Maternal obesity in mice not only affects fresh embryo quality but also aggravates injury due to vitrification

Ma, Wudi; Huang, Xiaodong; Yang, Xing; Liang, Xiaoyan

doi:10.1007/s10815-016-0790-5

Cited by 3 publications

(3 citation statements)

References 52 publications

(70 reference statements)

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“…Metabolic programming during maternal overnutrition and obesity leads to ER stress activation [ 13 , 14 , 31 , 51 , 52 ], and mitochondrial dysfunction in oocytes and embryos [ 14 , 20 ], and impairs hypothalamic glucose metabolism in male offspring [ 53 ]. It is known that mitochondrial dynamics is regulated by cellular bioenergetic demands [ 54 ].…”

Section: Discussionmentioning

confidence: 99%

Maternal overnutrition by hypercaloric diets programs hypothalamic mitochondrial fusion and metabolic dysfunction in rat male offspring

et al. 2018

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BackgroundMaternal overnutrition including pre-pregnancy, pregnancy and lactation promotes a lipotoxic insult leading to metabolic dysfunction in offspring. Diet-induced obesity models (DIO) show that changes in hypothalamic mitochondria fusion and fission dynamics modulate metabolic dysfunction. Using three selective diet formula including a High fat diet (HFD), Cafeteria (CAF) and High Sugar Diet (HSD), we hypothesized that maternal diets exposure program leads to selective changes in hypothalamic mitochondria fusion and fission dynamics in male offspring leading to metabolic dysfunction which is exacerbated by a second exposure after weaning.MethodsWe exposed female Wistar rats to nutritional programming including Chow, HFD, CAF, or HSD for 9 weeks (pre-mating, mating, pregnancy and lactation) or to the same diets to offspring after weaning. We determined body weight, food intake and metabolic parameters in the offspring from 21 to 60 days old. Hypothalamus was dissected at 60 days old to determine mitochondria-ER interaction markers by mRNA expression and western blot and morphology by transmission electron microscopy (TEM). Mitochondrial-ER function was analyzed by confocal microscopy using hypothalamic cell line mHypoA-CLU192.ResultsMaternal programming by HFD and CAF leads to failure in glucose, leptin and insulin sensitivity and fat accumulation. Additionally, HFD and CAF programming promote mitochondrial fusion by increasing the expression of MFN2 and decreasing DRP1, respectively. Further, TEM analysis confirms that CAF exposure after programing leads to an increase in mitochondria fusion and enhanced mitochondrial-ER interaction, which partially correlates with metabolic dysfunction and fat accumulation in the HFD and CAF groups. Finally, we identified that lipotoxic palmitic acid stimulus in hypothalamic cells increases Ca2+ overload into mitochondria matrix leading to mitochondrial dysfunction.ConclusionsWe concluded that maternal programming by HFD induces hypothalamic mitochondria fusion, metabolic dysfunction and fat accumulation in male offspring, which is exacerbated by HFD or CAF exposure after weaning, potentially due to mitochondria calcium overflux.

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Section: Discussionmentioning

confidence: 99%

Maternal overnutrition by hypercaloric diets programs hypothalamic mitochondrial fusion and metabolic dysfunction in rat male offspring

et al. 2018

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“…Human [119], mouse [145], rat [142], cattle [146], sheep [137], pig [143], rabbit [48], goat [22], dog [138], horse [130], buffalo [139] Early embryo Cattle [129] Early placenta or pregnant endometrium Human [147], rat [142], rabbit [48], dog [144], cat [148] IGFR-1…”

Section: Blastocystmentioning

confidence: 99%

Pluripotency and Growth Factors in Early Embryonic Development of Mammals: A Comparative Approach

Llobat

2021

Veterinary Sciences

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The regulation of early events in mammalian embryonic development is a complex process. In the early stages, pluripotency, cellular differentiation, and growth should occur at specific times and these events are regulated by different genes that are expressed at specific times and locations. The genes related to pluripotency and cellular differentiation, and growth factors that determine successful embryonic development are different (or differentially expressed) among mammalian species. Some genes are fundamental for controlling pluripotency in some species but less fundamental in others, for example, Oct4 is particularly relevant in bovine early embryonic development, whereas Oct4 inhibition does not affect ovine early embryonic development. In addition, some mechanisms that regulate cellular differentiation do not seem to be clear or evolutionarily conserved. After cellular differentiation, growth factors are relevant in early development, and their effects also differ among species, for example, insulin-like growth factor improves the blastocyst development rate in some species but does not have the same effect in mice. Some growth factors influence genes related to pluripotency, and therefore, their role in early embryo development is not limited to cell growth but could also involve the earliest stages of development. In this review, we summarize the differences among mammalian species regarding the regulation of pluripotency, cellular differentiation, and growth factors in the early stages of embryonic development.

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“…One of the main advantages from vitrification is the absence of crystallization that causes cell damage [4-7], whereas, in the other freezing methods, the crystallization occurs. To avoid crystallization damaging in the blastomere cell in the vitrification, this method needs the use of high concentration cryoprotectant [8,9].…”

Section: Introductionmentioning

confidence: 99%

The profiling of pre- and post-warming DNA in mouse embryos with microsatellite method

2018

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Aims:This research aimed to identify the deoxyribonucleic acid (DNA) profile and changes of post-warming embryo after being frozen with vitrification method using microsatellite method.Materials and Methods:This research examined the mouse embryo blastocysts that were divided into four groups: Post-warming living blastocyst, post-warming living blastocyst with half fragmented cell, post-warming dead blastocyst, and pre-freezing living blastocyst. The isolation sample applied phenol-chloroform method. After obtaining polymerase chain reaction results, all the samples of pre-freezing fresh embryo, post-warming living embryo, dead embryo, and degenerated embryo were then examined by single-strand conformation polymorphism (SSCP).Results:The amplification with D18mit14 primer was 100 bp and 150bp with D18mit87 primer, 150bp with D7mit22, and 300bp with D7mit25. The result of SSCP with D18mit14 primer showed that the blastocysts were fragmented and dead after warming process and formed into two DNA strand fragments, while the fresh embryos which passed freezing process did not form any fragment. D18mit87 primer SSCP indicated different fragments for each treatment. The result of SSCP using D7mit22 formed two different fragments for each treatment. While using D7mit25, the SSCP result formed some different fragments for each sample. Post-warming living embryo had similar ribbon to pre-freezing fresh embryo.Conclusion:D7mit222, D7mit25, and D18mit87 primers could be used as the aneuploidy marker on mouse embryos that were induced by post-warming process. The profile of living blastocyst, dead blastocyst, and post-warming fragmented blastocyst had different DNA tapes.

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Maternal obesity in mice not only affects fresh embryo quality but also aggravates injury due to vitrification

Cited by 3 publications

References 52 publications

Maternal overnutrition by hypercaloric diets programs hypothalamic mitochondrial fusion and metabolic dysfunction in rat male offspring

Maternal overnutrition by hypercaloric diets programs hypothalamic mitochondrial fusion and metabolic dysfunction in rat male offspring

Pluripotency and Growth Factors in Early Embryonic Development of Mammals: A Comparative Approach

The profiling of pre- and post-warming DNA in mouse embryos with microsatellite method

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