ArticleNutrition & metabolism2018
Maternal overnutrition by hypercaloric diets programs hypothalamic mitochondrial fusion and metabolic dysfunction in rat male offspring.
Article in Nutrition & metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
- Tert-Butylhydroquinone Reversed Age-Dependent Hypothalamic Mitochondrial Dysfunction Linking Maternal Fructose Exposure to Synaptic Vulnerability.Molecular neurobiology · 2026Article
- Mitochondrial Dysfunction: A Critical Link Between Maternal Diet and Offspring Metabolic Health.Biomolecules · 2026Review
- Maternal Programming with a Cafeteria Diet Leads to Glucose Intolerance, Increased Insulinemia, Inflammation, and Intestinal Dysbiosis in Rat Offspring.Preventive nutrition and food science · 2026Article
- Maternal Obesity in Pregnancy: Risk Factor for Neurodevelopmental Outcomes in Offspring.Journal of neurochemistry · 2025Review
- Prevention of Hepatalin-Dependent Insulin Resistance Induced by a High Sucrose Diet Using a Synergistic Combination of S-Adenosyl Methionine, Vitamin E and Vitamin C (SAMEC) in Virgin and Pregnant Sprague Dawley Rats.Journal of experimental pharmacology · 2025Article
- Maternal Supplementation withDiseases (Basel, Switzerland) · 2024Article
- Gene expression alterations of purinergic signaling components in obesity-associated intestinal low-grade inflammation in type 2 diabetes.Purinergic signalling · 2024Article
- Article
- Swimming training prevents obesity installation and normalizes hypothalamic expressions of GLP1 and leptin receptors in adult offspring born in small litters.Einstein (Sao Paulo, Brazil) · 2024Article
- Article
- Review
- Maternal methyl donor supplementation regulates the effects of cafeteria diet on behavioral changes and nutritional status in male offspring.Food & nutrition research · 2023Article
- Emerging role of hypothalamus in the metabolic regulation in the offspring of maternal obesity.Frontiers in nutrition · 2023Review
- Article
- Female and male C57BL/6J offspring exposed to maternal obesogenic diet develop altered hypothalamic energy metabolism in adulthood.American journal of physiology. Endocrinology and metabolism · 2022Article
- MCP-1 Signaling Disrupts Social Behavior by Modulating Brain Volumetric Changes and Microglia Morphology.Molecular neurobiology · 2022Article
- Animal Foetal Models of Obesity and Diabetes - From Laboratory to Clinical Settings.Frontiers in endocrinology · 2022Review
- Mothers' cafeteria diet induced sex-specific changes in fat content, metabolic profiles, and inflammation outcomes in rat offspring.Scientific reports · 2021Article
- Article
- Maternal cafeteria diet exposure primes depression-like behavior in the offspring evoking lower brain volume related to changes in synaptic terminals and gliosis.Translational psychiatry · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 Ca
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.