understood .Materials and Methods We examined the effects of feeding the pregnant mice with either a high fat diet or nornal chow diet throughout pregnancy and lactation on the glucose and lipid metabolism in their offsprings . Some glucose and lipid metabolism biomarkers and hepatic histology were analyzed .Results At weaning, for males of dams fed high-fat diet , they had heavier body weight , the blood glucose levels were significantly higher at 30 min ( P<0.001) and 60 min (P<0.01) after intraperitoneal glucose administration , and the AUC was also significantly larger (P=0.0016) and HOMA-IR was higher(P<0.05).For females of dams fed high-fat diet, they had higher blood glucose levels at 30 min ( P<0.01 ) after intraperitoneal glucose administration .No significant differences were observed of AUC and HOMA-IR.Both males and females of dams fed high-fat diet had elevated total cholesterol levels ( P<0.0001 and P=0.0004, respectively).Triglyceride levels showed no significant differences between the two groups of males and females . The offsprings of high-fat diet group indicated hepatic steatosis and there were no differences between males and females . Conclusions Maternal high fat diet during pregnancy and lactation can induce early -onset aberrant glucose and lipid me-tabolism in offspring mice , and the male offsprings are more prone to metabolic changes , such as obesity , glucose intoler-ance and insulin resistance .

2.
Rio de Janeiro; s.n; 2010. 85 p. ilus.
Thesis in Portuguese | LILACS | ID: lil-665409

ABSTRACT

A dieta hiperlipídica (high-fat, HF) materna durante a gestação e/ou lactação aumenta a susceptibilidade da prole para o desenvolvimento de doenças crônicas na fase adulta. Verificar a hipótese que a ingestão materna de dieta HF nos períodos críticos de desenvolvimento (gestação e/ou lactação) predispõe à doença não alcoólica do fígado gorduroso e alterações pancreáticas e no tecido adiposo de camundongos machos adultos. Camundongos C57BL/6 fêmeas receberam durante a gestação e/ou lactação dieta padrão (standard chow, SC) ou HF. Filhotes machos foram divididos em cinco grupos: SC - provenientes de mães SC; G - provenientes de mães HF durante a gestação; L - provenientes de mães HF durante a lactação; GL/HF - provenientes de mães HF durante a gestação/lactação, mantendo a mesma dieta HF no período pós-natal (do desmame aos 3 meses de idade); GL - provenientes de mães HF durante a gestação/lactação trocando a dieta para SC no período pós-natal (do desmame aos 3 meses de idade). Foi analisada ao longo do experimento a massa corporal da prole. No sacrifício (3 meses), o fígado, o pâncreas e a gordura epididimária foram removidos, pesados e processados e o sangue foi coletado para análise bioquímica. Ao nascimento e ao desmame, filhotes GL/HF foram mais pesados (+6% e +44%, p<0,05, respectivamente) que os filhotes SC. Os filhotes G apresentaram resistência à insulina e menor expressão do transportador de glicose no fígado (GLUT-2). A esteatose hepática foi observada nos grupos G, L, GL e principalmente nos filhotes do grupo GL/HF. A expressão hepática da proteína ligante de elementos regulatórios de esteróis (SREBP-1c) estava aumentada nos filhotes G, GL e GL/HF. Os filhotes G, GL e GL/HF apresentaram hipertrofia da ilhota pancreática e dos adipócitos quando comparados com o grupo SC. O consumo de dieta HF durante a gestação mostra-se ser o período mais prejudicial para os filhotes adultos de camundongos. A programação metabólica por dieta HF ...


Maternal high-fat diet (HF) during gestation and/or lactation period increases the susceptibility to development of chronic disease in offspring adult life. This work aimed to verify the hypothesis that maternal intake of high-fat diet in critical periods of pregnancy and/or suckling period predisposes to non alcoholic fatty liver disease, pancreatic and adipose tissue alterations in adulthood mice offspring. C57BL/6 female mice were fed, during gestation and/or lactation phases, with standard chow (SC) of HF diet. Male pups were divided into 5 groups: SC - from SC fed dam; G - from HF fed dam during gestation period; L - from HF fed dam during lactation period; GL - from HF fed dam during gestation and lactation periods and GL/HF - from HF fed dam during gestation and lactation, maintaining HF diet from post-weaning to adulthood. We analyzed body mass in all experiment, and at the euthanasia (3 mo-old), liver, pancreas and adipose tissue were removed, weighted and embedded. Blood was collected to biochemical analyses. At birth and at weaning, GL/HF pups were heavier than SC pups (+6% and +44%, p<0.05, respectively). G offspring showed insulin resistance and lower glucose transporter-2 expression (GLUT-2). Hepatic steatosis was present in G, L, GL and mainly in GL/HF offspring. Sterol regulatory element-binding protein-1c (SREBP-1c) expression was higher in G, GL and GL/HF offspring. It is important to mention that pancreatic islet hyperthophy and adipocyte hypertrophy were affected in G, GL and GL/HF offspring in comparison to SC. HF diet administration during gestation period is worse than lactation period. Furthermore, this type of programming by HF predisposes to adverse remodeling in liver, pancreas and adipose tissue in adult mice offspring


Subject(s)
Animals , Male , Female , Pregnancy , Mice , Dietary Fats/adverse effects , Dietary Fats/metabolism , Maternal Nutritional Physiological Phenomena , Prenatal Exposure Delayed Effects/physiopathology , Prenatal Exposure Delayed Effects/metabolism , Fatty Liver/physiopathology , Liver Diseases/etiology , Pancreas/physiopathology , Adipose Tissue/physiopathology
SELECTION OF CITATIONS
SEARCH DETAIL