OBJECTIVES: Epidemiological and animal studies have shown that maternal obesity predisposes the offspring to obesity and the metabolic syndrome, possibly via late-onset metabolic programming of the fetus. Little is known, however, about the metabolic effect of maternal obesity on the fetus. This study investigated the effect of a maternal high-fat diet (HFD) on fetal growth and glucose metabolism using a diet-induced obesity mouse model. STUDY DESIGN: Female mice (6 weeks old; C57BL/6N) were fed either a normal chow diet (NCD, 10 kcal% fat) or an HFD (60 kcal% fat) for 4 weeks before mating and throughout pregnancy. At 17 days of gestation, gene expression of inflammatory markers and adipokines in fetal subcutaneous adipose tissue was analyzed by quantitative real-time polymerase chain reaction. RESULTS: HFD mice were overweight, glucose intolerant and insulin resistant compared with NCD mice of the same gestational age. Although fetal body weight was not significantly different, fetal plasma glucose and insulin levels were higher in the HFD group than the NCD group. Furthermore, examination of fetal subcutaneous adipose tissue in the HFD group revealed hypertrophy with an increase in the levels of cluster of differentiation-68, chemokine receptor-2 and tumor necrosis factor-α mRNA, but a decrease in the level of glucose transporter-4 mRNA. CONCLUSION: Maternal HFD causes inflammatory changes in the adipose tissue of offspring.
OBJECTIVES: Epidemiological and animal studies have shown that maternal obesity predisposes the offspring to obesity and the metabolic syndrome, possibly via late-onset metabolic programming of the fetus. Little is known, however, about the metabolic effect of maternal obesity on the fetus. This study investigated the effect of a maternal high-fat diet (HFD) on fetal growth and glucose metabolism using a diet-induced obesitymouse model. STUDY DESIGN: Female mice (6 weeks old; C57BL/6N) were fed either a normal chow diet (NCD, 10 kcal% fat) or an HFD (60 kcal% fat) for 4 weeks before mating and throughout pregnancy. At 17 days of gestation, gene expression of inflammatory markers and adipokines in fetal subcutaneous adipose tissue was analyzed by quantitative real-time polymerase chain reaction. RESULTS: HFD mice were overweight, glucose intolerant and insulin resistant compared with NCD mice of the same gestational age. Although fetal body weight was not significantly different, fetal plasma glucose and insulin levels were higher in the HFD group than the NCD group. Furthermore, examination of fetal subcutaneous adipose tissue in the HFD group revealed hypertrophy with an increase in the levels of cluster of differentiation-68, chemokine receptor-2 and tumor necrosis factor-α mRNA, but a decrease in the level of glucose transporter-4 mRNA. CONCLUSION: Maternal HFD causes inflammatory changes in the adipose tissue of offspring.
Authors: Matthew W Hale; Sarah J Spencer; Bruno Conti; Christine L Jasoni; Stephen Kent; Morgan E Radler; Teresa M Reyes; Luba Sominsky Journal: Neurosci Biobehav Rev Date: 2014-12-15 Impact factor: 8.989
Authors: Mina Desai; Juanita K Jellyman; Guang Han; Marie Beall; Robert H Lane; Michael G Ross Journal: Am J Obstet Gynecol Date: 2014-03-14 Impact factor: 8.661
Authors: Brianna F Moore; Katherine A Sauder; Anne P Starling; James R Hébert; Nitin Shivappa; Brandy M Ringham; Deborah H Glueck; Dana Dabelea Journal: J Pediatr Date: 2017-12-06 Impact factor: 4.406