Maternal high-fat feeding leads to alterations of brain glucose metabolism in the offspring: positron emission tomography study in a porcine model

Sanguinetti, Elena; Liistro, Tiziana; Mainardi, Marco; Pardini, S.; Salvadori, Piero A.; Vannucci, Alessandro; Burchielli, Silvia; Iozzo, Patricia

doi:10.1007/s00125-015-3848-5

Cited by 17 publications

(21 citation statements)

References 47 publications

(48 reference statements)

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“…In our model, brain response to INI in the offspring of HFDm was significantly greater at weaning and blunted (statistical significance reached only in 4 brain regions out of 11 examined) in adult age compared to controls. This is consistent with our previously published data showing that during peripheral insulin infusion in a hyperinsulinaemic-isoglycaemic clamp, brain glucose uptake in minipigs of HFD mothers was elevated in early life, and defective during young adulthood, being paralleled by cortical and hypothalamic expression of insulin receptors and insulin-sensitive glucose transporters 57 . The study suggested that the brain of animals born to obese sows was initially hypersensitive to insulin, and then became insulin resistant 57 .…”

Section: Discussionsupporting

confidence: 93%

Microbiota signatures relating to reduced memory and exploratory behaviour in the offspring of overweight mothers in a murine model

Sanguinetti

Guzzardi

Tripodi

et al. 2019

Sci Rep

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An elevated number of women of reproductive age are overweight, predisposing their offspring to metabolic and neuropsychiatric disorders. Gut microbiota is influenced by maternal factors, and has been implicated in the pathogenesis of neurodegenerative diseases. Our aim was to explore the effects of maternal high-fat feeding on the relationship linking gut microbiota and cognitive development in the offspring. Murine offspring born to dams undergoing normal diet (NDm) and high-fat diet (HFDm) were studied at 1 or 6 months of age to assess cognitive function by Y-maze test, cerebral glucose metabolism and insulin sensitivity by Positron Emission Tomography, brain density by Computed Tomography, microbiota profile (colon, caecum) and inferred metabolic pathways (KEGG analysis) by 16S ribosomal RNA sequencing. From 3 weeks post-weaning, mice born to HFDm developed hyperphagia and overweight, showing reduction in memory and exploratory behaviour, and brain insulin resistance in adulthood. We identified a panel of bacteria characterizing offspring born to HFD dams from early life, and correlating with dysfunction in memory and exploratory behaviour in adults (including Proteobacteria phylum, Parabacteroides and unclassified Rikenellaceae genera). Microbiota-derived metabolic pathways involved in fatty acid, essential aminoacid and vitamin processing, sulphur metabolism, glutaminergic activation and Alzheimer’s disease were differently present in the HFDm and NDm offspring groups. Our results document tight relationships between gut dysbiosis and memory and behavioural impairment in relation to maternal HFD. Persistent bacterial signatures induced by maternal HFD during infancy can influence cognition during adulthood, opening the possibility of microbiota-targeted strategies to contrast cognitive decline.

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Section: Discussionsupporting

confidence: 93%

Microbiota signatures relating to reduced memory and exploratory behaviour in the offspring of overweight mothers in a murine model

Sanguinetti

Guzzardi

Tripodi

et al. 2019

Sci Rep

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“…Maternal intake of a Western-style diet during pregnancy/lactation led to changes in microbiota profile, blood lipids, cognitive responses, and hippocampal neurogenesis in swine offspring ( 45 ). Recent work by Sanguinetti et al has also shown that maternal HF feeding results in marked alterations in brain glucose metabolism in offspring thus predisposing to metabolic-neurodegenerative diseases ( 46 – 48 ).…”

Section: Experimental Models Of Maternal Obesitymentioning

confidence: 99%

Experimental Models of Maternal Obesity and Neuroendocrine Programming of Metabolic Disorders in Offspring

2017

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Evidence from epidemiological, clinical, and experimental studies have clearly shown that disease risk in later life is increased following a poor early life environment, a process preferentially termed developmental programming. In particular, this work clearly highlights the importance of the nutritional environment during early development with alterations in maternal nutrition, including both under- and overnutrition, increasing the risk for a range of cardiometabolic and neurobehavioral disorders in adult offspring characterized by both adipokine resistance and obesity. Although the mechanistic basis for such developmental programming is not yet fully defined, a common feature derived from experimental animal models is that of alterations in the wiring of the neuroendocrine pathways that control energy balance and appetite regulation during early stages of developmental plasticity. The adipokine leptin has also received significant attention with clear experimental evidence that normal regulation of leptin levels during the early life period is critical for the normal development of tissues and related signaling pathways that are involved in metabolic and cardiovascular homeostasis. There is also increasing evidence that alterations in the epigenome and other underlying mechanisms including an altered gut–brain axis may contribute to lasting cardiometabolic dysfunction in offspring. Ongoing studies that further define the mechanisms between these associations will allow for identification of early risk markers and implementation of strategies around interventions that will have obvious beneficial implications in breaking a programmed transgenerational cycle of metabolic disorders.

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“…A recent study showed that maternal HFD resulted in an increase in the brain insulin receptors (IRβs) in offspring at birth followed by a long-term decrease in brain glucose uptake and expression of glucose transporter 4 and IRβ in minipigs, which may increase the offspring predisposition to metabolic-neurodegenerative diseases. [ 43 ] Our team also established the mouse model of maternal HFD during pregnancy and lactation and investigated the intergenerational effects of maternal overnutrition on offspring. Similarly, our results also verified that perinatal overnutrition (HFD) changed health and disease trajectory in offspring and significantly increased the risks of glucose and lipid metabolic disorders.…”

Section: Over-nutrition In Early Life and Energy Metabolism In Later mentioning

confidence: 99%

Early-life nutrition and metabolic disorders in later life: a new perspective on energy metabolism

Zhou

Deng

Zhang

et al. 2020

Chinese Medical Journal

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Type 2 diabetes mellitus and metabolic disorders have become an epidemic globally. However, the pathogenesis remains largely unclear and the prevention and treatment are still limited. In addition to environmental factors during adulthood, early life is the critical developmental window with high tissue plasticity, which might be modified by external environmental cues. Substantial evidence has demonstrated the vital role of early-life nutrition in programming the metabolic disorders in later life. In this review, we aim to overview the concepts of fetal programming and investigate the effects of early-life nutrition on energy metabolism in later life and the potential epigenetic mechanism. The related studies published on PubMed database up to March 2020 were included. The results showed that both maternal overnutrition and undernutrition increased the riskes of metabolic disorders in offspring and epigenetic modifications, including DNA methylation, miRNAs, and histone modification, might be the vital mediators. The beneficial effects of early-life lifestyle modifications as well as dietary and nutritional interventions on these deleterious metabolic remolding were initially observed. Overall, characterizing the early-life malnutrition that reshapes metabolic disease trajectories may yield novel targets for early prevention and intervention and provide a new point of view to the energy metabolism.

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Maternal high-fat feeding leads to alterations of brain glucose metabolism in the offspring: positron emission tomography study in a porcine model

Cited by 17 publications

References 47 publications

Microbiota signatures relating to reduced memory and exploratory behaviour in the offspring of overweight mothers in a murine model

Microbiota signatures relating to reduced memory and exploratory behaviour in the offspring of overweight mothers in a murine model

Experimental Models of Maternal Obesity and Neuroendocrine Programming of Metabolic Disorders in Offspring

Early-life nutrition and metabolic disorders in later life: a new perspective on energy metabolism

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