PPARγ links maternal malnutrition and abnormal glucose and lipid metabolism in the offspring of mice.
Yi Chuan
; 37(1): 70-76, 2015 Jan.
Article
em En
| MEDLINE
| ID: mdl-25608816
ABSTRACT
Peroxisome proliferator-activated receptors (PPARs) are a group of nuclear receptor proteins that regulate gene transcription. PPARs play essential roles in modulating cell differentiation, development, and metabolism (carbohydrate, lipid, protein). Here, we investigated whether PPARγ plays a role in linking maternal malnutrition and aberrant metabolism in the offspring of mice. After feeding dams with high fat (HF) and low protein (LP) diet during pregnancy and lactation, we examined the effects on the offspring at weaning (age of 3-week). The results showed that the LP offspring had lower body weight and length than the control. The HF offspring had heavier body weight and longer body length than LP. The blood glucose levels in HF group were significantly higher at 30 min and 60 min after intraperitoneal glucose administration and the area under curve was also significantly larger than the control. The blood glucose levels in HF group were significantly higher at 30 min than LP. HF group had elevated total cholesterol levels and LP group had decreased total cholesterol levels compared with the control. All results were statistically significant as examined by t-test. More importantly, PPARγ expression levels detected by qRT-PCR were significantly increased in HF and LP groups compared with the control. In conclusion, maternal HF and LP diet during pregnancy and lactation can induce impaired glucose and lipid metabolism in the early life of mouse offspring, where PPARγ may play an important role.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Efeitos Tardios da Exposição Pré-Natal
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Fenômenos Fisiológicos da Nutrição Materna
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Desnutrição
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PPAR gama
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Metabolismo dos Lipídeos
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Glucose
Aspecto:
Determinantes_sociais_saude
Limite:
Animals
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Female
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Humans
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Male
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Pregnancy
Idioma:
En
Revista:
Yi Chuan
Assunto da revista:
GENETICA
Ano de publicação:
2015
Tipo de documento:
Article
País de afiliação:
China