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

Overview of attention for article published in Nutrition & Metabolism, June 2018
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  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (82nd percentile)
  • Above-average Attention Score compared to outputs of the same age and source (57th percentile)

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92 Mendeley
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Title
Maternal overnutrition by hypercaloric diets programs hypothalamic mitochondrial fusion and metabolic dysfunction in rat male offspring
Published in
Nutrition & Metabolism, June 2018
DOI 10.1186/s12986-018-0279-6
Pubmed ID
Authors

Robbi E. Cardenas-Perez, Lizeth Fuentes-Mera, Ana Laura de la Garza, Ivan Torre-Villalvazo, Luis A. Reyes-Castro, Humberto Rodriguez-Rocha, Aracely Garcia-Garcia, Juan Carlos Corona-Castillo, Armando R. Tovar, Elena Zambrano, Rocio Ortiz-Lopez, Jennifer Saville, Maria Fuller, Alberto Camacho

Abstract

Maternal 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. We 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. Maternal 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. We 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.

X Demographics

X Demographics

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 92 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 92 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 15 16%
Researcher 12 13%
Student > Ph. D. Student 12 13%
Student > Bachelor 9 10%
Other 5 5%
Other 13 14%
Unknown 26 28%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 17 18%
Medicine and Dentistry 11 12%
Neuroscience 10 11%
Agricultural and Biological Sciences 5 5%
Nursing and Health Professions 4 4%
Other 11 12%
Unknown 34 37%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 12. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 27 October 2023.
All research outputs
#2,964,084
of 24,696,958 outputs
Outputs from Nutrition & Metabolism
#292
of 996 outputs
Outputs of similar age
#58,622
of 335,282 outputs
Outputs of similar age from Nutrition & Metabolism
#7
of 14 outputs
Altmetric has tracked 24,696,958 research outputs across all sources so far. Compared to these this one has done well and is in the 87th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 996 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 27.6. This one has gotten more attention than average, scoring higher than 70% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 335,282 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 82% of its contemporaries.
We're also able to compare this research output to 14 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 57% of its contemporaries.