Lean maternal hyperglycemia alters offspring lipid metabolism and susceptibility to diet-induced obesity in mice†

Talton, Omonseigho O.; Bates, Keenan; Salazar, Shirley Rojas; Ji, Tieming; Schulz, Laura C.

doi:10.1093/biolre/ioz009

Cited by 14 publications

(15 citation statements)

References 93 publications

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“…In a mouse model of GDM, maternal GDM had no long-lasting effects on offspring weight as long as they were maintained on a control diet; however, when they were fed a high fat and high sugar diet (HFHS), the weight of offspring from GDM dams was significantly elevated in comparison to control animals. Interestingly, although increased adiposity was observed in GDM-exposed offspring of both sexes at 4, 12 and 20 weeks of age, adult offspring (31 weeks) exhibited increased adiposity only if they were fed with a HFHS [66]. These data are in agreement with numerous previous studies suggesting that critical phases in the process of developmental programming are conditions influencing both prenatal and postnatal life.…”

Section: Do the Epigenetic Changes Acquired Due To Maternal Gdm Expossupporting

confidence: 91%

Gestational Diabetes Mellitus Affects Offspring’s Epigenome. Is There a Way to Reduce the Negative Consequences?

2020

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Gestational diabetes mellitus (GDM) is the most common pregnancy complication worldwide and may result in short-term and long-term consequences for offspring. The present review highlights evidence of epigenetic programming, mostly from human studies, which occurs in offspring exposed to maternal GDM during different stages of development, paying special attention to the differences in sensitivity of offspring to maternal hyperglycemia as a result of sex-related factors. We also aim to answer the following question: If these epigenetic changes are constant throughout the lifetime of the offspring, how do they present phenotypically?

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Section: Do the Epigenetic Changes Acquired Due To Maternal Gdm Expossupporting

confidence: 91%

Gestational Diabetes Mellitus Affects Offspring’s Epigenome. Is There a Way to Reduce the Negative Consequences?

2020

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Section: Discussionmentioning

confidence: 79%

“…Our finding that exposure to maternal GDM was associated with an adverse lipid profile that is likely related to the occurrence of perturbed maternal lipid metabolism in the context of gestational hyperglycaemia, 41 which in turn, may affect offspring lipid metabolism. 42 Mechanistic pathways are difficult to disentangle in humans, but animal models indicate an impact of maternal hyperglycaemia on hepatic lipid content and metabolism through oxidative stress and inflammatory pathways. 43 Although we adjusted for pubertal status in multivariable analyses, the female-specific nature of the relationship between exposure to maternal GDM and offspring lipid profile may be related to unmeasured confounding by tempo of sexual maturation (which exists on a spectrum that is likely not wholly captured by discrete Tanner staging) given recent findings that GDM-exposed girls undergo puberty earlier than their male counterparts.…”

Section: Girlsmentioning

confidence: 99%

In utero exposure to gestational diabetes mellitus and cardiovascular risk factors in youth: A longitudinal analysis in the EPOCH cohort

et al. 2020

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Summary Objective To examine associations of maternal gestational diabetes mellitus (GDM) with offspring cardiovascular biomarkers from late childhood through adolescence. Methods We used mixed effects linear regression models to examine associations of maternal GDM (n = 92 cases of 597) with average offspring levels of serum lipids (total cholesterol, high‐density lipoprotein [HDL], low‐density lipoprotein [LDL], and triglycerides) and systolic blood pressure (SBP) across two research visits spanning approximately 10.6 and 16.9 years of age. In sex‐stratified analysis, we evaluated the impact of adjustment for sociodemographic characteristics, pubertal status, physical activity and total energy intake, maternal body mass index (BMI), GDM treatment, and child's BMI. Results After adjusting for child's age, pubertal status, race/ethnicity, and maternal education and smoking, GDM exposure was associated with higher total (0.38 [95% CI, 0.16‐0.61] mmol/L) and LDL cholesterol (0.34 [95% CI, 0.14‐0.53] mmol/L) in girls. These estimates were robust to adjustment for lifestyle characteristics and maternal BMI but were attenuated after accounting for GDM treatment with no appreciable change following further adjustment for current BMI. In boys, maternal GDM corresponded with 4.50 (1.90‐7.10) mmHg higher SBP. This association persisted after accounting for sociodemographic/lifestyle characteristics, maternal BMI, and GDM treatment but was attenuated after adjusting for current BMI. Conclusions Maternal GDM is related to offspring lipid profile and SBP in a sex‐specific manner.

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Section: Animal Procedures and Tissue Collectionmentioning

confidence: 99%

“…Ovarian tissue utilized in this study was obtained as part of a larger study [42]. Briefly, gestational diabetes was induced in female C57B16/J mice (n = 14) by feeding a high fat, high sucrose (HFHS; 45% kcal/fat (lard and soybean oil) and 17% kcal/sucrose) diet (D12451, Research Diets, Inc) one week prior to mating and for the duration of gestation, for a total of 4 weeks as described [41,42]. Control female C57B16/J mice (Jackson Laboratories; n = 20) were fed a chow breeder diet (17% kcal/fat (lard) and 2.4% kcal/sucrose; LabDiet 5008, Purina) throughout the duration of the study.…”

Section: Animal Procedures and Tissue Collectionmentioning

confidence: 99%

Developmental origins of ovarian disorder: impact of maternal lean gestational diabetes on the offspring ovarian proteome in mice†

Clark

Talton

Ganesan

et al. 2019

Biology of Reproduction

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Gestational diabetes mellitus (GDM) is an obstetric disorder affecting approximately 10% of pregnancies. The four high-fat, high-sucrose (HFHS) mouse model emulates GDM in lean women. Dams are fed a HFHS diet 1 week prior to mating and throughout gestation resulting in inadequate insulin response to glucose in mid-late pregnancy. The offspring of HFHS dams have increased adiposity, thus, we hypothesized that maternal metabolic alterations during lean GDM would compromise ovarian function in offspring both basally and in response to a control or HFHS diet in adulthood. Briefly, DLPL were lean dams and control diet pups; DLPH were lean dams and HFHS pups; DHPL were HFHS dams and control diet pups; and DHPH were HFHS dams and HFHS pups. A HFHS challenge in the absence of maternal GDM (DLPL vs. DLPH) increased 3 and decreased 30 ovarian proteins. Maternal GDM in the absence of a dietary stress (DLPL vs. DHPL) increased abundance of 4 proteins and decreased abundance of 85 proteins in the offspring ovary. Finally, 87 proteins increased, and 4 proteins decreased in offspring ovaries due to dietary challenge and exposure to maternal GDM in utero (DLPL vs. DHPH). Canopy FGF signaling regulator 2, deleted in azoospermia-associated protein 1, septin 7, and serine/arginine-rich splicing factor 2 were altered across multiple offspring groups. Together, these findings suggest a possible impact on fertility and oocyte quality in relation to GDM exposure in utero as well as in response to a western diet in later life.

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Lean maternal hyperglycemia alters offspring lipid metabolism and susceptibility to diet-induced obesity in mice†

Cited by 14 publications

References 93 publications

Gestational Diabetes Mellitus Affects Offspring’s Epigenome. Is There a Way to Reduce the Negative Consequences?

Gestational Diabetes Mellitus Affects Offspring’s Epigenome. Is There a Way to Reduce the Negative Consequences?

In utero exposure to gestational diabetes mellitus and cardiovascular risk factors in youth: A longitudinal analysis in the EPOCH cohort

Developmental origins of ovarian disorder: impact of maternal lean gestational diabetes on the offspring ovarian proteome in mice†

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